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Piracetam is a cyclical derivative of GABA, synthesized by converting 2-pyrrolidinone into an amide.
It was discovered in 1964 by Romanian chemist, Corneliu E. Giurgea, who later coined the term “nootropic” to describe the novel effects of this compound.
Piracetam is the archetype of the Racetam class of nootropics. It is observed to increase cholinergic neurotransmission without exhibiting stimulant properties.
Additional effects observed in research trials include the following:
- Improves general cognition and working memory
- Increases oxygen utilization and glucose metabolism in the brain
- Slows signs of aging and reverses some forms of neuron damage
- Enhances cellular membrane fluidity and exerts a neuroprotective effect
Product Name: Piracetam (Nootropil)
Chemical Name: 2-(2-oxopyrrolidin-1-yl)acetamide
Formula: C6H10N2O2
Molecular Weight: 142.16 g/mol
CAS Number: 7491-74-9
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Brain Health- Promotes neuron health & synaptic plasticity
- Supports memory recall & learning
- Boosts focus, visual perception & attention
Piracetam Nootropic Research
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Piracetam (Nootropil, Breinox, Lucetam, Nootropyl) is also known as 2-(2-oxopyrrolidin-1-yl)acetamide.
It was the first nootropic substance discovered by Dr. Corneliu E. Giurgea, who remarked that it exhibited a cognitive enhancement effect without causing stimulation or depression of the central nervous system.
His research showed that Piracetam could increase learning and memory, protect the brain from injury, and that it exhibited few side effects and extremely low toxicity.
Giurgea coined the phrased “nootropic” from the Greek words, nous, or “mind”, and trepein, or “to turn”, to describe Piracetam. This Racetam thus became the first in a new class of compounds that could “bend the mind.”
Chemical Structure
Piracetam (2-oxo-1-pyrrolidine-acetamide) is a cyclical derivative of the neurotransmitter Gamma-Aminobutyric acid (GABA), although it is not observed to interact with GABA receptors. Like other Racetam nootropics, it features a 5-carbon oxopyrrolidone ring structure.
Piracetam can be formed by removing a molecule from GABA, resulting in a cyclical shape that retains two nitrogen atoms with one amide containing a side chain with two carbon atoms and the other nitrogen molecule. [5]
Piracetam is synthesized by condensing 2-pyrrolidinone with ethyl chloroacetate and a metal hydride. The resulting ester is then converted into an amide with ammonia. [6]
Pharmacokinetics
Piracetam absorption occurs rapidly and peak plasma levels have been recorded within 1.5 hours following oral administration. Oral bio-availability has been assessed at almost 100% based on Area Under Curve (AUC0-24) analysis.
The plasma half-life has been established at 5.0 hours in young adult men with a volume of distribution of 0.7 L/kg. No metabolites of Piracetam have been detected so far. [1]
Initial researchers concluded that Piracetam was almost entirely eliminated via renal pathways and excreted in urine. [1] A recent study suggests that there may be extrarenal elimination pathways as only two-thirds of the oral dosage was detected in urine. [4]
Piracetam Mechanism of Action
Piracetam is observed to increase brain oxygen consumption and reduce the negative effects of oxidative stress. Oxygen utilization is one measure of brain activity with increased consumption linked to increased alertness.
Piracetam may have a beneficial effect under conditions of hypoxia (oxygen deficiency) due to activity of adenylate kinase. [2]
In one study, dosages of between 100-500 mg/kg Piracetam a day resulted in improved mitochondrial function following oxidative stress (deprivation of sufficient oxygen levels). Subjects first underwent a state of mild serum deprivation which is associated with decreased mitochondrial membrane potential and ATP production.
Administration of Piracetam resulted in near complete reversal of the negative effects and reduced antioxidant enzyme activities in aged mouse brains. The results were more pronounced in aged animals than in young healthy animals. [7]
Heiss et al. studied the effects of Piracetam on cerebral glucose metabolism in human patients with Alzheimer’s disease and multiinfarct dementia or unclassified dementia.
The nootropic was found to increase utilization of glucose in the Alzheimer’s group, but not in the dementia groups. [8] This compound was also found to increase local cerebral glucose utilization in the rat cerebral cortex following induction of hypoxia. [9]
The stimulation of metabolic glucose pathways has been suggested as one mechanism for Piracetam’s neuroprotective effect against oxygen insufficiency. [10]
- Promotes neuron health & synaptic plasticity
- Supports memory recall & learning
- Boosts focus, visual perception & attention
Glutamatergic Receptors
Piracetam is theorized to positively modulate AMPA-sensitive glutamate receptors, but not NMDA or Kainate receptors.
Using Piracetam (as well as Aniracetam and Oxiracetam) leads to increased max density of the binding sites for the [3H]AMPA receptors in synaptic membranes taken from the rat cerebral cortex. This leads to increased efficacy, but not potency, of AMPA action potentials. [11]
Both Piracetam and Aniracetam bind to GluA2 and GluA3 AMPA receptor subtypes, however differences have been observed between the specific binding sites of these two Racetam nootropics. [13]
When administered to aged mice, 500mg/kg of Piracetam for 14 days was found to elevate N-methyl-D-aspartate (NMDA) glutamate receptor density.
Deficits of NMDA receptors may be one cause for age-associated cognitive impairments. It is theorized that Piracetam may help to reduce these impairments. [12] In vitro studies have demonstrated that Piracetam can enhance the release of glutamate from neuronal synapses. [14]
Membrane Fluidity
Neuronal membrane fluidity gradually declines with aging and may lead to diminished functions associated with age-related cognitive decline.
Piracetam appears to increase neuronal membrane fluidity as measured by decreased anisotropy of a membrane probe. This effect appears to be limited to aged animals.
In vitro analysis showed that chronic treatment of 300 mg/kg Piracetam once daily significantly enhanced membrane fluidity in aged rats and humans, but not in young rats. The same treatment was correlated with improvements in avoidance learning only in the aged rats. [15]
Hippocampal neuron membranes from patients with Alzheimer’s Disease show significantly lower membrane fluidity compared to elderly patients not diagnosed with Alzheimer’s Disease.
Piracetam was found, in vitro, to reverse the differences in hippocampal membrane fluidity. Following administration, neurons from the Alzheimer’s group showed the same level of fluidity as those from the control group. [16]
Cholinergic Receptors
Administering 500 mg/kg a day orally for two weeks was found to increase muscarinic cholinergic receptor density in the frontal cortex in aged female mice by 30-40%.
However, there was no effect on m-cholinoceptor density for young mice. This limited efficacy could explain why memory-enhancing effects of Piracetam are more pronounced in elderly adults.[16]
Administration of Piracetam has been demonstrated to decrease acetylcholine concentrations in the hippocampus. [19] Taking choline alongside Piracetam has been observed to increase the cognitive enhancement effects of the nootropic.
In one memory study, mice were given two sessions within a photo-cell activity cage and measured of activity were used to determine retention of information. One group of mice received 2000 mg/kg piracetam IP and 50 mg/kg piracetam plus 50 mg/kg choline IP administered post-session.
Additional groups received either choline alone (between 10 to 200 mg/kg IP) or piracetam alone (between 10 to 1000 mg/kg IP) as well as other combinations of piracetam and choline. The first group performed the best at the memory test. [25]
This suggests a synergistic mechanism of action, though studies have not yet been conducted in humans. [24]
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Piracteam for Memory and Mental Performance
Piracetam has been observed to improve short-term working memory. In one study of 16 healthy adult subjects, participants were given 3×4 capsules at 400 mg per day.
No differences were recorded after 7 days of treatment for a memory test in which a series of words were presented on a memory drum. However, after 14 days, those in the group that received Piracetam performed significantly better in the memory test. [27]
In another double-blind, cross-over comparison of mental performance, 18 aging individuals who did not show signs of cognitive decline were given two 4-week periods of Piracetam or placebo administration. Those individuals who took Piracetam performed significantly better than those given the placebo in a majority of the examination tasks. [28]
Alcohol Withdrawal
Piracetam is observed to prevent neuronal damage following chronic alcohol consumption. Prolonged consumption of ethanol (alcohol) due to alcoholism has been found to increase hippocampal neuronal loss, resulting in impaired memory.
Following treatment with Piracetam, the numbers of hippocampal cells in experimental animals undergoing alcohol withdrawal were significantly higher than those that were not given Piracetam. This result suggests that this nootropic can prevent or reduce neuronal degeneration during alcoholism withdrawal. [20]
Researchers also found that alcohol-fed rats treated with the compound showed higher numbers of synapses than in those that were not treated with Piracetam. The researchers concluded that Piracetam promotes synaptic reorganization at the mossy fiber level and that this may be caused by a protective effect upon glutamatergic receptors. [21]
Chronic alcohol use is also shown to increase lipofuscin deposits in the hippocampus, accelerating age-related decline. Piracetam has been shown to reduce lipofuscin deposits in alcohol-withdrawn experimental animals. [20]
Piracetam Toxicology
Piracetam shows extremely low toxicity in non-human acute exposure studies. Lethal doses were observed at 18.2 g/kg and higher in mice, but were not observed in rats at 21 g/kg or in dogs at 10 g/kg. The dosage 18.2 g/kg is greater than 100 times the standard therapeutic dose in humans. [1]
By comparison, the median lethal dose (LD50) in mice for table salt is 3 g/kg and the lethal dose for caffeine is 192 mg/kg. Therefore, Piracetam shows lower toxicity than both table salt and caffeine in animal models.
Adverse Effects
Piracetam exhibits few mild side effects and no serious side effects when used on its own by healthy adults. It is well-tolerated and has been found safe when administered in humans at dosages of 3.2g per day for up to 18 months. [30]
In one trial, patients with early probably Alzheimer’s Disease reported no side effects during one year of 8g dosages per day. [31] Some patients reported drowsiness during the first two week of use. [30] When administered with synthetic thyroid hormones (T3 and T4), some patients reported sleep disorders, confusion and irritability.
Common adverse reactions (affecting between 1 – 10 users out of 100) can include nervousness, weight gain, and hyperkinesia. Uncommon side effects (affecting less than 1 out of 100 users) can include depression, somnolence, and asthenia.
Additional rare side effects can include agitation, anxiety, confusion, hypersensitivity, hallucinations, ataxia, balance impairment, headache, aggravation of epilepsy symptoms, insomnia, abdominal pain, diarrhea, nausea, and vomiting. [1]
Interactions
Due to Piracetam’s effect on platelet aggregation, it should not be used by patients with blood-clotting disorders. Caution is recommended before combining this drug with pharmaceutical blood thinners or using in patients at risk of internal bleeding including gastrointestinal ulcer.
Its use is contraindicated in patients with disorders of hemostasis, cerebral hemorrhage, Huntington’s Chorea or individuals undergoing major surgery.
It is also contraindicated for patients with severe renal impairment as measured by a renal creatinine clearance of lower than 20 mL/min. [1]
Piracetam should not be used by pregnant or breastfeeding mothers. This compound is excreted in human breast milk. There has not been sufficient research to determine safety of this compound if ingested by developing fetuses or breastfeeding children, therefore caution is advised by medical experts. [1]
Regulatory Status
Piracetam is an unscheduled and unregulated substance that has not been approved as a drug or dietary supplement by the FDA in the United States. It is currently classified as an Investigational New Drug (IND). It is not permitted to be sold in the US. It can be legally imported and owned for personal use.
In Canada, Piracetam has not been given a Drug Identification Number (DIN), and therefore cannot be sold there. It is legal to import for personal use.
In the UK, Piracetam is a Prescription Only Medicine. In Australia, it is a Schedule 4 Prescription Only Medicine under the Australian Therapeutic Goods Administration.
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Article last updated on: July 24th, 2018 by Nootriment
1 Comment
Piracetam was first approved in Europe in the early 1970s for treatment of vertigo and age related disorders. Oryginal Piracetam (Aluid Pharma)
It is a parent molecule of all racetam compounds (Aniracetam, Oxiracetam, Coluracetam, Nefiracetam, Fasoracetam, etc). A meta-analysis of studies also supports the effectiveness of piracetam in treating:
Epilepsy, Convulsion, Seizure
Neurodegenerative Disorders: Ataxia
Stroke/Ischaemia