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Aniracetam is a compound in the group of Racetams due to its common pyrrolidone structure. It is one of the more common Racetamic structures. It is fat-soluble and thus needs to be ingested with fatty acids. Additionally, Aniracetam is Cholinergic
Aniracetam acts as a positive modulator of some excitatory receptors known as AMPA receptors and decreases the rate of receptor desensitization. This typically manifests as a controlled and prolonged neurological stimulation effect. Since AMPA receptors differ in structure across the brain, different AMPA modulators affect the brain in different ways.
Anecdotally, Aniracetam has been know to aid in 'collective and holistic thinking', or putting the pieces of the puzzle together. It also increases blood flow and activity in the area of the brain known for this action, the association cortex.
Aniracetam, as an AMPA modulator, is currently being studied for usage in depression and other CNS disorders such as Alzheimer's disease.
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1-p-anasoyl-2-pyrrilidinone, Ro 13-5057, CAS 72432-10-1, 1(4-methoxybenzoyl)-2-pyrrolidinone
As is the nature of dissecting a brain, the majority of the studies on Aniracetam have been done in laboratory animals such as mice and monkeys. Extrapolation is used in many cases when applied to humans, which is an unavoidable consequence since cellular studies would require taking brain tissue out of a living human.Examine.com Medical Disclaimer
Doses between 10mg/kg bodyweight and 100mg/kg bodyweight have been used in rats with efficacy in laboratory settings, suggesting high variability of the range of efficacy. However, there is a lack of evidence to suggest that this extrapolates well to humans.
Limited human trials suggest a dose of 1000-1500mg, taken with food. Doses as low as 400mg have shown rises in blood levels.
It is common practise to use Aniracetam with a Cholinergic compound.
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Aniracetam is a pyrrolidinone compound of the racetam family.
Aniracetam appears to be greatly taken up from the gut even in a fasted state, but is subject to extensive first pass hepatic metabolism. Due to this, it has an overall bioavailabiliy of around 8.6-11.4%. Bioavailability is presumed higher when taken with fatty acids, but unexplored.
Is fat-soluble and logically enhanced when taken with fatty acids, does not appear to need fatty acids to be absorbed
After doses of 300mg and 1200mg, peak plasma levels of 2.3mcg/L and 14.1mcg/L (respectively) with an elimination half-life of 35 minutes. It appears to have extensive first pass metabolism in the liver with the main metabolites being N-anisoyl-GABA, 2-pyrrolidinone, and anisic acid. 95.8% of the dose is recovered, mostly in the urine, 28 hours post ingestion.
In a study of healthy male volunteers, Aniracetam showed a Cmax (max concentration) of 8.75+/-7.82 and 8.65+/-8.7ng/mL over two testing periods which correspond to a Tmax (time at max) of 0.4+/-0.1 hour each time; in response to 400mg oral Aniracetam. The plasma elimination half-lives were 47+/-0.16 and 49+/-0.24 hours and plasma AUC 4.53+/-6.62 and 4.76+/-6.65ng/h/mL in this study as well. These relatively low peaks of Aniracetam may be due to extensive metabolism after oral administration.
It appears that superloading Aniracetam (50-100mg/kg bodyweight) does not augment the Cmax or Tmax significantly, and tends to only prolong the AUC to 1.7-2.1 hours.
Appears to be rapidly absorbed in under 30 minutes, and rapidly metabolized; higher doses do not change the time it takes to work, but may prolong the AUC (Area-Under-Curve) of Aniracetam, either by delaying excretion or metabolism
The main human metabolite of Aniracetam is a compound known as N-Anisoyl-GABA (aka. 4,p-Anisaminobutyric acid or ABA), which accounts for 70% of orally ingested Aniracetam by weight after hepatic (liver) biotransformation. Alternate pathways lead to production of P-Anisic Acid (which can be conjugated by wither glucuronic acid or glycine) and 2-pyrrolidinone (which then goes on to the Kreb's Cycle to produce energy via the succinate intermediate).
Aniracetam is heavily metabolized into N-anisoyl-GABA and P-Anisic Acid, which should be considered for bioactivity in the body
Aniracetam has been found to specifically decrease the rate of receptor desensitization in lab animal hippocampus (specifically quisqualate receptors), suggesting a potential benefit to memory formation. It does not seem affect choline uptake into hippocampal cells in any way, and actually encourages acetylcholine release.
Aniracetam also increases the release of dopamine and serotonin via Cholinergic mechanisms in the prefrontal cortex, with implications in improving judgement. This may also in part explain it's involvement as an anti-depressant. Via either the same or alternate mechanisms (positive AMPA modulation) Aniracetam has also been shown to reduce impulsiveness in the rat.
Through the general mechanism of AMPA modulation (and thus applicable to Piracetam and Oxiracetam), Ampakines can upregulate Brain-derived Neurotrophic factor (BDNF) for periods longer than the Ampakine's AUC due to a long BDNF half-life. These effects may be free of downregulation given some time away from the ampakine's existence in serum exists. BDNF is implicated in increasing adult neural plasticity.
Aniracetam seems to be able to alleviate damage done to memory and learning impairment caused by various agents and traumas such as cholinergic antagonists, cerebral ischaemia and electroconvulsive shock. Aniracetam can also protect against scopolamine-induced damage, and does so (at 1.5g) to a greater extent than Piracetam (at 2.4g).
Aniracetam has been shown to reduce measures of anxiety in rats, and has anecdotally reported to do the same in humans. It is suspected to do so via a mix of serotonergic, dopaminergic, and cholinergic interactions. Improvements as measured by social interactions were seen in doses ranging from 10mg/kg body weight to 100mg/kg bodyweight.
It has demonstrated efficacy in reducing depression in aged rats at 100mg/kg bodyweight, but was ineffective at exerting anti-depressive effects in younger mice. These effects were mimicked with Aniracetam metabolites, and were abolished with haloperidol and mecamylamine, and thus the mechanism was theorized to be enhancing dopaminergic signalling via the nicotinic acetylcholinergic receptors.
There may also be interactions with depression and downstream effects of Aniracetam's main mechanism of action, AMPA receptor modulation.
Aniracetam has been shown at 50mg/kg oral ingestion (rats) to decrease the turnover rates for dopamine in the striatum and reducing dopamine levels in the hypothalamus and striatum; serotonin levels decreased in the hypothalamus but increased in the cortex and striatum, where it reduced turnover (hypothalamus) and increase turnover (cortex, striatum, brain stem).
AMPA receptors mediate the majority of fast excitatory amino acid transmission in the synapse (as opposed to kainate and NMDA receptors, which mediate some postsynaptic responses/presynaptic release and modulation of excitatory synaptic transmission, respectively). AMPA receptors are heterogeneously expressed across the brain, which is possibly due to variations in the four subunits that make up AMPA receptors (GluR1 through R4), expression of each subunit as either a 'flip' or 'flop' variant, or more specific sub-subunit differences.
Aniracetam is a modulator of the AMPA receptor that works by binding to a non-active site of AMPA receptors and allosterically modifying the binding site, of which the final result is a reduced rate of desensitization in the presence of positive stimuli (such as glutamate, which is intrinsically produced).
Aniracetam does not directly agonize NDMA receptors, but does not appear to hinder agonism of NMDA receptors either.
Aniracetam has also been implicated in rats to alleviate some cognitive deficits in the hippocampus onset by Fetal Alcohol Syndrome (FAS) in a dosage of 50mg/kg bodyweight.
It is also being studied in other cognitive deficits such as Alzheimer's disease or other cognitive ailments as either a mechanism to biologically reverse neurological changes or to alleviate symptoms of said disorders.
(Common misspellings for Aniracetam include aniractam, anracetam, aniracetm)
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