In elderly patients that suffered moderate brain pathology, Aniracetam nootropics have been tested as a possible treatment. In one study, researchers administered 1500mg of Aniracetam supplements daily to roughly 30 participants while the other 30 were given a placebo. The trial ran for four months, and those on the aniracetam nootropic treatment at the two and four-month check-in saw marked improvements.
A clinical study in rats of both aniracetam and piracetam found that the substances could help with turnover of serotonin and dopamine.Aniracetam. (2019). =MeSH-Pharmacological-Classification These are two important neurotransmitters that can affect your overall mood. They can also help with sleep quality, appetite, and weight maintenance.
One review of ADHD treatments published in Adolescent Psychiatry found that aniracetam can be helpful without unwanted side effects. The authors suggested 750 mg twice per day.Sharma A, et al. (2016). Non-pharmacological treatments for ADHD in youth.
While nootropics are most commonly taken by mouth, emerging research is suggesting better efficacy when aniracetam is taken intravenously.Goldsmith SD, et al. (2018). Designing a formulation of the nootropic drug Aniracetam using 2-hydroxypropyl-B-cyclodextrin suitable for parenteral administration. More research is needed.
Aniracetam can be available in capsule, tablet and powder forms. Tablets and capsules typically contain 500 mg each. Because aniracetam is an fat-soluble nootropic that you can take in conjunction with a healthy meal that contains fats. You can also take it with a tablespoon of unrefined coconut oil, or extra olive oil that is virgin.
Aniracetam is another AMPAkine created by modifying the piracetam molecule by replacing the acetamide moiety with a 4-methoxybenzoyl group . Aniracetam has few side effects (e.g. anxiety, insomnia, diarrhoea), a wide therapeutic window and a short half-life, making it very safe [13, 14], and has demonstrated a restorative effect in animal models of impaired memory. Aniracetam improves memory to healthy levels following disruption via scopolamine injection [13, 15, 16], sleep deprivation , surgical brain damage [18, 19], or as part of normal aging [14, 18, 20, 21]. Aniracetam also has a protective effect when administered prior to disruption. When administered before testing, aniracetam protects against memory loss caused by electrical brain stimulation [11, 22], haloperidol administration , and CO2-induced learning impairment .
The plasma concentration-time data after oral administration of aniracetam were analysed by noncompartmental pharmacokinetic methods performed using Phoenix 64 (WinNonlin, Certara LP). The area under the concentration-time curve (AUC) up to the last sampling point was calculated using the trapezoidal method.
DMS performance following no injection, saline, 100 mg/kg aniracetam, and 200 mg/kg aniracetam in the Inject-30 condition. A total of six birds were tested. Three birds were tested with delays of 0, 2, 4, and 8 sec (Delay set 2), and three were tested with delays of 0, 3, 6, and 12 sec (Delay set 3). Chance is 50% correct. Error bars are +/- SEM.
DMS performance following no injection, saline, 100 mg/kg aniracetam, and 200 mg/kg aniracetam in the Inject-60 condition. A total of eight birds were tested. Four birds were tested with delays of 0, 1, 2, and 4 sec (Delay set 1), one was tested with delays of 0, 2, 4, and 8 sec (Delay set 2), two were tested with delays of 0, 3, 6, and 9 sec (Delay set 3) and one was tested with delays of 0, 5, 10, and 20 sec (Delay set 5). Chance is 50% correct. Error bars are +/- SEM.
DMS performance following no drug (corn) or drug (corn + 200 mg/kg aniracetam in the Oral-30 condition. A total of five birds were tested. One bird was tested on delays of 0, 1, 2, and 4 sec (Delay set 1), one was tested on delays of 0, 2, 4, and 8 sec (Delay set 2), two were tested on delays of 0, 3, 6, and 9 sec (Delay set 3), and one was tested on delays of 0, 5, 10, and 20 sec (Delays set 5). Chance is 50% correct. Error bars are +/- SEM.
Five birds were tested in the Oral-60 group. Three of the birds were drawn from birds in the Inject-30 group, and two were drawn from birds in the Inject-60 group. One bird was tested on delays of 0, 1, 2, and 4 sec (Delay set 1), two were tested on delays of 0, 2, 4, and 8 sec (Delay set 2), and two were tested with delays of 0, 3, 6, and 12 sec (Delay set 3). The performance of these five birds across the two different drug conditions and their respective four different delay durations is shown in Fig 6. There was again a significant effect of delay, F (3, 12) = 84.53, p < 0.001, indicating that performance fell as the delay increased in length. There was a significant effect of drug in that aniracetam reduced performance, F (1, 4) = 12.67, p < 0.05, but no Drug x Delay interaction, F (3, 12) = 2.28, p = 0.17.
DMS performance following no drug (corn) or drug (corn + 200 mg/kg aniracetam in the Oral-60 condition. A total of five birds were tested. One bird was tested on delays of 0, 1, 2, and 4 sec (Delay set 1), two were tested on delays of 0, 2, 4, and 8 sec (Delay set 2), and two were tested with delays of 0, 3, 6, and 12 sec (Delay set 3). Chance is 50% correct. Error bars are +/- SEM.
There was no indication that aniracetam improved short-term memory in pigeons, evidenced by a lack of increase in matching accuracy at any of the delays used on the DMS task. Additionally, the absence of any improvement was observed for both the intramuscular and oral delivery routes, and similarly there was no improvement when aniracetam was administered at either 30 or 60 minutes before testing. The lack of improvement was not due to a floor or ceiling performance effect, as the retention functions displayed on the DMS task were ideal for observing any improvement. Finally, the results of the pharmacokinetic study suggest that, at least for the oral administration, we chose the correct testing times in relation to the time-points at which the blood aniracetam and N-anisoyl-GABA concentrations were highest.
In humans, rats, and dogs, aniracetam is rapidly and completely absorbed from the gastrointestinal tract following oral administration and is extensively metabolised in the liver, primarily to N-anisoyl-GABA [27, 28]. There is however, a wide variability reported in the literature for the maximum plasma concentrations following oral administration of aniracetam [25, 29]. The present study is the first to investigate the pharmacokinetics following oral administration aniracetam in pigeons and the plasma concentrations observed were within the range reported [29, 30], however were higher than that reported for rats . The concentrations of N-anisoyl-GABA were higher in the present study than reported for rats  and humans . Investigations into the pharmacokinetics following IV administration is needed for pigeons, however there are currently methodological limitations due to the low solubility of aniracetam. Consequently, subsequent studies are needed to produce a formulation that can be used for IV administration in pigeons.
Another difficulty in drug treatment is determining the best time to administer the drug in relation to testing times. Aniracetam has a short half-life  and, in a previous study no effect was found when pigeons were treated with aniracetam administered intramuscularly 50 minutes before testing. Given that it is possible that the aniracetam had already been metabolised by the time testing occurred, we tested both 30-minute and 60-minutes time-points, and conducted a pharmacokinetic study to determine whether our testing times were appropriate based on the peak blood concentration levels of aniracetam. While the results of the pharmacokinetic study did indicate that peak concentration levels were occurring just before testing began, it did not guarantee that aniracetam was getting into the brain in a timely manner, so future research should investigate a wider array of times for administering the drug. Amakusa et al.  report that the metabolite N-anisoyl-GABA was found in the cerebrospinal fluid of elderly patients when administered 200 mg aniracetam, providing evidence that aniracetam and/or its metabolites are able to traverse the blood-brain barrier. Further studies could be conducted in pigeons to investigate the availability of aniracetam and N-anisoyl-GABA in the brain, perhaps by collecting brain tissue at different time-points and correlating this to the disappearance of these compounds in the blood.
There is growing evidence supporting the restorative effect of aniracetam in animal models of disease or injury. Aniracetam has been shown to reverse impairment caused by scopolamine during a passive avoidance task , help to restore lost memory function following trauma to the brain , and improve memory function in aged individuals . Similarly, aniracetam has a protective effect when administered prior to scopolamine or CO2 disruption . The restorative and protective effects were dose-dependent, with the optimal dose being around 50 mg/kg. The evidence seems convincing, therefore, that aniracetam does improve performance in brains that have been subject to insult.
Whether aniracetam can improve memory performance in healthy brains is much less certain. Neurologically-healthy monkeys treated with aniracetam demonstrated improved performance on a DMS task [16, 23], and rats experienced an increased ability to discriminate between novel and familiar objects following aniracetam (50 mg/kg) administration . Rats also exhibited improved performance on the radial arm maze test when treated with high doses (400 and 800 mg/kg) of aniracetam , and improved performance on an active avoidance task when given aniracetam (50 mg/kg) 60 minutes before testing . That all said, the improvements, although significant, are often small, and are observed in a varying range of doses, making it difficult to determine where exactly the enhancement, if any, occurs. For example, a study using rats failed to find an enhancement at doses lower than 400 mg/kg, but did notice an enhancement at 400 and 800 mg/kg , whereas another study in rats found an enhancement at 50 mg/kg, but not at 25 or 100 mg/kg . 59ce067264