Haven't tried it and wouldn't.
I found this.....
MECHANISMS OF ACTION
Since the action of phosphatidylserine has not been established, any discussion of the mechanism of action is speculative. However, some findings from animal studies are of interest. Cholinergic hypofunction is thought to account in part for the cognitive deficits found in Alzheimer's disease. The most commonly used drugs for the treatment of Alzheimer's disease are reversible acetylcholinesterase inhibitors. The rationale of these drugs is to increase acetylcholine levels in the brains of Alzheimer's patients, and they may be somewhat effective in some cases. Animal studies indicate that phosphatidylserine restores acetylcholine release in aging rats by maintaining an adequate supply of the molecule and is able to increase the availability of endogenous choline for de novo acetylcholine synthesis.
The hippocampus of the brain is believed to be important for cognitive processes and is affected in those with Alzheimer's disease. The dendritic spines of pyramidal cells, the post-synaptic target of the excitatory input to the hippocampus, have been proposed as a substrate for information storage. Age-dependent dendritic spine loss in pyramidal neurons has been reported in the human brain, and the extent of synaptic loss appears to correlate with the degree of cognitive impairment. Rat experiments indicate that phosphatidylserine treatment prevents the age-related reduction in dendritic spine density in rat hippocampus. Protein kinase C facilitation of acetylcholine release has been reported in rats. Phosphatidylserine was found to restore protein kinase C activity in aging rats. Stimulation of calcium uptake by brain synaptosomes and activation of protein kinase C are yet other speculative mechanisms of phosphatidylserine's putative cognition-enhancing action.
And then doing a brief pub med search, i found this......
Effects of phosphatidylserine on the neuroendocrine response to physical stress in humans.
Monteleone P, Beinat L, Tanzillo C, Maj M, Kemali D.
Institute of Medical Psychology and Psychiatry, First Medical School, University of Naples, Italy.
The activity of brain cortex-derived phosphatidylserine (BC-PS) on the neuroendocrine and neurovegetative responses to physical stress was tested in 8 healthy men who underwent three experiments with a bicycle ergometer. According to a double-blind design, before starting the exercise, each subject received intravenously, within 10 min, 50 or 75 mg of BC-PS or a volume-matched placebo diluted in 100 ml of saline. Blood samples were collected before and after the exercise for plasma epinephrine (E), norepinephrine (NE), dopamine (DA), adrenocorticotropin (ACTH), cortisol, growth hormone (GH), prolactin (PRL) and glucose determinations. Blood pressure and heart rate were also recorded. Physical stress induced a clear-cut increase in plasma E, NE, ACTH, cortisol, GH and PRL, whereas no significant change was observed in plasma DA and glucose. Pretreatment with both 50 and 75 mg BC-PS significantly blunted the ACTH and cortisol responses to physical stress.
Hope this helps
