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L-Alpha glycerylphosphorylcholine (α-GPC, choline alfoscerate) is a natural choline compound. It is parasympathomimetic, meaning it activates the “rest and digest” branch of the nervous system.

α-GPC rapidly delivers choline to the brain across the blood–brain barrier and is a biosynthetic precursor of the neurotransmitter acetylcholine.

α-GPC is readily hydrolyzed and absorbed through oral intake to form free choline. It is able to increase both dopamine and serotonin concentrations in the frontal cortex and cerebellum of rats following ingestion.

Is it safe? Are there side effects?

Yes, α-GPC is approved as a dietary supplement component under provisions of the Dietary Supplement Health and Education Act of 1994. It is classified as generally recognized as safe (GRAS).

There are no reported major side effects of α-GPC. Minor side effects include headache and heartburn, but these are rare if α-GPC is taken in safe quantities. Most individuals should be able to safely tolerate up to 1.2 g of α-GPC per day.

Effects on Cognition


A study on 19 healthy college students showed that a nootropic blend consisting of α-GPC in addition to other compounds (choline bitartrate, phosphatidylserine, vitamins B3, B6, and B12, folic acid, L-tyrosine, anhydrous caffeine, acetyl-L-carnitine, and naringin), resulted in increased reaction time and alertness, as measured by both a self-report questionnaire and reaction time measured by a Makoto testing device.


A study in 26 individuals showed that daily ingestion of a nootropic blend containing α-GPC was effective in improving memory (recall, recognition, and short-term memory) at both 2 weeks and 10 weeks into the treatment period.

Effects on Medical Conditions

Many studies have consistently showed efficacy and safety of α-GPC. Thus, α-GPC is a promising therapeutic resource in “association with cholinesterase inhibitors or in particular situations in which treatment with inhibitors is not tolerated or contraindicated”.

Alzheimer’s Disease

There is evidence that α-GPC may have potential for the treatment of Alzheimer’s disease and dementia. Choline has been found to improve Alzheimer’s Disease patients’ performance on cognitive tests including the mini mental status exam (MMSE), Alzheimer’s Disease Assessment Scale (both behavioral and cognitive subscales), Global Deterioration Scale, and the Clinical Gobal Impression Scale. These effects were seen in a study in which patients took 400 mg choline alfoscerate for 180 days.

Vascular Cognitive Impairment

Vascular dementia or cognitive impairment is found in individuals with problems such as stroke.

A meta-analysis of α-GPC studies across 4315 patients with vascular dementia or vascular cognitive impairment showed that there were positive effects of α-GPC on various cognitive tasks. Patients with neurodegenerative dementia saw an improvement on the Mini Mental State Evaluation (MMSE). Those with vascular dementia performed better on the Sandoz Clinical Assessment Geriatric (SCAG) scale.

A 2001 meta-analysis assessed the effect of α-GPC on cognitive performance in 1570 patients with senile dementia of the Alzheimer’s type (SDAT) and vascular dementia. It was found that patients undergoing treatment with α-GPC performed significantly better than their counterparts receiving standard treatments. The patients improved performance on the MMSE if they had SDAT and the SCAG scale if they were suffering from vascular dementia. When compared against CDP-choline, α-GPC tended to result in better SCAG scores in vascular dementia patients.


Administration of α-GPC has been found to reverse the effects of scopolamine-induced amnesia. Scopolamine is an anticholinergic drug.

Stroke and Ischemia

The clinical tolerability was measured in an Italian open multicenter trial on 2044 patients suffering from a recent stroke or transient ischemic attack (TIA). Patients recieved injections of α-GPC for one month and oral dosages for five months afterwards. Patients improved their performance on the MMSE by regaining function up to normal baseline within 3 months of treatment. By the end of the trial period, 75% of the patients improved to a state where there was “no cognitive decline”. Patients showed excellent tolerability for the drug, as there were no major adverse effects.

Structure & Synthesis

Choline can be supplemented from several different sources. Popular sources include α-GPC, choline bitartate and CDP-choline. By weight, choline represents 40% of α-GPC, 18% of CDP-choline, and 40% of choline bitartate. Choline bitartate is inexpensive, but is not as bioavailable as α-GPC or CDP-choline and cannot cross the brain-blood barrier. CDP-choline is a less efficient delivery mechanism of choline; one needs to take more than twice as much CDP-choline than α-GPC to get the same amount of choline.

α-GPC naturally occurs in the brain. When the brain is low on free choline for acetylcholine, the brain breaks down cell membranes to cannabalize choline. α-GPC is that catabolic byproduct, and thus is reliably able to cross the blood brain barrier intact.

The best natural source of α-GPC is in red meat. Its natural availability is otherwise scarce.

α-GPC can be synthesized synthetically via phosphorylation and reduction steps with (R)-glycidol as a starting material.

Mechanisms of Action

Choline (various quaternary ammonium salts containing the N,N,N-trimethylethanolammonium cation) is a chemical precursor or “building block” needed to produce acetylcholine.

This is clinically important because there is a large body of research suggesting that learning, memory, intelligence, and mood are mediated at least in part by acetylcholine metabolism in the brain. This is commonly referred to as the “cholinergic effect”.

Role of cholinergic receptors in memory

Increased binding to cholinergic receptors has been implicated in memory.

The role of cholinergic receptors in memory has been studied extensively in animal models by administering cholinergic antagonists and measuring resulting changes in memory. Injection of cholinergic antagonists in the perirhinal cortex has resulted in impaired encoding of information for stimuli recognition. Scopolamine injection into the hippocampus impairs spatial encoding, and infusions into the medial septum impair spatial learning and reduce acetylcholine release in the hippocampus.

Infusions of carbachol (a cholinergic agonist) were able to reverse memory impairment caused by a certain dosage of scopolamine. However, impairment caused by a higher dosage was not reversible. Meanwhile, infusions of scopolamine into the CA3 region of the hippocampus have been shown to cause impairments in memory encoding in rats as tested with the Hebb-Williams maze.


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