Combination of Modafinil and an Ampakine for Improving Cognition Field of the invention The present invention is directed to treating or ameliorating cognitive deficit as for example observed in (amnestic) mild cognitive impairment/early stages (i.e., mild and moderate stages) of established Alzheimer’s Disease (AD) or in age-related cognitive decline or in dementia by a combination of modafinil (including enantiomers, in particular armodafinil) and an ampakine, wherein these two actives are administered in a specifically timed administration regimen based on the PK profiles of the actives used. In certain embodiments, the present invention is directed to a method of treating or preventing diseases or disorders associated with cognitive deficit in a subject (e.g., an elderly human). One embodiment provides that the cognitive deficit is associated with AD pathology. Background of the invention Cognitive deficit is a major challenge in modern society, in particular in a society comprising increasing numbers of older people. There are typical forms of cognitive deficit, such as mild cognitive impairment (MCI) or a specific subtype of MCI, namely “amnestic MCI” or “aMCI”, which is frequently seen in the early stages of established Alzheimer's disease (AD). The use of modafinil in connection with the treatment of AD, but also in connection with hypersomnia, depression, dementia, and loss of memory, has been reported. When it comes to AD, an effect on the cognitive function impaired by AD upon the administration of modafinil has not been described. Modafinil has been approved by the United States Food and Drug Administration (FDA) for use in the treatment of narcolepsy. WO 01/58439 A1 discloses that modafinil is known to provide wake-promoting activity. WO 01/58439 further discloses novel compositions of modafinil that are effective at improving cognitive function in aged rats to levels comparable to young controls at doses much lower than the approved doses known to promote wakefulness. WO 2008/086483 A2 discloses methods for treating diseases and conditions of the central and peripheral nervous system by stimulating or increasing neurogenesis by use of modafinil or a prodrug thereof, optionally in combination with a neurogenic agent with activity to stimulate or activate the formation of new nerve cells. Although there are drugs available for the treatment of established AD, there are currently only a few treatments for early AD and none approved for MCI or age-related cognitive decline. Active agents for use in AD include acetylcholinesterase inhibitors and, possibly, memantine. However, these active agents thus far do not show the desired efficacy and there is accordingly a need for a more potent treatment of cognitive deficit. Summary of the Invention The present invention is based on the finding that the combination of two active pharmaceutical ingredients (APIs or actives), namely of modafinil and an ampakine, addresses and improves at least one, preferably simultaneously at least two or all three sub- domains affected in cognitive deficit, more specifically affected in MCI including amnestic MCI (aMCI), AD, in age related cognitive decline or in dementia. In a first aspect, the present invention is directed to modafinil or an enantiomer thereof, or a pharmaceutically acceptable salt thereof, in combination with an ampakine or a pharmaceutically acceptable salt thereof, for use in the treatment of cognitive deficit, wherein the modafinil or enantiomer thereof, or pharmaceutically acceptable salt thereof, and the ampakine or pharmaceutically acceptable salt thereof, are administered such that the onset of the effect of modafinil or enantiomer thereof, or pharmaceutically acceptable salt thereof, is established before the onset of the effect of the ampakine or pharmaceutically acceptable salt thereof is established. In doing so, the Executive Function (EF) will be boosted first, followed by (shortly thereafter or even simultaneously) a boost of the Episodic Memory (EM). Since the enantiomers of modafinil are included as well, the present invention is directed to modafinil, to armodafinil, which is the R-enantiomer of modafinil, to the S-enantiomer of modafinil, or to a pharmaceutically acceptable salt of any of those, in combination with an ampakine or a pharmaceutically acceptable salt thereof, for use in the treatment of cognitive deficit. In one embodiment of the first aspect, the cognitive deficit is mild cognitive impairment (MCI). It can be preferred that the mild cognitive impairment is amnestic mild cognitive impairment (aMCI). It can further be preferred that the amnestic mild cognitive impairment is an early stage of Alzheimer’s disease (AD), in particular a mild or moderate stage of established Alzheimer’s disease. In another embodiment of the first aspect, the cognitive deficit is age-induced cognitive deficit. In another embodiment of the first aspect, the disease or disorder associated with cognitive deficit is dementia. As outlined in detail below, the present invention is to provide a boost of Executive Function (EF) and – as soon as this boost of Executive Function (EF) is established – to provide also a boost in Episodic Memory (EM). It is preferred that these two boosts are – after the EF-boost has been established first and shortly thereafter (or even simultaneously) the EM-boost has been established – provided simultaneously at least for some time. The effect of modafinil or enantiomer thereof, or pharmaceutically acceptable salt thereof is the provision of a boost of Executive Function (EF). The effect of the ampakine or pharmaceutically acceptable salt thereof is the provision of a boost in Episodic Memory (EM). In order to provide for the timed onset of the two effects, it is important to take into account that the time to the onset of effect of the ampakine depends on the particular ampakine or pharmaceutically acceptable salt thereof that is used in combination with the modafinil or enantiomer thereof, or pharmaceutically acceptable salt thereof. Accordingly, depending on the onset time of the particular ampakine or pharmaceutically acceptable salt thereof that is used, 1) modafinil or an enantiomer thereof, or a pharmaceutically acceptable salt thereof, may be administered first followed by the administration of the ampakine or pharmaceutically acceptable salt thereof, or 2) the ampakine or pharmaceutically acceptable salt thereof may be administered first followed by the administration of modafinil or enantiomer thereof, or pharmaceutically acceptable salt thereof. In case of 1), the time it takes for the modafinil (preferably upon oral administration) to have the desired effect, i.e. the onset time, is longer than the time it takes for the specific ampakine (preferably upon oral administration) to have the desired effect. Since the effect of the modafinil must be established (shortly) before the effect of the ampakine is established, the modafinil will be administered first. In case of 2), the time it takes for the modafinil (preferably upon oral administration) to have the desired effect, i.e. the onset time, is shorter than the time it takes for the specific ampakine (preferably upon oral administration) to have the desired effect. Since the effect of the modafinil must be established (shortly) before the effect of the ampakine is established, the ampakine will in this situation be administered first to make sure that the time in between the onset of the effect of the modafinil and the onset of the effect of the specific ampakine will be short, thus ensuring that the time where the effects of the two actives are overlapping is as long as possible. A skilled person is well-aware that pharmacokinetics (PK) describes drug concentration-time courses in body fluids resulting from administration of a certain drug dose. Further, the skilled person knows that pharmacodynamics (PD) describes the effect resulting from a certain drug concentration. PK/PD modeling is a known tool to link PK and PD in order to establish and evaluate dose-concentration-response relationships and thereby describe and predict the effect-time courses resulting from a drug dose. The skilled person is well aware that certain parameters do have an influence in particular on the PK of an API, such as particularly the age of a patient as well as whether or not food is present when orally administering the API (known as “food effect”). It might thus take longer in an elderly person until the effect of an active is established. Also, of course depending on the particular active, food may prolong the time until the effect of the particular active is established. Thus, depending on the circumstances, it might be necessary to add some time until the onset of the effect of an active is achieved. This in turn will have an influence on the staggering in time for the two actives used, i.e. the modafinil or enantiomer thereof, or pharmaceutically acceptable salt thereof and the ampakine or pharmaceutically acceptable salt thereof. Given the above, the skilled person can establish a suitable order and timing of administration for any ampakine that is used in the present invention, preferably for any low impact ampakine, even more preferably for aniracetam, CX516, CX691, CX717, CX1632, or CX1739, including pharmaceutically acceptable salts thereof, in view of and relative to the administration of modafinil or an enantiomer thereof, or a pharmaceutically acceptable salt thereof, in order to provide for the effect mentioned above, namely that the EF is boosted first by the modafinil or enantiomer thereof, or pharmaceutically acceptable salt thereof, before the EM is shortly thereafter or preferably simultaneously boosted by the ampakine or pharmaceutically acceptable salt thereof. The order and timing of administration for aniracetam or a pharmaceutically acceptable salt thereof as the ampakine in combination with modafinil is outlined in the following embodiment, and this order and timing is a result of the PK and PD data for aniracetam as well as for modafinil. Thus, according to one embodiment, the ampakine or pharmaceutically acceptable salt thereof is aniracetam or a pharmaceutically acceptable salt thereof. In this embodiment, the modafinil or an enantiomer thereof, or a pharmaceutically acceptable salt thereof, is administered first followed by the administration of aniracetam or a pharmaceutically acceptable salt thereof, wherein the time in between the two administrations ranges from about 70 minutes to about 110 minutes. In a certain embodiment, the time in between the two administrations ranges from about 80 to about 100 minutes, such as e.g. from about 85 minutes to about 95 minutes or from about 80 minutes to about 90 minutes. A particular embodiment provides that the time is about 85 minutes. In another embodiment, the time is 85 minutes. The afore-mentioned administration scheme in particular applies for elderly patients. For younger patients (i.e. patients of 65 years of age or older), the time in between the two administrations may range from about 80 minutes to about 120 minutes. Certain embodiments provide that the time in between the two administrations ranges from about 90 to about 110 minutes, such as e.g. from about 95 minutes to about 105 minutes or from about 90 minutes to about 100 minutes. A particular embodiment provides that the time is about 95 minutes or about 100 minutes. One example provides that the time is 95 minutes or 100 minutes. Since a food effect is known for modafinil, which delays the onset of action of modafinil for about thirty minutes, and since a slight food effect is known for aniracetam, which delays the onset of action of aniracetam for about 5 minutes, the administration scheme may differ in fed patients: in fed patients, the time in between the two administrations may range from about 100 minutes to about 140 minutes. Certain embodiments provide that the time in between the two administrations ranges from about 110 to about 130 minutes, such as e.g. from about 120 minutes to about 130 minutes. One instance provides that the time is about 130 minutes, more specifically, 130 minutes. According to a certain embodiment of the present invention, the modafinil or enantiomer thereof, or pharmaceutically acceptable salt thereof, and the ampakine or pharmaceutically acceptable salt thereof, are administered in the form of separate dosage forms, wherein separate oral dosage forms are particularly preferred. One specific embodiment of the present invention provides that modafinil or the R- enantiomer of modafinil, namely armodafinil, or pharmaceutically acceptable salts thereof, are used. In another embodiment of the present invention, the ampakine is a low-impact ampakine. The suitable ampakine includes, but is not limited to, aniracetam, CX516, CX691, CX717, CX1632, CX1739, and mixtures thereof. In certain embodiments, one of aniracetam, CX717 and CX1739is employed in the invention. A suitable single dose of modafinil may be in the range of about 50 mg to about 800 mg or in the range of about 100 mg to about 400 mg or preferably in the range of about 150 mg to about 250 mg. A most suitable single dose of modafinil may be about 200 mg. This dose preferably refers to the daily dose. In one embodiment, this daily dose is given once daily. One example provides that modafinil is administered at about 200 mg once daily, in the form of an oral dosage form. In a certain embodiment of the invention, armodafinil is administered. A suitable single dose of armodafinil may be in the range of about 50 mg to about 800 mg or in the range of about 100 mg to about 400 mg or preferably in the range of about 150 mg to about 250 mg. One instance provides a single dose of armodafinil at about 200 mg. This dose may refer to the daily dose. In one embodiment, this daily dose is given once daily. One embodiment of the invention provides that armodafinil is administered about 200 mg once daily, in the form of an oral dosage form. A suitable single dose of aniracetam may be in the range of about 500 mg to about 2500 mg or in the range of about 750 mg to about 2250 mg or in the range of about 1000 mg to about 2000 mg. A certain embodiment provides that a single dose of aniracetam at about 1500 mg. This dose may refer to the daily dose. One embodiment of the invention provides that this daily dose is given once daily. Accordingly, aniracetam is administered about 1500 mg once daily, in the form of an oral dosage form. Certain embodiments provide that the combination of the present invention is administered to elderly patients suffering from cognitive deficit, i.e. patients of 65 years of age or older. In another embodiment, the elderly patients suffer from cognitive deficit associated with AD pathology. Typically, the combination of the two actives of the present invention will be administered over a period of days, weeks, months or even years. It is known that modafinil has an elimination half-life generally in the 10-12 hours range, that armodafinil has an elimination half-life of about 13 hours, and that aniracetam has a half-life of about 0.5 hours. Accordingly, the boost of EM caused by the onset of action of aniracetam might be short while the boost of EF caused by the onset of action of modafinil or armodafinil might last rather long. This means, however, that also the simultaneous boost of EF and EM may be rather short in case the ampakine is aniracetam. It is therefore within the ambit of the present invention that a second dose of aniracetam might be given after a suitable time, e.g. one hour, after the first dose, optionally a third, fourth, or fifth dose, wherein each further dose is given e.g. one hour after the dose given before. In one embodiment, the modafinil or an enantiomer thereof (e.g., armodafinil), or a pharmaceutically acceptable salt thereof, and the ampakine or a pharmaceutically acceptable salt thereof are administered orally. In a second aspect, the present invention relates to a kit comprising - a first dosage form comprising modafinil or an enantiomer thereof, or a pharmaceutically acceptable salt thereof; and a second dosage form comprising an ampakine or a pharmaceutically acceptable salt thereof. Certain embodiments provide that the kit further includes instructions for administration of the dosage forms contained therein for treating or preventing a specific disease or disorder associated with cognition deficit in a subject (e.g., a human patient). In one embodiment, the subject is an elderly patient suffering from aMCI, MCI, mild or moderate AD, or dementia. In one embodiment of the second aspect, modafinil or a pharmaceutically acceptable salt thereof, or the R-enantiomer of modafinil, namely armodafinil, or a pharmaceutically acceptable salt thereof, is comprised in the first dosage form. In another embodiment of the second aspect, the ampakine comprised in the second dosage form is a low-impact ampakine. One embodiment provides that the ampakine comprised in the second dosage form is selected from the group consisting of aniracetam, CX516, CX691, CX717, CX1632, CX1739, and mixtures thereof. A separate embodiment provides that the ampakine comprised in the second dosage form is selected from the group consisting of aniracetam, CX717 and CX1739. In yet another embodiment of the second aspect, both the first and the second dosage form are oral dosage forms. In another embodiment of the second aspect, the first dosage form and the second dosage form are once-a-day dosage forms, i.e. they are administered once daily. In particular embodiments of the second aspect, the kit comprises - a first dosage form comprising a pharmaceutically effective amount of modafinil or an enantiomer or a pharmaceutically acceptable salt thereof; - a second dosage form comprising a separate pharmaceutically effective amount of aniracetam or a pharmaceutically acceptable salt thereof, and - instructions for administration to treat or prevent diseases or disorders associated with cognition deficit (such as, aMCI, MCI, dementia, mild or moderate AD) in a subject. One embodiment provides that the first dosage form and the second dosage forms are both oral dosage forms. In another embodiment of the second aspect, the first dosage form comprises from about 50 mg to about 800 mg, preferably from about 100 mg to about 400 mg, more preferably from about 150 mg to about 250 mg modafinil or a pharmaceutically acceptable salt thereof. A particular suitable amount of modafinil or a pharmaceutically acceptable salt thereof is about 200 mg. The afore-mentioned amounts apply for armodafinil or a pharmaceutically acceptable salt thereof as well. In another embodiment of the second aspect, the second dosage form comprises aniracetam or a pharmaceutically acceptable salt thereof as the ampakine in an amount of from about 500 mg to about 2500 mg, preferably from about 750 mg to about 2250 mg, more preferably from about 1000 mg to about 2000 mg. A particular suitable amount of aniracetam or a pharmaceutically acceptable salt thereof, is about 1500 mg. In yet another embodiment of the second aspect, the first dosage form comprises modafinil or a pharmaceutically acceptable salt thereof in an amount of about 200 mg, whereas the second dosage form comprises aniracetam or a pharmaceutically acceptable salt thereof as the ampakine in an amount of about 1500 mg. For the second aspect, it is understood that the timing of the administration of the first dosage form and the second dosage form is of course in accordance with the specific timely sequence of administration as described herein. In a third aspect, the present invention relates to a dosage form comprising modafinil or an enantiomer thereof, or a pharmaceutically acceptable salt thereof; and an ampakine or a pharmaceutically acceptable salt thereof. In one embodiment of the third aspect, modafinil or a pharmaceutically acceptable salt thereof or the R-enantiomer of modafinil, namely armodafinil, or a pharmaceutically acceptable salt thereof, is comprised in the dosage form. In another embodiment of the third aspect, the ampakine comprised in the dosage form is a low-impact ampakine. It can be preferred that the ampakine comprised in the dosage form is selected from the group consisting of aniracetam, CX516, CX691, CX717, CX1632, CX1739, and mixtures thereof. It can be even more preferred that the ampakine comprised in the dosage form is selected from the group consisting of aniracetam, CX717 and CX1739. In yet another embodiment of the third aspect, the dosage form is an oral dosage form. In another embodiment of the third aspect, the dosage form is a once-a-day dosage form, i.e. it is administered once daily. In another embodiment of the third aspect, the dosage form comprises from about 50 mg to about 800 mg, preferably from about 100 mg to about 400 mg, more preferably from about 150 mg to about 250 mg modafinil or a pharmaceutically acceptable salt thereof. A particular suitable amount of modafinil or a pharmaceutically acceptable salt thereof is about 200 mg. The afore-mentioned amounts apply for armodafinil or a pharmaceutically acceptable salt thereof as well. In still another embodiment of the third aspect, the dosage form comprises aniracetam or a pharmaceutically acceptable salt thereof as the ampakine in an amount of from about 500 mg to about 2500 mg, preferably from about 750 mg to about 2250 mg, more preferably from about 1000 mg to about 2000 mg. A particular example provides that the suitable amount of aniracetam or a pharmaceutically acceptable salt thereof, is about 1500 mg. In yet another embodiment of the third aspect, the dosage form comprises modafinil or a pharmaceutically acceptable salt thereof in an amount of about 200 mg and aniracetam or a pharmaceutically acceptable salt thereof as the ampakine in an amount of about 1500 mg. For the third aspect, it is understood that the two actives are released from the dosage form in accordance with the specific timely sequence, in which they shall be released from the dosage form in order to achieve the onsets of effects as described herein. Reference is made in this respect to example 3, which in an exemplary way shows formulation systems that can achieve a different release pattern for two active agents such that a specific timely administration is achieved. In another aspect, the present invention provides a method of treating or preventing a disease or disorder associated with cognitive deficit in a subject (e.g., a human) identified as in need thereof, comprising administering a therapeutically effective amount of modafinil or an enantiomer or a pharmaceutically acceptable salt thereof to the subject, followed by administering to the subject a separate therapeutically effective amount of an ampakine or a pharmaceutically acceptable salt thereof. In this aspect, the present invention achieves in the subject the onset of therapeutic effects of the modafinil, or enantiomer or pharmaceutically acceptable salt thereof, before the onset of therapeutic effects of the ampakine or pharmaceutically acceptable salt thereof. In certain embodiments, the time interval between the two administrations (i.e., the modafinil administration and the ampakine administration) ranges from about 70 minutes to about 110 minutes. Certain embodiments of the invention provide that the modafinil administration occurs to 80 to 90 minutes prior to the ampakine the administration. One particular embodiment provides that the time interval is about 85 minutes. One embodiment of the cognitive deficit identified in the subject is mild cognitive impairment, for example, amnestic mild cognitive impairment. The cognitive deficit can also be age-induced cognitive deficit. The method of the present invention is effective in treating or preventing a mild or moderate stage of established Alzheimer’s disease in the subject. In another embodiment, the method of the invention is useful for treating or preventing dementia. In a certain embodiment, the ampakine used in accordance with the method of the invention is aniracetam or a pharmaceutically acceptable salt thereof. Certain embodiments of the invention provide that the method administers the modafinil, or enantiomer or pharmaceutically acceptable salt thereof, and the ampakine or pharmaceutically acceptable salt thereof in separate dosage forms. In a certain embodiment, both the modafinil administration and the ampakine administration are oral administrations. The ampakine that can be used in accordance with the method of the invention includes a low-impact ampakine. BRIEF DESCRIPTION OF THE DRAWINGS The above and other features of the present invention, their nature, and various advantages will become more apparent post consideration of the following detailed description, taken in conjunction with the accompanying drawings, in which: Figure 1 depicts the effects of vehicle and modafinil (25, 50, 100 mg/kg) on delay-induced amnesia (or forgetting) in rats in a Social Recoginition Test; The vehicle and the modafinil were administered p.o. 60 minutes before the second contact (C2). Figure 2 depicts the effects of vehicle and aniracetam (25, 50, 100 mg/kg) on delay-induced amnesia (or forgetting) in rats in a Social Recoginition Test; the vehicle and the aniracetam were administered p.o. 30 minutes before the second contact (C2). Figure 3 depicts the effects of vehicle and various combinations of modafinil (25 mg/kg) with aniracetam (25, 50, 100 mg/kg, respectively) on delay-induced amnesia (or forgetting) in rats in a Social Recoginition Test. Figure 4 depicts the effects of vehicle and various combinations of modafinil (50 mg/kg) with aniracetam (25, 50, 100 mg/kg, respectively) on delay-induced amnesia (or forgetting) in rats in a Social Recoginition Test. Figure 5 depicts the effects of vehicle and various combinations of modafinil (100 mg/kg) with aniracetam (25, 50, 100 mg/kg, respectively) on delay-induced amnesia (or forgetting) in rats in a Social Recoginition Test. Figure 6 summarizes the Recoginition Index (C2/C1) achieved by vehicle and various modafinil and aniracetam combinations. Figure 7 depicts the position of the SCD subjects in the Example 2 clinical trial within the disease progression chart. Figure 8 depicts the OTS Problems Solved to First Choice score achieved by the subjects in the active arm and by those in the placebo arm in a One-Touch Stockings of Cambridge (OTS) test in Example 2 clinical trial. Figure 9 presents the break-down analysis of OTS Problems Solved to First Choice score achieved by the amnestic and non-amnestic subjects in the active and placebo arms in the OTS test. Figure 10 depicts the Pattern Recoginition Memory (PRM) % correct (Immediate) score achieved by the subjects in the active arm and by those in the placebo arm in a PRM test in Example 2 clinical trial. Figure 11 presents the break-down analysis of PRM % correct (Immediate) score achieved by the amnestic and non-amnestic subjects in the active and placebo arms in the PRM test. Figure 12 depicts the Pattern Recoginition Memory (PRM) % correct score (Delayed) achieved by the subjects in the active arm and by those in the placebo arm in a PRM test in Example 2 clinical trial. Figure 13 presents the break-down analysis of PRM % correct score (Delayed) achieved by the amnestic and non-amnestic subjects in the active and placebo arms in the PRM test. Figure 14 depicts the Rapid Visual Information Processing (RVP) response latency score achieved by the subjects in the active arm and by those in the placebo arm in a RVP test in Example 2 clinical trial. Figure 15 presents the break-down analysis of Rapid Visual Information Processing (RVP) response latency score achieved by the amnestic and non-amnestic subjects in the active and placebo arms in the PRM test. Figure 16 depicts the Rapid Visual Information Processing (RVP) A Prime score achieved by the subjects in the active arm, compared to subjects in the placebo arm in a RVP test in Example 2 clinical trial. Figure 17 presents the break-down analysis of Rapid Visual Information Processing (RVP) A Prime score achieved by the amnestic and non-amnestic subjects in the active and placebo arms in the PRM test. Figure 18 depicts the Spatial Working Memory (SWM) Between Errors score obtained by subjects in the active arm, compared to subjects in the placebo arm in a SWM test in Example 2 clinical trial. Figure 19 presents the break-down analysis of SWM Between Errors score achieved by the amnestic and non-amnestic subjects in the active and placebo arms in the SWM test. Figure 20 depicts the PAL total errors adjusted (PAL TEA) score achieved by the subjects in the active arm and by those in the placebo arm in a Paired Associates Learning (PAL) test in Example 2 clinical trial. Figure 21 shows the PAL Mean Errors to Success (PAL METS) score obtained by subjects in the active arm, compared to subjects in the placebo arm. Figure 22 shows a schematic of the design of Part A of the clinical study of Example 2. Figure 23 shows a more detailed schedule of assessments in Part A of the clinical study of Example 2. Figure 24 shows a schematic of Part B of the clinical study of example 2. Figure 25 shows a more detailed schedule of assessments in Part B of the clinical study of Example 2. Definitions The term “cognitive” refers to any cognitive domain, which is not restrictive to memory (Jessen et al., Alzheimers Dement. 2014 November; 10(6):844-852). There are multiple cognitive domains, of which three are particularly relevant to this invention. These are Episodic Memory (EM), Executive Function (EF) and Motivation. Many drugs are known to target these sub-domains individually but currently there is no therapy providing improvements across all three cognitive sub-domains. It is believed that this is due to different mechanistic pathways underlying each subdomain. When reference is made herein to the “treatment of cognitive deficit”, this refers to an improvement in at least one cognitive sub-domain, namely of at least EM, preferably in at least two cognitive sub-domains, namely of at least EM and EF, which will ultimately have an overall positive effect on the cognitive deficit. The term “cognitive deficit” as used herein is defined as a perceivable decline of at least one of the above-mentioned sub-domains in an individual, i.e. cognitive impairment. The decline is often recognized by those experiencing it and by those around them. In certain embodiments of the invention, the cognitive deficit is associated with AD pathology. “Mild cognitive impairment” or “MCI” is an intermediate, defined stage between the expected cognitive decline of normal aging and the more pronounced decline of dementia or Alzheimer’s disease (AD) or dementia (see R.C. Petersen in N Engl J Med 2011;364:2227– 34 and in J Intern Med. 2014 March; 275(3): 214–228). It involves problems with memory, language, thinking and judgment that are greater than typical age-related changes. In elderly people, MCI may be defined as a disease that can be diagnosed by subjective and objective cognitive decline without significant influence on the activities of daily living, i.e. the individuals are functionally independent. MCI is the earliest stage of cognitive decline that is considered a labelable “indication” by mainstream regulators such as the FDA, i.e. drug developers are able to conduct clinical trials in an MCI population, with the potential of getting a drug approved. MCI may also be a symptom of early stage of a disease, such as early Alzheimer’s disease (AD), namely in its subtype “amnestic MCI” or “aMCI”. Amnestic MCI is typically referred to when memory loss is the predominant symptom of MCI. However MCI can also be a manifestation of other pathologies unrelated to AD, such as frontotemporal dementia, Lewy Body dementia, dementia caused by vascular causes such as stroke or Transient Ischemic Attack, cognitive decline or dementia caused by a particular lifestyle or drug being used. “Subjective Cognitive Decline subjects“ (SCD subjects) refers to a group of subjects who report feelings that his/her cognition is worsening, nonetheless who have a normal performance on an objective level (Jessen F et al., Alzheimers Dement 2014;10:844–852). This is distinct from mild cognitive impairment (MCI), in which cognition is already below what is expected for age (Petersen RC, J Intern Med 2004; 256:183–194). While a subjective report of cognitive decline in an unimpaired individual was formerly considered of little relevance (patients were referred to as the “worried well”), SCD has recently gained increasing attention as a risk condition for dementia (Mitchell AJ, et al. Acta Psychiatr Scand 2014;130:439–451). In the presence of Alzheimer disease (AD) pathology, SCD is now considered its first symptomatic manifestation (stage 2) (Jack CR Jr, , et al. Alzheimers Dement 2018;14:535–562). SCD is not considered a labelableindication“ by mainstream regulators. It can be considered the last phase before MCI manifests in the patient. In another embodiment, it has been appreciated that SCD is a prelimnary stage of aMCI, along a disease progression contiuum that proceeds to MCI, Mild AD, Moderate AD and dementia (Severe AD). A schematic depiction of where SCD fits along the disease progression timeline is presented in Figure 7. Just like MCI, numerous causes of SCD other than preclinical AD also exist. These include, but are not limited to, SCD in MCI due to AD/prodromal AD, dementia, normal aging, psychiatric and neurologic disorders other than AD, or related to effects of medication and substance use, or a particular lifestyle (Jessen et al., Alzheimers Dement. 2014 November; 10(6):844-852). In certain embodiments, the SCD subjects are prone to (or have symptoms predictive of) preclinical AD. “Age-induced cognitive deficit” is a well-known observation, namely that the cognitive skills of a person decrease while the person gets older. The term is used herein in this common understanding. “Dementia” is a well-known term. The term is used herein in its common understanding. Typically, in patients with dementia, cognitive deficits are affecting daily functioning to the extent that there is loss of independence in the community (see R.C. Petersen in N Engl J Med 2011;364:2227-34). Episodic memory (EM) is the ability to remember information and experiences that occurred at a particular time and place. Executive function (EF) refers to a collection of “higher-level” cognitive processes that include planning, reasoning, working memory and mental manipulation, response inhibition and cognitive flexibility. The term “onset of the effect” of a specific API as used herein means that this particular API has reached a certain level or certain concentration in a patient that is suitable to create a specific pharmacological effect in this patient (this may also be referred to as “MEC”, see below). This effect will then last in the patient depending on the action of the API, the elimination half-life of the API, etc. The onset of the effect can correlate with the peak plasma concentration (c _max ) that is reached at a certain time (t _max ) but does not necessarily correlate. Thus, the onset of the effect can also be achieved prior to the c _max being achieved. If so, reference is typically made to the “MEC”, i.e. the minimal effective concentration, that is reached at “t _onset ”, wherein MEC < c _max and t _onset < t _max . As used in the specification and the claims, the singular forms of “a” and “an” also include the corresponding plurals unless the context clearly dictates otherwise. The term “about” in the context of the present invention denotes an interval of accuracy that a person skilled in the art will understand to still ensure the technical effect of the feature in question. The term typically indicates a deviation from the indicated numerical value of ±10% and preferably ±5%. It needs to be understood that the term “comprising” is not limiting. For the purposes of the present invention, the term “consisting of” is considered to be a preferred embodiment of the term “comprising”. If hereinafter a group is defined to comprise at least a certain number of embodiments, this is also meant to encompass a group which preferably consists of these embodiments only. “Modafinil” as referred to herein is 2-[(diphenylmethyl)-sulfinyl]acetamide and has the following structure represented by Formula I: Armodafinil as the R-enantiomer is accordingly 2-[(R)-(diphenylmethyl)-sulfinyl]acetamide represented by Formula Ia “Ampakines” as referred to herein – which are often also referred to as AMPAkines – are known as a class of compounds which act on the central nervous system (CNS). Ampakines are positive allosteric modulators of the ionotropic alpha-amino-3-hydroxy-5-methyl-4- isoxazole-propionic acid (AMPA) receptor. Ampakines enhance the excitatory actions of the neurotransmitter glutamate at the AMPA receptor complex, which mediates most excitatory transmission in the CNS. The present invention relates to the presently known ampakines as well as to ampakines that will be identified or developed in the future. This includes all pharmacological agents, which are presently well-known but have thus far not been identified to have an ampakine activity, for example, through a biological assay well within the routine experimentation of a skilled person in the field. Ampakines are categorized into “high-impact” and “low-impact” ampakines. They differ in their effects on the AMPA receptor-mediated current. Whilst the low-impact ampakines increase the amplitude of the current, there is little effect on receptor deactivation. In contrast, the high impact ampakines increase both the amplitude and duration of the current. As noted herein, the low-impact ampakines with the above effect are preferred for the present invention. “Aniracetam” as referred to herein is 1-(4-methoxybenzoyl)-2-pyrrolidone and has the following structure represented by Formula II: “CX516” as referred to herein is piperidin-1-yl(quinoxalin-6-yl)methanone and is also known as Ampalex. It has the following structure represented by Formula III: “CX691” as referred to herein is 2,1,3-benzoxadiazol-6-yl-piperidin-1-ylmethanone and is also known as Farampator. It has the following structure represented by Formula IV: “CX717” as referred to herein is benzo[c][1,2,5]oxadiazol-5-yl(morpholino)methanone and has the following structure represented by Formula V: “CX1632” as referred to herein is 8-cyclopropyl-3-[2-(3-fluorophenyl)ethyl]-7H- [1,3]oxazino[6,5-g][1,2,3]benzotriazine-4,9-dione and has the following structure represented by Formula VI: “CX1739” as referred to herein is N-methyl-N-tetrahydro-2H-pyran-4-yl-[2,1,3]- benzoxadiazol-5-carboxamide and has the following structure represented by Formula VII: The terms “treatment of” and “treating” include the administration of an active agent(s) with the intent to lessen the severity of a condition. The terms “prevention of” and “preventing” include the delay or avoidance of the onset of a condition by a prophylactic administration of the active agent. Detailed Description of the Invention Although there are many cognitive sub-domains covering different aspects of memory and thinking, there are three cognitive sub-domains of interest in the context of the general MCI, AD, dementia and age-related cognitive decline populations. These are Episodic Memory (EM), Executive Function (EF) and Motivation. The present invention is based on the finding that the combination of modafinil and an ampakine improves at least one, preferably simultaneously at least two, if not all three sub-domains that are affected in cognitive deficit, more specifically in MCI including aMCI or in age related decline of the cognitive function. When it comes to the above three sub-domains, modafinil provides the required boost in Executive Function (EF) and Motivation while the ampakine provides the required boost in Episodic Memory (EM). In order to achieve the above effect, the inventors have surprisingly determined that it is the combination and, more preferably and strikingly, the particular timing of the onset of effect of the two active agents that is required. Thus, the concept of the present invention is to provide a boost of Executive Function (EF), namely by the modafinil or enantiomer thereof (to be more precise, to provide this boost by the onset of the effect of the modafinil or enantiomer thereof) and – as soon as this boost of Executive Function (EF) is established – to provide (shortly thereafter or even simultaneously) a boost of Episodic Memory (EM), namely by an ampakine (to be more precise, to provide this boost by the onset of the effect of an ampakine). Accordingly, at the onset of the effect of the ampakine (resulting in improved Episodic Memory (EM), see above), the patient is already in a higher state of awareness, namely from the modafinil effect. A synergistic or additive efficacy is accordingly gained via the timed administration of the two actives. “Timed administration” means that the EF is boosted first while then, shortly thereafter or even simultaneously, the EM is boosted. When looking at the PK data of modafinil, it takes about 120 minutes to about 240 minutes after oral administration until the peak plasma concentration is reached. It is assumed that the onset of the effect is reached at about 120 minutes. The ampakine therefore has to be administered such that its onset of the effect is reached shortly after the onset of the effect of the modafinil has been achieved or even simultaneously. Taking into account that the ampakines have different PK values including different times it takes until the respective MEC / respective peak plasma concentration is reached, the actual timing of the administration of the specific ampakine depends on its PK data. As an example, the time it takes for aniracetam to reach its peak plasma concentration is 30 to 40 minutes after oral administration. It is assumed that the onset of the effect is reached at about 15 to 25 minutes, with 15 to 20 minutes being most suitable in the present setup, where the modafinil effect must be established first. Accordingly, for the specific combination of modafinil and aniracetam, the timed administration will be that modafinil is administered first, followed by the administration of aniracetam, namely the administration of aniracetam at about 100 minutes after the modafinil has been administered (120 minutes for modafinil – 20 minutes for aniracetam = 100 minutes). It is then a more preferred embodiment of this concept that the two actives provide for their respective effects simultaneously over at least some period of time, ideally for about 8 hours. Examples Example 1: Social Recognition Test in Rat This study was performed with the purpose of evaluation of modafinil and aniracetam alone or in combination in the social recognition test with 2-hour delay-induced normal forgetting in rats. The aim of this study was to evaluate Modafinil and Aniracetam for their potential beneficial effects on episodic-like memory using the Social Recognition Test with 2-hour delay-induced forgetting in the rat. Modafinil and aniracetam were administered alone or in combination to determine whether the effects of these compounds are additive or synergistic. The social recognition test has been validated to detect the cognitive enhancing effects of substances on the performance of young rats (Fox et al, 2005) or to evaluate the restorative effects of substances on short term memory deficits associated with age or those induced pharmacologically (Lemaire et al, 1994). Briefly, based on its olfactory selections, when a juvenile congener is placed in the home cage of an adult rat, the adult rat is able to recognize the juvenile as familiar for approximately one hour (juvenile is presented twice). This test exploits some aspects that are relevant to episodic memory in humans (what:juvenile; where: home cage, when: delay between the two exposures). The term episodic-like memory is thus preferable to episodic memory as this has not been truly verified in rodents. Using a 2-hour delay between presentations, control adult animals reliably demonstrate a similar level of investigation during the two exposures. In comparison, donepezil or memantine-treated adult animals display a reproducible decrease in the level of investigation of the juvenile at the second contact compared with the first, indicating improved recognition of the juvenile. However, it should be noted that cognition in the human brain is vastly different from cognition in the rat brain. Therefore, specific cognitive sub-domains that are defined in human terms will not apply to rats in the same manner. This is a limitation of all animal models of cognition. (Al Dahhan NZ, De Felice FG, Munoz DP. Potentials and Pitfalls of Cross-Translational Models of Cognitive Impairment. Front Behav Neurosci. 2019) Animals 205 adult rats were included at the beginning of the study, among which 204 rats were included at the behavioral testing, with the rest were saved as the spare rats. 68 male juvenile Wistar rats (4-week old, weighing 81-137 grams at testing) were used as social stimuli in the test. Experimental Procedures The social recognition test can be used to evaluate ‘episodic-like’ memory in rats as it exploits some of the aspects of episodic memory in humans. The method, as the means to detect memory enhancing activities, is described in Lemaire et al. (Psychopharmacology, 115, 435-440, 1994). The test is based on the tendency of rodents to preferentially explore a novel compared to a familiar object. Test subjects are exposed to a sample stimulus (object), and after a delay of minutes to hours, are presented with the sample object together with a novel object. Memory of the familiar object is gauged by a time difference score spent exploring each object. An unfamiliar juvenile rat was introduced into the individual home cage of a mature adult rat for 5 minutes. Following this first contact (C1), the juvenile rat was returned to its isolation cage until a second contact (C2) of 5 minutes with the same mature adult rat, 120 minutes later. The time the adult rat spends investigating (sniffing, grooming, licking, closely following) the juvenile at each contact was recorded. A recognition index (=C2/C1) was also calculated. Under such conditions, a mature adult rat fails to recognize the juvenile rat as familiar, as indicated by an absence of reduction in the duration of social investigatory behavior at C2. The test was performed blind using vials containing different formulations. There were 12 rats for each group. The experiment was divided into 6 sub-experiments. To avoid potential inter-day variability, in each sub-experiment, equal numbers of animals from each treatment group (N = 2) were tested. Modafinil was evaluated alone at 25, 50 and 100 mg/kg, respectively, administered p.o. 60 minutes before C2; or in combination with aniracetam at 25, 50 and 100 mg/kg, respectively. Aniracetam was also evaluated alone at 25, 50 and 100 mg/kg, respectively., administered p.o. 30 minutes before C2. A control group receiving administrations of vehicle was used in the experiment. To keep blind conditions, all animals received 3 administrations as described Table 1 below. When a dosing was not due, animals received an administration of vehicle. Table 1 Blood Collection At the completion of behavioral evaluation, all animals from the control (vehicle), modafinil, and aniracetam-treated groups (12 animals x 16 groups, 192 in total) were placed under isoflurane anesthesia and approximately 1 mL of blood was collected by cardiac puncture using a sterile disposable syringe. The blood samples were immediately transferred into identified tubes containing anticoagulant agent (Li-Heparin) for plasma preparation. After sealing each tube, the blood samples were gently agitated and stored on ice until centrifugation (within 30 minutes of sampling). The samples were centrifuged at +4°C, at 2000 g, for 10 minutes. The entire resultant plasma was immediately transferred into 2 suitably labelled polypropylene tubes (2 aliquots of approximately 250 µL). The tubes were stored upright at approximately -80°C. Statistical Analysis Data were analyzed by comparing the duration of social investigation at the second contact (C2) with the first contact (C1) for each group. Data were analyzed by comparing all test substances-treated groups with the vehicle control group at each contact and for the index of recognition using one-way Anova followed by Bonferroni’s multiple comparisons test. At the request of the sponsor study monitor, no chemical analyses of the test substances formulations were performed. Post-hoc on-way ANAVA analyses were performed using Bonferroni’s multiple comparisons test instead of Dunnett’s tests. These deviations were not considered to have affected the validity of the study. Test Results Effects of test substances on investigation duration(s) for the first contact (C1) and the second contact (C2) (120 min after C1) were provided in Table 2 and presented in Figures 1- 6. Table 2

NS = Not Significant; * = p < 0.05; ** = p < 0.01; *** = p < 0.001. As shown in Figures 1 through 5, the level of investigation at the initial contact (C1), i.e. before any treatment, was similar in the different groups (that is, no significant difference was observed as compared with vehicle controls). Vehicle-treated rats showed a similar level of social investigation of the familiar juvenile at the second contact (C2), as compared with the first contact (+8%, NS; recognition index C2/C1 = 1.08), indicating the absence of social recognition after a 2-hour delay (normal forgetting). Figure 1 shows that modafinil (25, 50 and 100 mg/kg) administered p.o. 60 minutes before the second contact (C2) did not significantly affect the duration of investigation of the familiar juvenile rat at the second contact (C2), as compared with the first contact (C1) (+9%, +9% and -8%, NS, respectively). The recognition index was not significantly modified, as compared with vehicle controls (1.12, 1.14 and 0.94 versus 1.08, respectively, NS). Figure 2 shows that aniracetam (25, 50 and 100 mg/kg, respectively) administered p.o. 30 minutes before the second contact (C2) did not affect the duration of investigation of the familiar juvenile rat at the second contact (C2), although a significant increase was observed at 50 mg/kg, as compared with the first contact (C1) (-3%, NS; +24%, p < 0.01 and 0%, NS, respectively). The recognition index was not significantly modified, as compared with vehicle controls (0.99, 1.26 and 1.03 versus 1.08, respectively, NS). As shown in Figure 5, modafinil (100 mg/kg) administered in combination with aniracetam (25 mg/kg) significantly decreased the duration of investigation of the familiar juvenile rat at the second contact (C2), as compared with the first contact (C1) (-16%, p < 0.05). Nonetheless, other combinations of modafinil and aniracetam did not demonstrate apparent effects on the duration of the second contact (C2), relative to the first (C1) (Figures 3-5). The recognition index was not significantly modified at any combination dose, as The results indicate that a combination dose of modafinil (100 mg/kg) and aniracetam (25 mg/kg) significantly decreased the duration of investigation of the juvenile rat on second contact (C2) (-16%, p<0.05), indicating a potential effect of episodic-like memory in the Social Recognition Test with 2-hour delay-induced forgetting in the rat. One the other hand, neither modafinil or aniracetam on its own significantly decreased the second contact time, nor did any of the other modafinil/aniracetam dose combinations. Example 2: Human Clinical Study This was a Phase 1B study designed to assess the safety and tolerability of modafinil coadministered with aniracetam, and the PK of modafinil administered alone or in combination with aniracetam in generally healthy elderly adults with subjective cognitive decline (SCD), as determined at screening. As a proof-of-concept, exploratory evaluations of the effect of modafinil in combination with aniracetam on cognitive function in this study population was also performed. It was designed as a two-part, randomized, two-period, two- sequence crossover and placebo-controlled parallel-group, Phase 1b trial. Study Rationale The rationale for a combination of modafinil and aniracetam is based on an assessment of cognitive subdomains that are in deficit among patients exhibiting age-related cognitive decline and mild cognitive impairment. Based on existing published literature around cognitive dysfunction among individuals with amnestic MCI (aMCI) and mild-to-moderate dementia, the core domains of cognition that are adversely affected in these populations were identified as episodic memory, executive function, and motivation, in order of priority. These same domains, in particular episodic memory and executive function are likely to be affected in patients exhibiting age-related cognitive decline or subjective cognitive decline (SCD) in elderly people. After assessing the neuroanatomical correlates of these domains and linking these correlates to the likely neurotransmitters involved in these domains, pharmacological agents that are known to influence the targeted neurotransmitters were determined, selecting modafinil and aniracetam. Neither agent appears efficacious enough on its own to alleviate the cognitive deficits relevant to the targeted patient population. However, by combining the 2 agents, coverage of episodic memory, executive function, and motivation can be expected. This study will assess the safety and tolerability of modafinil coadministered with aniracetam and the PK of modafinil administered alone or in combination with aniracetam in generally healthy elderly adults with SCD, as determined at screening. As a proof-of-concept, exploratory evaluations of the effect of modafinil in combination with aniracetam on cognitive function in this study population will also be performed. Study Objectives The objectives of this Phase 1b trial are outlined below: Primary objective • To assess the safety and tolerability of modafinil administered in combination with aniracetam in generally healthy elderly subjects with SCD Secondary objective • To evaluate the PK profile of modafinil administered alone or in combination with aniracetam in generally healthy elderly subjects with SCD Explanatory Objective • To evaluate the efficacy of modafinil in combination with aniracetam on objective function in generally healthy elderly subjects with SCD. Subjective Cognitive Decline To have an SCD diagnosis for a generally healthy elderly subject, the following inclusion criteria have been met for the “healthy elderly” subject to be eligible for inclusion in the study: • Good general health, as determined by medical history, physical examination, clinical laboratory, vital signs, 12-lead electrocardiogram (ECG), and Columbia Suicide Severity Rating Scale (C-SSRS), in the opinion of the Investigator • Has a clinical SCD diagnosis confirmed during screening, by answering ‘yes’ on the question: “During the past 12 months, have you experienced confusion or memory loss that is happening more often or is getting worse?” • by having a score of ³23/30 to £29/30 on the Mini-Mental State Exam [MMSE] Cognitive decline tends to be accumulative over time. There is a long sub-clinical period wherein structural brain changes occur without any cognitive of functional complaints. The first possible “diagnosed” stage is Mild Cognitive Impairment (MCI), which can be of multiple etiologies but >35% are amyloid heavy, suggesting Alzheimer’s Disease (AD). Most patients are diagnosed much later, once Mild-Moderate AD or other early dementias have set in. The selection of SCD subjects within the disease progression/severity chart is shown in Figure 7. It is believed that a signal generated in healthy elderly SCD subjects that can be extrapolated to infer the efficacy on other elderly patients with advanced disease progression and severity (e.g., aMCI, MCI, Mild AD, Moderate AD). Timing and Sequence of doses in the study Dosing of modafinil and aniracetam was staggered in time such that the peak plasma concentration (C _max ) for each compound occurs at approximately 2 hours post-dose for modafinil and 30 to 40 minutes post-dose for aniracetam. Aniracetam was administered 85 minutes after modafinil. To maintain blinding, when modafinil was administered alone, 2 placebo capsules were administered along with the active modafinil capsule, for a total of 3 matching over-encapsulated capsules. In Part A, aniracetam or placebo capsules were administered 85 minutes after modafinil. In Part B, aniracetam or placebo capsules were administered 85 minutes after modafinil or placebo. Study Design and Plan Part A was conducted in a crossover manner to facilitate intrasubject comparisons, allowing for a smaller sample size (compared to a parallel design). The goal of Part A was to establish that it is safe to give modafinil and aniracetam together in elderly humans, and that neither agent interferes with the known PK or the other. Part A of the study was conducted at clinical site 1 (PRA). In Part B, the parallel group design was chosen to evaluate the safety of the modafinil and aniracetam treatment while avoiding the confounding issues related to practice effects on tasks of executive and memory function in crossover studies. To investigate the effect of the experimental treatments on test performance, differences between group mean performances for single measures are analyzed. The goal of Part B was to explore the efficacy of modafinil and aniracetam on cognition. Part B of the study was conducted at 2 clinical sites (PRA and Subjects were screened for eligibility on Day -35 through Day -2 relative to the first study drug administration on Day 1. In Part A, 6 qualified subjects were admitted into the clinical research unit (CRU) on Day -1 of Periods 1 and 2 for baseline measurements. On Day 1 of Period 1, subjects were randomized to 1 of 2 sequences (AB or BA) consisting of the following treatments, separated by a 7-day washout: • A: modafinil 200 mg once daily (qd) for 7 days • B: modafinil 200 mg + aniracetam 1500 mg qd for 7 days In each period, subjects initiated the study treatment in the CRU on Day 1, self-administered the study treatment at home on Day 2 through Day 6, and reported to the CRU in the afternoon of Day 6 for an overnight visit, with discharge on Day 8. The final study drug administration on Day 7 was completed at the CRU followed by end of treatment (EOT) assessments. In Part B, qualified, generally healthy elderly male and female subjects with SCD were admitted into the CRU in the morning of Day -1 for baseline measurements. On Day 1, subjects were randomized to placebo qd for 7 days (n=28) or modafinil 200 mg + aniracetam 1500 mg qd for 7 days (n=28). Subjects initiated their assigned study treatment in the CRU on Day 1 and undergo Day 1 assessments followed by discharge from the CRU. They then self-administered the study treatment at home on Day 2 through Day 6, and returned for an overnight visit to the CRU on Day 6 for final study drug administration and EOT assessments on Day 7. Aniracetam was administered 85 minutes after modafinil. To maintain blinding, the placebo treatment consisted of 3 over-encapsulated placebo capsules to match the number of capsules for modafinil + aniracetam. For both study parts, study drugs were administered at the clinical research unit (CRU) on Day 1 and Day 7. On Days 2 through 6 study drugs were self-administered by subjects at home. Each subject was only dosed in 1 part of the study. Design of Part A of the clinical study is presented as a schematic in Figure 22. A more detailed schedule of assessments in Part A are presented in Figure 23 with explanations below. a. a: Including years of full-time education starting from the beginning of secondary education onwards. b. b: Complete physical examination at screening; targeted physical examination at other time points. c. c: At screening though EOT assessments, a total of 5 BP measurements, one every 6 minutes, are taken over a 30-minute period during which subject are laying supine. At follow-up, a single BP measurement is taken after 5 minutes of rest in the supine position. Temperature and respiratory rate are measured after completion of BP measurements. d. d: From 3.5 hours through 4 hours post-modafinil dose. e. e: Four hours post-modafinil dose. f. f: Screening/Baseline version at screening; Since Last Visit version at EOT and Follow-up. g. g: Modafinil is administered in the morning after a fast of approximately 1.5 hours. Fasting continue through 1.5 hours after administration of aniracetam or aniracetam placebo. For Treatment B, aniracetam or aniracetam + placebo are administered 85 minutes after modafinil. On Day 1 and Day 7, study drugs are administered in the CRU. On Day 2 through Day 6, they are self-administered by subjects at home. h. h: Samples for modafinil are collected pre-dose (0 hour) and at 0.25, 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 12, 24 hours post-modafinil administration on Day 7. The 24-hour post- dose sample is taken on Day 8. Samples for aniracetam are collected at 1, 1.5, 2, 2.5, 3, 4, 6, 8, 12, 24 hours post-modafinil administration on Day 7. The 24-hour post-dose samples are taken on Day 8. i. i: Study diary to record the timing of drug self-administration, concomitant medications, and any clinical symptoms are issued on Day 1 and reviewed on Day 6. j: Where possible, subjects receive phone calls twice daily at the time of dosing with modafinil and aniracetam or placebo. Figure 24 shows the schedule of assessments in Part B of the clinical study. A more detailed schedule of assessments in Part A are presented in Figure 25 with explanations below. a. a: Including years of full-time education starting from the beginning of secondary education onwards. b. b: Complete physical examination at screening; targeted physical examination at other time points c. c: Performed 3.5 hours post-modafinil dose. See Section 3.5.10 for the order of assessments. d. d: Body weight is taken prior to the aniracetam dose. e. e: At screening through the EOT assessments, a total of 5 BP measurements, one every 6 minutes, are taken over a 30-minute period during which subject are laying supine. At follow-up, a single BP measurement is taken after 5 minutes of rest in the supine position. Temperature and respiratory rate are measured after completion of BP measurements f. f: Between 3 hours and 3.5 hours post-modafinil dose. g. g: Screening/Baseline version at screening; Since Last Visit version at EOT and Follow-up h. h: May be performed within 2 hours of the time CANTAB test battery is expected to be performed on Day 7. i. i: Two hours post-modafinil dose j. j: Performed immediately after completion of CANTAB test battery k. k: Modafinil or placebo is administered in the morning after a fast of approximately 1.5 hours. Fasting continues through 1.5 hours after administration of aniracetam or placebo. Aniracetam or placebo is administered 85 min after modafinil or placebo, respectively. On Day 2 through Day 6, study drugs are administered at home. On Day 1 and Day 7, study drugs are administered in the CRU. l. l: Study diary to record the timing of drug self-administration, concomitant medications, and any clinical symptoms are issued on Day 1 and reviewed on Day 6. m: Where possible, subjects receive phone calls twice daily at the time of dosing with modafinil and aniracetam or respective placebos. The inclusion and exclusion criteria for the subjects are described in the following. Inclusion criteria: 1. Sex: male or female 2. Age: ³ 65 years to £ 85 years of age at screening 3. Body mass index: ³ 19 kg/m2 to £ 35 kg/m ² at screening 4. Good general health, as determined by medical history, physical examination, clinical laboratory, vital signs, 12-lead electrocardiogram (ECG), and Columbia Suicide Severity Rating Scale (C-SSRS), in the opinion of the Investigator 5. Has SCD confirmed during screening (“During the past 12 months, have you experienced confusion or memory loss that is happening more often or is getting worse?”) 6. Able to swallow capsules 7. Fluent in and able to read and comprehend the respective site languages 8. Able to understand and willing to comply with all study requirements and provide written informed consent 9. Males who are sexually active with a partner of child bearing potential must use a condom plus an additional method of contraception by their partner for sexual intercourse from screening until at least 90 days after last dose of study drug, unless they have been surgically sterilized (e.g., vasectomy) for a minimum of 6 months prior to the Screening visit. An additional method of contraception for the female partner can include hormonal contraceptives, an intrauterine device, a diaphragm, or a cervical cap. Total abstinence, in accordance with the lifestyle of the subject, is also acceptable. Females who are not women of child bearing potential defined as meeting one of the following criteria: a) Surgically sterile (has had a hysterectomy, bilateral salpingectomy or bilateral oophorectomy) for a minimum of 6 months prior to screening; or, b) Postmenopausal, defined as no menses for 12 months prior to screening without an alternative medical cause. Exclusion criteria: 1. History or current evidence of a clinically significant cardiovascular disease, including myocardial infarction, cerebrovascular accident, unstable angina, New York Heart Association Class II or greater heart failure, severe cardiac arrhythmia requiring medication or implanted defibrillator or pacemaker, syncope, uncontrolled hypertension, defined by systolic blood pressure > 150 mmHg and/or diastolic blood pressure > 90 mmHg (measured while subject is lying supine over a 30-minute duration) with or without antihypertensive medications; or clinically significant hypotension, in the Investigator’s judgment 2. Finding of any of the following on the screening or baseline ECG: QT interval corrected using Fridericia’s formula (QTcF) > 450 msec (males) and >470 msec (females), frequent supraventricular or ventricular ectopy, complete left bundle branch block, or any other ECG findings that, in the opinion of the investigator, would preclude participation in this study. 3. A score of 30/30 on the Mini-Mental State Exam (MMSE) 4. Major surgery within 6 months prior to the Screening visit, or any history of significant gastrointestinal, liver, or kidney surgery that may affect drug bioavailability, excluding appendectomy and cholecystectomy, which are allowed. 5. Any history or presence of significant gastrointestinal (GI), liver or kidney disease, or any other conditions known to interfere with the absorption, distribution, metabolism, or excretion of medications 6. Any of the following laboratory abnormalities at screening/baseline: - estimated glomerular filtration rate (eGFR) <50 mL/min/1.73 m2 calculated using the Modification of Diet in Renal Disease equation (screening only) - aspartate aminotransferase (AST) or alanine aminotransferase (ALT) >1.5 x the upper limit of normal (ULN), or total bilirubin >1.5 x ULN 7. Positive hepatitis B surface antigen (HBsAg), antihepatitis C virus (HCV) antibodies, or anti-HIV 1 and 2 antibodies at screening 8. Any other abnormal laboratory result deemed clinically significant by the Investigator 9. History of malignancy within 5 years prior to the screening visit (within 1 year for adequately treated carcinoma in situ of the cervix and nonmelanoma skincarcinoma) 10. Severe infection requiring oral or IV antibiotics within 2 weeks prior to the first dose of study drug 11. Any history of psychiatric disorders including psychosis, major depressive disorder as defined by the DSM-5 diagnostic criteria, mania, major anxiety, agitation, insomnia, or substance abuse; or neurological disorders (including seizure disorder). Subjects with mild depression that is not clinically significant, in the opinion of the Investigator, are allowed to participate. 12. Any history of attempted suicide or clinically significant suicidal ideation, in the opinion of the Investigator, or C-SSRS score >0 on any of the C-SSRS categories at screening 13. History of hypersensitivity reaction or intolerance to modafinil, aniracetam, or any of the inactive excipients of the study drugs, or to any of the substances in the placebo 14. History of systemic allergic reaction to any drug that is considered clinically significant by the Investigator 15. History of alcohol or drug abuse or dependence, as determined by the Investigator 16. History of noncompliance or other reason to anticipate noncompliance with the study visits, assessments, or study drug intake 17. Exposure to any investigational product (small molecule or biological drugs) within 60 days prior to the first dose of study drug 18. Use of cholinesterase inhibitors or other agents known to have cognitive enhancer properties, such as memantine, piracetam, nefiracetam, sunifiram, gingko biloba, ginseng, golden or Arctic root, Brahmi, etc, within 30 days preceding screening 19. Use of any medication that could interact adversely with modafinil, within the following intervals prior to the Screening visit (whichever is longest): A) 5 half-lives of the prior medication or its active metabolite(s), whichever is longer B) 2 weeks C) interval recommended by the prior medication’s product labeling. Medications that fall into this category include: - bupropion, antipsychotics, neuroleptics, psychostimulants, tricyclic antidepressants, anxiolytics, central nervous system depressants (tranquilizers), and monoamine oxidase inhibitors - Prescription and nonprescription medications known to be sensitive substrates, inducers, or inhibitors of cytochrome P450 (CYP)3A4* - Prescription and nonprescription medications known to be sensitive substrates of CYP2A9 or CYP2C19* (*As listed in the Food and Drug Administration (FDA) Drug Development and Drug Interactions: Table of Substrates, Inhibitors and Inducers (2017)) 20. Concomitant use of any other prohibited medication that cannot be stopped or replaced safely within 2 weeks prior to Day 1, as judged by the Investigator 21. Participants who have smoked or used nicotine-containing products (including, but not limited, to e-cigarettes, pipes, cigars, chewing tobacco, nicotine patches, nicotine lozenges, or nicotine gum) within 3 months of the first dose of study treatment 22. Any other condition/disease which, in the opinion of the Investigator, could compromise subject safety or interfere with the subject’s participation in the study or with the evaluation of the study results. In case of any doubt, the Investigator should consult the Medical Monitor 23. Previous participation in the current study 24. Employee of PRA, HMR, or the Sponsor 25. Positive drug and alcohol screen (opiates, methadone, cocaine, amphetamines [including ecstasy], cannabinoids, barbiturates, benzodiazepines, tricyclic antidepressants, cotinine, and alcohol) at screening or admission to the clinical research center 26. Average intake of more than 21 units (female subjects) or 24 units of alcohol (male subjects) per week: 1 unit of alcohol equals approximately 250 mL of beer, 100 mL of wine, or 35 mL of spirits) 27. Donation or loss of more than 100 mL of blood within 60 days prior to the first drug administration 28. Unsuitable veins for infusion or blood sampling The Study Drugs are • [Active medication] active substance 1: modafinil; activity: centrally acting sympathomimetic; Strength: 100 mg; Dosage form: Oral tablets, over-encapsulated • [Active medication] active substance 2: aniracetam; activity: nootropic; Strength: 750 mg; Dosage form: Oral tablet, over-encapsulated • [Placebo] visually matching active medication; Substance: silicified microcrystalline cellulose, carboxymethylamylum natricum A, magnesium stearate, and lactose; Strength: Not applicable; Dosage form: Oral tablet, over-encapsulated Study Schedule Part A Screening : Between Day -35 and Day -2 Confinement : Day -1, Day 6, and 7; discharge on Day 1 and Day 8 Follow-up : Day 14 ± 2 of Period 2 Part B Screening : Between Day -35 and Day -2 Confinement : Day -1 and Day 6; discharge on Day 1 and Day 7 Follow-up : Day 14 ± 2 Subjects Part A : 6 generally healthy elderly male and female subjects with SCD Part B : 56 generally healthy elderly male and female subjects with SCD The study measurements and variables are: 1. Pharmacokinetic Measurements 1.1 Blood Sampling and Bioanalysis Blood samples of 4 ml were taken for analysis of both modafinil and its metabolite modafinil acid and aniracetam and its metabolite 4-[(4-methoxybenzoyl)amino] butanoic acid (ABA). Plasma concentrations of modafinil and aniracetam were determined using validated bioanalytical methods. In addition, plasma samples may also be subjected to analysis for drug-related metabolites. 1.2 Safety and Tolerability Measurements Safety and tolerability assessments consist of AEs, clinical laboratory, vital signs, 12-lead ECG, physical examination, and C-SSRS. Assessments were performed in accordance with the schedules of assessments. 1.2.1 Adverse Events AEs were recorded from signing of the ICF until completion of the follow-up visit. Any clinically significant observations in results of clinical laboratory, 12-lead ECGs, vital signs, physical examinations, or C-SSRS were recorded as AEs. A treatment-emergent AE (TEAE) is defined as any event not present prior to the first administration of the study drug or any event already present that worsens in either severity or frequency following exposure to the study drug. An AE that occurs prior to the first administration of the study drug are considered a pretreatment AE. 1.2.2 Clinical Laboratory Blood and urine samples for clinical laboratory assessments were collected according to each site’s respective SOPs. The following parameters are measured: - Clinical chemistry (serum quantitatively): total bilirubin, alkaline phosphatase, gamma glutamyl transferase, AST, ALT, lactate dehydrogenase, creatinine, urea, total protein, glucose, inorganic phosphate, sodium, potassium, calcium, chloride - Hematology (blood quantitatively): leukocytes, erythrocytes, hemoglobin, hematocrit, thrombocytes, partial automated differentiation: lymphocytes, monocytes, eosinophils, basophils, neutrophils, mean corpuscular volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration, and at Screening only, HbA1c - Urinalysis (urine qualitatively): hemoglobin, urobilinogen, ketones, glucose, protein. - Serology: HBsAg, anti-HCV, and anti-HIV. - Drug and alcohol screen: opiates, methadone, cocaine, amphetamines (including ecstasy), cannabinoids, barbiturates, benzodiazepines, tricyclic antidepressants, cotinine, and alcohol. 1.2.3 Vital Signs At screening through EOT assessments, systolic and diastolic blood pressure (BP) (including pulse) is recorded during a 30-minute period during which the subject is resting in the supine position. A total of 5 BP measurements, 1 every 6 minutes, are taken during this period. These assessments are made using an automated device. For assessment of eligibility, the lowest of the 5 BP measurements is considered. At follow-up, a single BP measurement is taken after 5 minutes in the supine position. Body temperature and respiratory rate are measured (a single measurement) after the BP measurements. 1.2.4 Electrocardiogram A standard 12-lead ECG is recorded after the subject has been resting for at least 5 minutes in the supine position. The ECG are recorded using an ECG machine with computer-based interval measurements. The following ECG parameters are recorded: heart rate, PR interval, QRS duration, QT interval, QTc-interval (Fridericia's), and the interpretation of the ECG profile by the Investigator. 1.2.5 Physical Examination Physical examination are performed according to each site’s respective SOPs. In addition, body weight and height are measured according to each site’s respective SOPs. A complete physical examination is performed at screening and targeted physical examinations at time points thereafter. 1.2.6 Columbia-Suicide Severity Rating Scale The C-SSRS is a brief questionnaire that provides for the identification, quantification and standardized assessment of the occurrences and severity of suicidal ideation and behavior (see http://cssrs.columbia.edu). The “Baseline/Screening” version of the C-SSRS is assessed at Screening. The C-SSRS “Since Last Visit” version is assessed at EOT and at Follow-up. 1.3 Cognitive Measurements After completion of dosing, subjects are asked to spend the time between dosing and cognitive testing engaged in low-arousal activities (reading, watching TV, or napping) under supervision by site staff. 1.3.1 Rey’s Auditory Verbal Learning Test (RAVLT) The RAVLT is be administered at baseline and EOT of Part B as an objective measure of subject’s memory. The RAVLT is a neuropsychological tool that is used for assessing episodic memory by providing scores for evaluating different aspects of memory. Briefly, the RAVLT consists of presenting a list of 15 words across 5 consecutive trials. The list is read aloud to the participant, and then the participant is immediately asked to recall as many words as he/she remembers. This procedure is repeated for 5 consecutive trials (Trials 1 to 5). After that, a new list (List B) of 15 new words is read to the participant, who then is immediately asked to recall the words. After the List B trial, the examiner asks the participant to recall the words from the first list (Trial 6). After 20 minutes of interpolated testing (timed from the completion of List B recall), the participant is again asked to recall the words from the first list (delayed recall). Different summary scores are derived from raw RAVLT scores. These include RAVLT Immediate (the sum of scores from the first 5 trials [Trials 1 to 5]), RAVLT Learning (the score of Trial 5 minus the score of Trial 1), RAVLT Forgetting (the score of Trial 5 minus score of the delayed recall) and RAVLT Percent Forgetting (RAVLT Forgetting divided by the score of Trial 5). 1.3.2 Cambridge Neuropsychological Test Automated Battery (CANTAB) The selected CANTAB tests assess the cognitive domains affected in MCI, aMCI, and early AD populations. The cognitive domains assessed in this battery ensure there is a broad evaluation of the cognitive safety profile as well as potential pro-cognitive effects of the test compounds. The tests in this battery are performed in the order listed in this protocol. 1.3.2.1 Motor Screening Task (MOT) The MOT provides a general assay of whether sensorimotor or comprehension difficulties limit collecting valid data from a subject. Participants must touch a flashing cross that appears on different locations of a screen. 1.3.2.2 Paired Associates Learning (PAL) The PAL task assesses episodic memory. It is designed to assesses simple visual pattern and visuospatial associative learning, which contains aspects of both delayed response procedure and a conditional learning task. For each stage, boxes are displayed on the screen. All are opened in a randomized order. One or more of them contain a pattern. The patterns shown in the boxes are then displayed in the middle of the screen, one at a time, and the subject must touch the box where the pattern was originally located. Each stage may have up to 10 attempts (trials) in total (the first presentation of all the shapes, then up to 9 repeat presentations). If the subject makes an error, the patterns are re-presented to remind the subject of their locations. When the subject gets all the locations correct, they proceed to the next stage. If the subject cannot complete a stage correctly, the test terminates. As the test progresses so the stages become more difficult as the number of patterns to be remembered increases, up to a maximum of 12 patterns. For participants who fail to complete all levels, an adjusted total is calculated that allows for errors predicted in the stages that were not attempted. Successful performance of the PAL test is dependent on functional integrity of the temporal lobe, particularly the entorhinal cortex (Owen, Sahakian, Semple, Polkey, & Robbins, 1995). The key measure for this task isTotal Errors Adjusted and Mean Errors to Success. “PAL total errors adjusted” (aka, PAL TEA) means the number of errors committed by the subject plus an adjustment for the estimated number of errors they would have made on any stages that were not reached. For subjects who fail to complete all levels, an adjusted total is calculated that allows for errors predicted in the stages that were not attempted. 1.3.2.3 Spatial Working Memory (SWM) SWM assesses the ability of the participant to retain spatial information and manipulate it in working memory. It is a self-ordered task that also gives a measure of strategy. A number of colored boxes are presented on the screen, and the computer hides a token in these boxes one at a time. The participant is instructed to touch the boxes in turn to search for the token that has been hidden. When a token is found it should be placed in a home area on the right side of the screen. The participant then searches for more tokens until the same number of tokens as the number of colored boxes has been found. The key task instruction is that the computer will never hide a token in the same colored box twice in the same problem. As the test progresses, so it becomes more difficult. SWM performance is impaired by damage to the prefrontal cortex, especially the dorsolateral prefrontal cortex. Similarly, in neuroimaging studies in healthy volunteers, SWM performance is associated with activations in the dorsolateral and mid-ventrolateral prefrontal cortex. The 12-box version of the SWM task will be used in this study. Performance at the harder levels of this task is enhanced by the use of a heuristic search strategy. SWM Between errors are defined as times the subject revisits a box in which a token has previously been found. Lower is better. SWM Strategy is obtained by counting the number of times the subject begins a new search with a different box for six- and eight-box problems only. A high score represents poor use of this strategy and a low score equates to effective use of strategy. 1.3.2.4 Pattern Recognition Memory (PRM) PRM measures both immediate and delayed visual recognition memory in a 2-choice forced discrimination paradigm. The participant is presented with a series of visual patterns, one at a time, in the center of the screen. A white box appears in the center of the computer screen, inside which digits, from 2 to 9, appear in a pseudo-random order, at the rate of 100 digits per minute. The test is in two parts; a ‘warm-up’ practice phase which lasts for two minutes (slow mode, five minutes) and is not scored, and a test phase which lasts for four, six or ten minutes, depending on the test mode, the last three/five/seven and a half of which are assessed. The subject is presented with a series of 12 visual patterns, one at a time, in the center of the screen. These patterns are designed so that they cannot easily be given verbal labels. In the recognition phase, the subject is required to choose between a pattern they have already seen and a novel pattern. In this phase, the test patterns are presented in the reverse order of the original order of presentation. The participant is required to touch the pattern they have seen before. The presentation phase is then repeated, with new patterns. The second recognition phase is given after a delay of at least 20 minutes. PRM Percent correct measures the number of correct responses, expressed as a percentage, with higher values indicating better pattern of recognition memory. 1.3.2.5 One-Touch Stockings of Cambridge (OTS) OTS is a test of executive function, planning and working memory based upon the ‘Tower of London’ and the CANTAB Stockings of Cambridge task. The participant sees 2 displays containing 3 colored balls. The displays are presented in such a way that they can easily be perceived as stacks of colored balls held in stockings or socks suspended from a beam. There is a row of numbered boxes along the bottom of the screen. An animated tutorial first demonstrates to the participant how to use the balls in the lower display to copy the pattern in the upper display, and completes one demonstration problem, where the solution requires one move. The participant must then complete 3 further problems, one each of 2 moves, 3 moves, and 4 moves. Next the participant is shown further problems, and must work out in their head how many moves the solutions to these problems require, then touch the appropriate box at the bottom of the screen to indicate their response. The 6-move version is used in this study. 1.3.2.6 Rapid Visual Information Processing (RVP) RVP is a sensitive measure of sustained attention, outputting measures of response accuracy, target sensitivity and reaction times. For the RVP task, single digits appear in a pseudorandom order at a rate of 100 digits per minute in box in the center of the screen. Subjects must detect a series of 3-digit target sequences (e.g., 3-5-7; 2-4-6; 4-6-8) and respond by touching the button at the bottom of the screen when they see the final number of the sequence. Nine target sequences appear every minute. . A Prime is the signal detection measure of sensitivity to the target, regardless of response tendency (range 0.00 to 1.00; bad to good). In essence, this measure is a measure of how efficient the subject is at detecting target sequences. 1.4 Task Motivation and Pleasure Task motivation and pleasure are measured after completion of the cognitive assessments (Part B) using a paper unipolar visual analog scale (VAS) (0 to 10 cm), anchored on one end with “0=not pleasant” and on the other end with “10=very pleasurable.” Subjects are asked “Please rate your feelings on the tasks you just completed” and provide their rating by making a clear vertical mark on the appropriate spot on the VAS scale. The length of the line from 0 to the point of intersection on the scale is measured manually and documented. 1.5 Leeds Sleep Evaluation Questionnaire Sleep quality during Part B of the study is assessed using the Leeds Sleep Evaluation Questionnaire (LSEQ), a 10-item, subjective, VAS scale. The LSEQ was designed to assess changes in sleep quality over the course of a psychopharmaco-logical treatment intervention. The scale evaluates 4 domains: ease of initiating sleep, quality of sleep, ease of waking, and behavior following wakefulness. The scores for each domain are obtained from a sum of the corresponding item scores for each domain. 1.6 Mini-Mental State Exam (MMSE) The MMSE is a widely used test of cognitive function among the elderly; it includes tests of orientation, attention, memory, language, and visual-spatial skills. 1.7 Short Form (36) Health Survey The SF-36 is a 36-item, patient-reported survey of general health. The items in SF-36 are divided into 8 different domains with overall physical and mental health component summary scores. Its domains are physical functioning, role limitations physical, bodily pain, social functioning, general mental health, role limitations emotional, vitality, and general health. 1.8 Timing of Assessments For PK, predose samples are obtained up to 30 minutes prior to dosing. Post-dose samples up to 20 minutes post-dose are obtained with a time window of ±1 minute. Thereafter, postdose samples will be obtained with time margins of ±5% of the time that has passed since modafinil dosing. In Part A, in the event assessments were planned for the same scheme time, the order of the assessments were arranged in such a way that PK blood sampling was done after the ECG and vital signs recordings have been conducted, with PK blood sampling as close to the nominal time as possible. On Day 1 and Day 7, the supine period for BP began at 3.5 hours post-modafinil dose. BP will be collected starting at 3.5 hours through 4 hours post-modafinil dose. Temperature, respiratory rate, and ECG werecollected after BP measurements are completed. On Day 1, physical examination and C-SSRS were done after ECG, and on Day 7, they were done after the 4-hour PK sampling. In Part B, the CANTAB cognitive assessments were done starting at 2 hours postdose, in the order presented in the protocol, followed immediately by the task motivation and pleasure VAS. On Day 1 and Day 7, the supine period for BP began at 3 hours post-modafinil dose. BP and pulse were collected starting at 3 hours through 3.5 hours post-modafinil dose. Temperature, respiratory rate, ECG, and clinical laboratory, in that order, were collected immediately after BP measurements are completed, followed by the RAVLT, SF-36, LSEQ, followed by physical examination, C-SSRS, and MMSE in that order. 1.9 Pharmacokinetic, Safety, and Cognitive Assessment Variables 1.9.1 Pharmacokinetic Variables Pharmacokinetic (aka “PK”) variables are the plasma concentrations of modafinil, modafinil acid, aniracetam, and its metabolite 4 [(4 methoxybenzoyl)amino]butanoic acid (ABA), and their PK parameters (Part A only). The PK parameters to be determined or calculated using noncompartmental analysis may include the parameters as given below. C _max : Maximum observed plasma concentration T _max : Time to attain maximum observed plasma concentration AUC _0-tau : Area under the plasma concentration-time curve over a dosing interval (24 hours) C _min : Minimum observed plasma concentration MR_C _max (metabolites only): metabolite/parent ratio based on C _max and corrected for molar weight MRAUC _0-tau (metabolites only): metabolite/parent ratio based on AUC _0-tau and corrected for molar weight 1.9.2 Cognitive Assessment Variables - Rey’s Auditory Verbal Learning Task (RAVLT): Total Sum Score and Delayed Recall Score - MOT: median latency to a correct response - Paired Associates Learning (PAL): a) Total errors and total errors (adjusted) from the 2,4,6,8,12 patterns assessment b) Mean Errors to Success c) First attempt memory score - Spatial Working Memory (SWM): between errors (working memory) and strategy (executive function, planning) - Pattern Recognition Memory (PRM): percent correct (immediate and delayed components) - One-Touch Stocking of Cambridge (OTS): problems solved on first choice and median latency to correct - Rapid Visual Information Processing (RVP): target sensitivity and reaction times via a) RVP A Prime b) RVP Response Latency Composite Cambridge Neuropsychological Test Automated Battery (CANTAB) Global Score of Cognitive Function 2. Statistical Procedures and Determination of Sample Size 2.1 Analysis Sets 2.1.1 Safety Set All randomized subjects who receive at least one dose of any study drug. 2.1.2 Pharmacokinetic Set All randomized subjects in Part A who receive at least one dose of study drug and have sufficient plasma concentration data for PK analysis. 2.1.3 Full Analysis Set All randomized subjects in Part B, who receive at least one dose of study drug, and have baseline and on-treatment cognitive assessment data 2.2 Statistical and Analytical Plan (SAP) for Pharmacokinetic, Pharmacodynamic, and Safety, and Exploratory Evaluation A SAP was generated and finalized prior to database lock and unblinding of study treatment codes. Any deviation from the SAP will be reported in the Section “Changes in Planned Analysis” in the Clinical Study Report. 2.2.1 Pharmacokinetic Evaluation Plasma concentrations of modafinil, aniracetam, and their respective metabolites was measured at specific timepoints, tabulated, and summarized. Standard noncompartmental PK parameters were determined for each analyte as applicable using WinNonlin™ Professional (Pharsight Corporation, Mountain View, CA, USA). Additional PK computations can also be performed in SAS for Windows® (SAS Institute Inc., Cary, NC, USA). Descriptive statistics for plasma concentrations and PK parameters include arithmetic means and SDs, geometric means, geometric coefficients of variation, medians, and minimum and maximum, as appropriate. The comparisons between Treatment A (modafinil alone [reference]) vs Treatment B (modafinil + aniracetam [test]) will be assessed using an analysis of variance (ANOVA) for natural logarithm (ln)-transformed PK parameters (AUC0-tau and Cmax). The ANOVA model will include sequence, period, and treatment as fixed effects and subject nested within sequence as a random effect. From these analyses, least squares (LS) means, LS mean treatment differences, and 90% confidence intervals (CIs) for the treatment differences on the ln-scale were estimated. These results were transformed back to the original scale by exponentiation to provide treatment geometric LS means, point estimates of the geometric LS mean ratios, and the 90% CIs for these ratios. The ratios of geometric means between treatments (B vs A) and their 90% CIs are presented. 2.2.2 Cognitive Assessment Evaluation The CANTAB Composite Score in the clinical trial study of Example 2 is attributed to the results of the 5 tests, with each having 20% weightage. Two of the tests are memory tests: (PAL, PRM), two are executive function tests (OTS, SWM), and one tests attention (RVP). All data was summarized using descriptive statistics and was listed and summarized in tabular and/or graphical form. 2.2.3 Evaluation of Safety and Tolerability Safety and tolerability were assessed through adverse events (“AEs”), clinical laboratory, vital signs, ECGs, and physical examination findings, and any other parameter that is relevant for safety assessment. 2.2.3.1 Adverse Events A listing of all individual AEs are provided. Summary tables of TEAEs are presented by system organ class based on the MedDRA terminology list (preferred terms): a table containing the number of TEAEs (frequency of occurrence, number of subjects experiencing the event) by treatment and a table containing the number of drug-related TEAEs (frequency of occurrence, number of subjects experiencing the event) per treatment. Additional tables of total counts by treatment and relationship and by treatment and severity are given. 2.2.3.2 Clinical Laboratory Clinical laboratory data are listed accompanied by an indication if the parameter is outside the reference range. A summary of all data outside the reference range of the clinical laboratory are provided. Clinical laboratory data are summarized by treatment group and study visit, using descriptive statistics. Shift tables may also be provided, if warranted by the data. 2.2.3.3 Vital Signs and Electrocardiograms Vital signs (including changes from baseline) are summarized by treatment group and study visit, using descriptive statistics. Shift tables may also be provided, if warranted by the data. Electrocardiogram (ECG) results are classified as normal or abnormal and summarized using frequency counts by treatment group and time point of collection. Descriptive statistics are provided for PR, RR, QRS, QT, and QTc intervals. 2.2.3.4 Physical Examination Changes from baseline for physical examination are described and listed. 2.3 Determination of Sample Size For this proof-of-concept study, no prospective calculations of statistical power have been made. Any p-values to be calculated according to the SAP will be interpreted in the perspective of the explorative character of this study. Results: Primary Objective of the Clinical Trial: Assessment of Safety and Tolerability Part A: Number of treatment-emergent adverse events (TEAEs): A total of 59 TEAEs were reported by 6 (100%) subjects. Of these, 36 were reported by 6 (100%) subjects on modafinil, and 23 were reported by 6 (100%) subjects on modafinil and aniracetam. Frequency: The most frequently reported TEAEs were dizziness (10 reports; modafinil=6 reports, modafinil and aniracetam=4 reports), headache (8 reports; modafinil=5 reports, modafinil and aniracetam=3 reports), fatigue (4 reports; all for modafinil), and insomnia (4 reports; modafinil=2 reports, modafinil and aniracetam=2 reports). The remainder of the TEAEs was reported 3 times or less. The percentage of subjects reporting TEAEs was comparable for subjects on modafinil and aniracetam, but the number of TEAEs was higher in Treatment A (36 TEAEs versus 23 TEAEs). Part B Number of TEAEs: A total of 106 TEAEs were reported by 41 (68.3%) subjects. Of these, 69 were reported by 22 (71.0%) subjects on modafinil and aniracetam and 37 were reported by 19 (65.5%) subjects on placebo. Frequency: The most frequently reported TEAEs were headache (28 reports; modafinil and aniracetam=15 reports, placebo=13 reports) and dizziness (12 reports; modafinil and aniracetam=9 reports, placebo=3 reports). In Part B, The percentage of subjects reporting TEAEs was comparable for the subjects treated with modafinil and aniracetam, and the placebo-treated subjects. The number of TEAEs was higher for subjects treated with modafinil and aniracetam compared to placebo-treated subjects (69 TEAEs versus 37 TEAEs). Subjects treated with modafinil and aniracetam reported more gastrointestinal disorders (17 TEAEs), nervous system disorders (27 TEAEs), and psychiatric disorders (9 TEAEs) than placebo-treated subjects (7, 18, and 2 TEAEs, respectively). There were no deaths or serious AEs reported during the study. It was concluded that a seven-day qd administration of modafinil in combination with aniracetam was safe and well tolerated in generally healthy elderly subjects with SCD. Secondary Objective of the Clinical Trial: Evaluation of PK variables The pharmacokinetic variables of the clinical trial Part A are provided in the following tables: Table 3_Statistical Assessment of Treatment (Analyte: Modafinil) Table 4_Statistical Assessment of Treatment (Analyte: Modafinil acid) Note: using proc mixed (ANOVA) with fixed effects of treatment on log-transformed parameters, period and sequence and subject nested within treatment as a random effect. %CVinter=100*sqrt(exp(Subject Covariance Parameter Estimate)-1). %CVintra=100*sqrt(exp(Residual Covariance Parameter Estimate)-1). LS=Least Squares. As shown by the data presented in the above tables, the pharmacokinetic parameters of modafinil in the presence (test) and absence (reference, i.e., modafinil alone) of aniracetam are superimposable, suggesting there was no pharmacokinetic interaction between modafinil and aniracetam under the current dosing regimen. The pharmacokinetics of modafinil and its acid metabolite were not affected by co-administration of aniracetam, more specifically, which was administered about 85 minutes after modafinil. As shown in Table 3 and Table 4 above, the exposures of modafinil and modafinil acid plasma were comparable after 7 days of qd modafinil dosing with and without 7 days of qd co-administration of aniracetam, in generally healthy elderly subjects with SCD. Explanatory Objective of the Clinical Trial Efficacy Signal It is known that cognitive or neuropsychological deficits, despite of being a consistent feautre of MCI and early AD, overlap with cognitive impairment associated with other disorders, such as, depression (Swainon, et al, Dement Geriat Cogn Disord, 2001; 12:265-280). A significant diagnostic value was placed on clinical differentiation on early detection of cognitive impairment signals that are predictive of future AD diagnosis from other neurological or psychiatric conditions, e.g., depression (Swainon, et al). A CDC report explicitly acknowledged the association of SCD with frequent mental distress (FMD), including such as stress, depression and problems with emotions (Retrieved from https://www.cdc.gov/aging/data/subjective-cognitive-decline- brief.html). The CDC report presented that 20.9% of the elderly subjects (adults of 65 years of age or older) with SCD reported FMD. K.S. Fowler et al. (J. of the Int. Neuropsychological Soc., 2002, 8, 58-71) found that that performance on the CANTAB PAL test more reliably identified the onset of progressive memory deterioration in a subgroup of questionable dementia (QD) subjects for probable dementia of the Alzheimer type (DAT) pertaining to progression of cognitive deficits, impaired functional ability, onset and conscious state. Swainson, et al also reported that “scores on a test of visuo-spatial PAL very accurately classified individuals as belonging to either the AD or the combined depression/control group”. For these reasons, and on the advice of a panel of experts, the CANTAB battery was chosen as the primary exploratory endpoint for efficacy in cognitive improvement, along with a few other endpoints. Thus, the study design envisioned gleaning an efficacy signal using the CANTAB battery in generally healthy elderly SCD subjects. Since this was a Ph 1 trial, the subjects cannot be classified as patients, i.e. they had not yet crossed the clinical threshold of cognitive and functional disability to qualify for a diagnosis. Hence by design, these patients were not expected to exhibit the level of disability that is typically seen in MCI or AD or dementia patients. This presented the challenge of finding a signal of improvement when the baseline deficit was expected to be substantial. To deal with this challenge, it was thus necessary to find a way to segregate subjects into two subgroups- those who displayed signs of higher cognitive deficit versus and those who displayed a lower or more “normal” cognitive deficit for their age and profile. This was achieved using the number of patterns the subject reached on initial assessment PAL assessment, specifically the number of patterns reached. This was done on the basis of evidence that this particular sub-test best predicted disease progression to AD (Swainson, et al). Thereby, SCD subjects in this clinical trial were classified into two subgroups, labelled „amnestic subjects” and “non-amnestic subjects”, which was determined by whether or not the subject managed to reach 8 patterns in the CANTAB PAL test (aka, PAL 8 cutoff). Amnestic subjects refer to the subgroup who did not reach 8 patterns in the PAL test, while non-Amnestic subjects are those that either reached 8 patterns or crossed 8 patterns in the PAL test. Using the PAL 8 cutoff, amnestic groups of subjects were generated to more closely resemble MCI and early AD patients. Therefore, an efficacy signal generated in this subgroup is more likely to predict the efficacy in an MCI or early AD population. Thus the signal that can be extroplated from amnestic subjects are a more liable predictor of the efficacy of the combined therapy within elderly subjects with greater progression and severity in cognitive deficit related diseases or disorders (e.g., MCI, mild or moderate AD). The number of the amnestic and non-amnestic subjects in the active and placebo arms was presented below: Table 5 0 The structure of the exploratory analysis shown below is as follows: Subjects were tested on each of the specified 5 CANTAB tests on Day -1 (before commencing therapy) and again on Day 7 (after taking modafinil and aniracetam for 7 days). The difference in their scores between Day -1 and Day 7 was calculated and assessed. The results are presented as the average improvement (or worsening) of scores before and after treatment. For each CANTAB test, the difference in averages of the selected groups (e.g. Active versus Placebo) or subgroups (Active versus Placebo within amnestic subjects or Active versus Placebo within non-amnestic subjects) was calculated. The difference in averages are first presented using the entire dataset (28 subjects on the active arm and 28 subjects in the placebo arm). Thereafter, the same averages are stratified using the PAL 8 cutoff to generate amnestic and non-amnestic subgroups, for which the same difference in averages is presented. Results are presented in Figures 8 to 21, showing the results of the 5 attentional, memory, and executive tests (i.e., OTS, PRM, RVP, SWM and PAL) that will contribute to the CANTAB Composite Score, weighed at 20% each. One-Touch Stockings of Cambridge (OTS) is a test of executive function, based upon the Tower of Hanoi test. It assesses both the spatial planning and the working memory subdomains. The OTS test results demonstrated that there was about 66% improvement in Problems Solved To First Choice score in the test subjects in the active arm, compared to the subjects in the placebo arm (Figure 8). In a further break-down analysis, the results showed that there was about 1045% improvement in terms of Problems Solved to First Choice score in the amnestic subjects in the active arm, compared to the amnestic subjects in the placebo arm, while non-amnestic subjects in the active arm saw about 93% worsening compared to the non-amnestic subjects in the placebo arm (Figure 9). The Pattern Recognition Memory (PRM) test results showed that there was about 377% improvement (3.77 vs 0.79) in the PRM % Correct Immediate score in the test subjects in the active arm, compared to the subjects in the placebo arm (Figure 10). In a further break-down analysis, the results showed that there was about 472% improvement (6.35 vs. 1.11) in PRM % Correct Immediate score in the amnestic subjects in the active arm, compared to the amnestic subjects in the placebo arm, while non-amnestic subjects in the active arm saw about 92% improvement (1.19 vs. 0.62), compared to the non-amnestic subjects in the placebo arm (Figure 11). Elaborating on the differentiation between amnestic and non- amnestic subgroups in the same arm, the amnestic subjects in the active arm gained about 6.35 points in the PRM % Correct Immediate score, with the non-amnestic subjects in the same arm having achieved only 1.11 points, which is a 5.7 times increase. Among non- amnestic subjects, those on the active arm averaged 1.19 points on their PRM % Correct (Immediate) scores, compared to 0.62 points obtained by the non-amnestic subjects in the placebo arm. Since PRM % Correct Immediate is a measure of immediate pattern-recognition memory, we also conducted a similar analysis on the Pattern Recognition Memory % Correct (Delayed) test, which measures a similar retention of pattern recognition memory but after a delay. It was noted that subjects in the active arm, compared to subjects in the placebo arm performed 40% better (4.2 vs. 3.0) (Figure 12) on their PRM % Correct Delayed scores. In a further break-down analysis, results from the PRM % Correct (Delayed) test showed that amnestic subjects on active arm also performed better than amnestic on the placebo arm (3.2 vs. 2.8), and that non-amnestic subjects on the active arms also performed better than non-amnestic subjects on the placebo arm (5.2 vs. 3.1) (Figure 13). Rapid Visual Information Processing (RVP) test is a computerized measure of sustained attention in a test subject. The RVP test results showed that there was about 76% improvement (41.3 vs. 23.4) in the RVP response latency score achieved by all the test subjects in the active arm, compared to all the subjects in the placebo arm (Figure 14). In a further break-down analysis, the results showed that there was about 91% improvement (36.3 vs. 19.0) in the RVP Response Latency score obtained by the amnestic subjects in the active arm, compared to the amnestic subjects in the placebo arm, with the non-amnestic subjects in the active arm seeing about 79% improvement (46.3 vs. 25.9), relative to the non- amnestic subjects in the placebo arm (Figure 15). This trend was reinforced via the results of the RVP A PRIME test, which is a signal detection measure of target sensitivity (i.e., successful response to targets and withholding of responses to non-targets). In the RVP A Prime test, there was minimal separation in scores between test subjects in the active arm compared to subjects in the placebo arm (0.022 vs. 0.025) (Figure 16). However, in a further breakdown analysis, the RVP A Prime score obtained by amnestic subjects in the active arm, compared to non-amnestic subjects in the active arm showed a 550% improvement (0.026 vs. 0.004). In the same analysis, non- amnestic subjects on the active arm compared to non-amnestic subjects in the placebo arm showed a 51% worsening of scores (0.018 vs. 0.037) (Figure 17). Spatial Working Memory (SWM) requires retention and manipulation of visuospatial information. This self-ordered test has notable executive function demands and provides a measure of strategy as well as working memory errors. SWM was measured using the SWM Between Errors metric (SWM BE). The results showed that there was an a small improvement (4.46 vs. 4.29) in the SWM BE score in all the test subjects in the active arm, compared to all the subjects in the placebo arm (Figure 18). In a further break-down analysis, the results showed that there was about 114% improvement (3.86 vs. 1.80) in the SWM score obtained by the amnestic subjects in the active arm, compared to the amnestic subjects in the placebo arm, with the non-amnestic subjects in the active arm seeing about 11% worsening effects (5.07 vs. 5.67), relative to the non-amnestic subjects in the placebo arm (Figure 19). Paired Associates Learning (PAL) assesses visual memory and new learning. Outcome measures include the errors made by the participant, the number of trials required to locate the pattern(s) correctly, memory scores and stages completed. The PAL TEA score showed a surprising finding that subjects in the active arm performed worse than subjects in the placebo arm (Figure 20). Further analysis revealed the presence of outliers in the active arm, with nothing comparable in the placebo arm. It is believed that these outliers were generated due to the statistical “adjustment” of the Total Errors a subject made. To deal with the possibility that the statistical adjustment of Total Errors (TEA) was leading to the generation of outliers, we used a different PAL sub-test, the PAL Mean Errors to Success test (PAL METS), to assess visual memory and new learning improvement. This test did not require a similar statiscal adjustment. PAL METS showed that subjects in the active arm, compared to subjects in the placebo arm performed about 12 times better (0.39 vs -0.04) (Figure 21). In summary, under the explanatory efficacy analysis, although the treatment of modafinil in combination with aniracetam for 7 days had not achieved a statistical difference compared to the placebo in terms of efficacy in all generally healthy elderly subjects with SCD through the five CANTAB tests, a further breakdown analysis of the results between the amnestic and non-amnestic subgroups in the majority of the tests revealed a promising signal that elderly subjects with amnestic mild cognitive impairment and/or even at more advanced disease progression state (for example, patients with MCI, Mild Alzheimer’s Disease, or Moderate Alzheimer’s Disease) could benefit from this combination therapy. Example 3: Dosage form comprising aniracetam and armodafinil Capsules comprising pellets with aniracetam and modafinil are prepared, wherein each capsule comprises pellets providing an overall amount of aniracetam of 1500 mg and an overall amount of modafinil of 200 mg. The release of the two actives is controlled in that there is a specific timing when these two actives are released from the pellets, which are present in the gastrointestinal tract shortly after ingestion of a capsule. The pellets have a setup, where a core is formed comprising the active agent aniracetam (the core former being e.g. saccharose, maize starch and/or povidone), followed by a layer delaying the release of the aniracetam from the core (the delayed release layer being based on e.g. a Surelease-coating, i.e. an ethylcellulose-coating; another possibility would be to delay the release by an enteric coating), followed by a layer comprising the active agent modafinil. The release is delayed by the delayed release layer such that the aniracetam is only released after about 1.5 hours after ingestion of a capsule. This specific timely release can be achieved by adjusting the thickness and/or the pore former of the layer delaying the release. The necessary adjustments to achieve the about 1.5 hours delay can be determined in particular by suitable standard in vitro release tests (e.g. the Paddle test according to USP in SGF). It is noted that it is preferred that the aniracetam, once the release is not delayed any more, is released in a regular, preferably immediate release manner, from the core. The dosage form then comprises a further component upon the layer delaying the release of the aniracetam, namely a layer comprising the modafinil. This layer may e.g. be a HPMC- layer comprising the modafinil (and further comprising triacetin as plasticizer), resulting in an immediate release of the modafinil right after ingestion of the capsule comprising the pellets. Using this setup, a dosage form can be provided, which release the first active agent, namely the modafinil, right after ingestion, followed by a delay of about 1.5 hours until the second active agent in the dosage form, namely the aniracetam, is released. This fits exactly with the desired onsets of the effects of the two active agents. The present invention has been described with reference to specific exemplary embodiments thereof. The disclosure and drawings are, accordingly, to be regarded in an illustrative rather than a restrictive sense. Various modifications of the invention in addition to those shown and described herein will become apparent to those skilled in the art and are intended to fall within the scope of the appended claims. For example, a skilled artisan will be able to choose the specific timely sequence of administration of two other actives (e.g., modafinil and another ampakine, or armodafinil and an ampakine), other than the specific combination provided in the examples, to achieve desired therapeutic effects including those noted above.