Phosphatidylserines

Lipids -> Unambiguous Lipids

Lipids -> Glycerophospholipids [GP] -> Glycerophosphoserines [GP03] -> Diacylglycerophosphoserines [GP0301]

280.7 Ų [M-H]- [CCS Type: DT; Buffer gas: N2; Sample Type: Brain (polar extract); Dataset: Unambiguous Lipids]

284.03 Ų [M-H]- [CCS Type: DT; Method: stepped-field]

Warning

H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]

P264, P264+P265, P280, P302+P352, P305+P351+P338, P321, P332+P317, P337+P317, and P362+P364 (click each P-code to see the statement)

The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.

Phosphatidylserine is indicated in the treatment of cognitive impairment, including Alzheimer's disease, age-associated memory impairment and some non-Alzheimer's dementias. Further research is required before phosphatidylserine can be indicated for immune enhancement or for reduction of exercise stress. Phosphatidylserine was first isolated from brain lipids called cephalins. The major cephalins are phosphatidylserine and phophatidylethanolamine. Phosphatidylserine is involved in signal transduction activity as well as being a basic structural component of biologic membranes.

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. Phosphatidylserine restores acetylcholine release in aging humans 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. 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.