Serine for Phosphatidylserine and the Aging Brain

Table of Contents

1. Phosphatidylserine as Inner-Leaflet Membrane Phospholipid
2. Why the Brain Concentrates Phosphatidylserine
3. Endogenous Biosynthesis — Base-Exchange and PSS1 / PSS2
4. The Crook Trials (1991, 1992) in Memory Impairment and Early Alzheimer's Disease
5. Bovine-Cortex vs Soy-Derived PS — The BSE-Driven Sourcing Shift
6. The U.S. Food and Drug Administration Qualified Health Claim (2003)
7. Attention and Attention-Deficit/Hyperactivity Disorder Trials
8. Exercise, Cortisol, and Athletic Performance
9. Dosing, Forms, and Bioavailability
10. Cautions and Drug Interactions
11. Key Research Papers
12. Connections
13. Featured Videos

Phosphatidylserine as Inner-Leaflet Membrane Phospholipid

Phosphatidylserine is one of the four major glycerophospholipids that build the lipid bilayer of every animal cell membrane. Its structure is straightforward: a glycerol backbone with two fatty-acid tails esterified at the sn-1 and sn-2 positions, and a phosphate-serine head group at sn-3. The serine carboxylate carries a negative charge at physiological pH, and the amino group carries a positive charge — net charge is −1, making PS the dominant anionic phospholipid of the cell membrane.

That anionic character has a striking consequence: phosphatidylserine is actively maintained on the inner leaflet of the plasma membrane by a family of adenosine triphosphate-dependent lipid transporters called flippases (P4-ATPases). The asymmetry is not accidental. It enables three crucial biological functions:

1. Apoptosis signaling — when a cell commits to programmed death, flippase activity stops and a scramblase enzyme flips PS to the outer leaflet. The externalized PS becomes the "eat me" signal that macrophages recognize through specific PS receptors (TIM-4, BAI1, stabilin-2) to clear the dying cell before it ruptures. Loss of PS asymmetry is the canonical biochemical marker of apoptosis — the annexin-V assay used in every immunology and cancer lab works by binding externalized PS.
2. Blood coagulation — activated platelets expose PS on their outer surface, and the PS surface provides a binding platform for the tenase (factors IXa and VIIIa) and prothrombinase (factors Xa and Va) complexes of the coagulation cascade. Without PS exposure, the cascade runs roughly 1,000-fold more slowly.
3. Membrane-bound enzyme regulation — protein kinase C, several Ras-family GTPases, and many other signaling proteins require PS in the inner leaflet for their membrane targeting and activation. PS depletion impairs all of these signaling cascades simultaneously.

The serine amino acid is consumed stoichiometrically in PS synthesis — one serine molecule per PS molecule. In a typical 70-kilogram adult, the steady-state turnover of phosphatidylserine consumes roughly 200 to 400 milligrams of serine per day for membrane maintenance alone, on top of all other serine-requiring pathways.

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Why the Brain Concentrates Phosphatidylserine

The brain is unusual among organs in the degree to which it concentrates phosphatidylserine. Lipidomic analyses of human brain tissue consistently report that PS represents approximately 13 to 15% of total phospholipid in gray matter and a slightly lower fraction in white matter — compared with 2 to 4% in skeletal muscle, 6 to 8% in liver, and roughly 1% in plasma. The total PS content of the adult human brain is on the order of 30 to 40 grams.

Three features of neural tissue drive this concentration:

1. Dendritic membrane area — the dendritic arborization of cortical pyramidal neurons creates an enormous surface-area-to-volume ratio, with up to 10,000 synaptic inputs per neuron each requiring a chemically distinct postsynaptic membrane patch. PS is enriched in these synaptic membranes and supports the receptor clustering and signal transduction at each synapse.
2. Synaptic vesicle traffic — presynaptic terminals contain pools of small synaptic vesicles that fuse with the plasma membrane during neurotransmitter release and are then recycled by endocytosis. PS in the cytoplasmic leaflet is required for the fusion and fission events at every cycle — specific proteins (synaptotagmin, syntaxin, complexin) bind PS as part of the regulated exocytosis machinery.
3. Myelin biosynthesis — oligodendrocytes synthesize enormous quantities of membrane lipid (each oligodendrocyte can myelinate up to 50 axons), and PS contributes to the cytoplasmic surface of the myelin sheath and to the paranodal junctions that organize axonal ion channels.

Brain PS content declines with age. Cross-sectional and longitudinal post-mortem studies show roughly a 10 to 20% reduction in cortical PS concentration between age 30 and age 80, with steeper declines in regions vulnerable to neurodegenerative disease (hippocampus, frontal cortex). This age-related PS decline is part of the rationale for exogenous PS supplementation in older adults — restoring membrane PS to younger-adult levels may support the receptor and signaling functions that PS enables.

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Endogenous Biosynthesis — Base-Exchange and PSS1 / PSS2

Animal cells — unlike yeast and bacteria — do not synthesize phosphatidylserine by direct condensation of CDP-diacylglycerol with serine. Instead, they use a base-exchange mechanism catalyzed by two enzymes: phosphatidylserine synthase 1 (PSS1, encoded by PTDSS1) and phosphatidylserine synthase 2 (PSS2, encoded by PTDSS2). Both are integral membrane proteins of the endoplasmic reticulum, concentrated at ER-mitochondria contact sites (MAM, mitochondria-associated membranes).

• PSS1 catalyzes the exchange of the choline head group of phosphatidylcholine for serine: phosphatidylcholine + L-serine → phosphatidylserine + choline.
• PSS2 catalyzes the analogous exchange for phosphatidylethanolamine: phosphatidylethanolamine + L-serine → phosphatidylserine + ethanolamine.

Both reactions are reversible, calcium-dependent, and feedback-inhibited by their own product (phosphatidylserine binds an allosteric site on each synthase and reduces activity). The feedback inhibition is so tight that intracellular PS concentration is held within a narrow range even when substrate supply varies widely — this is part of the homeostasis that prevents pathological PS accumulation.

Once synthesized in the ER, PS is transported to mitochondria via the MAM contact sites, where mitochondrial phosphatidylserine decarboxylase (PSD, encoded by PISD) converts a fraction of it to phosphatidylethanolamine. PE produced this way is then trafficked back to other organelles for membrane assembly. This serine → PS → PE pathway is, quantitatively, one of the two major routes by which animal cells make phosphatidylethanolamine.

The clinical importance of these enzymes was illustrated by the discovery that gain-of-function mutations in PTDSS1 cause Lenz-Majewski syndrome, a rare developmental disorder with hyperostosis, intellectual disability, and progeroid features. Loss-of-function mutations in PISD (mitochondrial PSD) cause a developmental and metabolic disorder with white-matter abnormalities. These rare disorders confirm that PS biosynthesis is non-redundant and that disruption produces severe neurological consequences.

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The Crook Trials (1991, 1992) in Memory Impairment and Early Alzheimer's Disease

The clinical literature on oral phosphatidylserine supplementation was established by a series of trials led by Thomas Crook at the Memory Assessment Clinics in Bethesda, Maryland, in the early 1990s. The two pivotal trials — published in Neurology in 1991 and Psychopharmacology Bulletin in 1992 — remain the most-cited demonstrations of PS efficacy in older adults with memory impairment. Both, like the Cenacchi trial below, used phosphatidylserine made from cow brain (bovine cortex), not the soy PS sold today (see the next section).

Crook et al. 1991, Neurology. Multicenter, randomized, double-blind, placebo-controlled trial of bovine-cortex-derived phosphatidylserine (BC-PS) at 300 mg per day (100 mg three times daily) for 12 weeks in 149 adults aged 50 to 75 with AAMI. The primary outcome was change on a computerized memory test battery (the MAC-S, Memory Assessment Clinics Self-Rating Scale, plus a battery of recall and recognition tasks).

• The PS group showed significant improvement on tests of name-face association (the canonical real-life memory complaint of older adults), telephone number recall, and misplaced-objects recall
• The greatest benefit was in the subgroup with the worst baseline performance (those with the most pronounced AAMI), suggesting PS works best in those who need it most
• The effect was equivalent, on the memory measures used, to a roughly 12-year reduction in apparent memory age — an unusually large effect size for a nutritional intervention
• Adverse effects were minimal and indistinguishable from placebo

In the published summary's own words, the 149 people treated with BC-PS 100 mg three times a day improved relative to placebo “on performance tests related to learning and memory tasks of daily life,” and those who performed at a relatively low level before treatment were the most likely to respond; in that subgroup, computerized and standard memory tests and doctors' overall ratings of improvement all got better.

Crook, Petrie, Wells, & Massari 1992, Psychopharmacology Bulletin. Trial in 51 patients meeting clinical criteria for probable Alzheimer's disease, using BC-PS 100 mg three times a day (300 mg/day) or placebo for 12 weeks. Those on PS improved on several cognitive measures relative to placebo, and the differences between the groups were most apparent among patients with less severe cognitive impairment; the authors suggested PS may be a promising candidate for study in the early stages of Alzheimer's disease. This is the origin of the common understanding that PS is most useful in the early stages of cognitive decline, before substantial neuronal loss has occurred.

A subsequent double-blind, placebo-controlled trial by Cenacchi and colleagues in Italy (1993) recruited 494 people aged 65 to 93 with moderate to severe cognitive decline in 23 geriatric or general medicine units, and gave BC-PS 300 mg/day or placebo for 6 months. The PS group showed statistically significant improvements over placebo in both behaviour (the Plutchik Geriatric Rating Scale) and memory (the Buschke Selective Reminding Test), and clinical checks and laboratory tests showed that PS was well tolerated.

A 2025 mixed-supplement trial. A randomized, double-blind, placebo-controlled trial in China (Duan and colleagues) gave 190 older adults with mild cognitive impairment (average age about 68) two capsules a day for 12 months. Each capsule contained 31.5 mg phosphatidylserine, 144 mg alpha-linolenic acid (a plant omega-3) and 3.6 mg ginkgo flavonoids, plus small amounts of vitamins B1 and B6 and folic acid. Compared with placebo, the supplement group improved significantly on arithmetic, a similarities (reasoning) test and short-term memory. Because the capsule was a mixture with a low PS dose, the result cannot be credited to PS alone.

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Bovine-Cortex vs Soy-Derived PS — The BSE-Driven Sourcing Shift

All of the foundational PS efficacy trials — Crook 1991, Crook 1992, Cenacchi 1993, and earlier European work — used bovine-cortex-derived phosphatidylserine (BC-PS). The bovine source was chosen because the fatty acid composition of bovine cortical PS most closely resembles human brain PS (high in stearic acid at sn-1, docosahexaenoic acid (DHA) at sn-2). This compositional similarity was thought to be important for clinical effect.

The bovine-source supply chain collapsed in the mid-1990s for an obvious reason: the bovine spongiform encephalopathy (BSE, "mad cow disease") crisis. By 1996, when the link between BSE and variant Creutzfeldt-Jakob disease in humans was confirmed, no responsible supplement manufacturer would ship bovine-brain-derived material. The U.S. Food and Drug Administration and European regulators effectively prohibited bovine-CNS-source phospholipids for oral consumption, and the BC-PS industry shut down.

The replacement was soy-derived phosphatidylserine (S-PS), manufactured by enzymatic conversion of soy lecithin using a phospholipase D enzyme that exchanges the choline of soy phosphatidylcholine for serine — essentially the same base-exchange chemistry as the endogenous PSS1 enzyme. By the late 1990s, soy PS was the universal commercial source for supplements.

The clinical question was: does soy-derived PS work as well as the bovine-cortex PS that was used in the original trials? The fatty-acid composition differs — soy PS has a much higher fraction of linoleic acid and a much lower fraction of docosahexaenoic acid. Several trials of soy PS published from 2000 onward have shown modest but real cognitive benefit in older adults, though typically smaller effect sizes than the historical BC-PS trials. The picture, on balance:

• Soy PS is clinically effective for memory and cognitive symptoms, particularly in age-associated memory impairment and early-stage cognitive decline
• The effect size may be smaller than that of bovine PS, but the difference has not been definitively quantified in head-to-head comparison
• Some manufacturers offer docosahexaenoic acid-enriched soy PS or krill-derived PS to better match the historical fatty-acid composition; these are more expensive but may produce somewhat larger benefit
• Marine-source PS (from herring roe, krill, or other marine sources) is increasingly available and provides a DHA-PS option from animal sources (krill and herring roe are not vegetarian)

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The U.S. Food and Drug Administration Qualified Health Claim (2003)

In May 2003, the United States Food and Drug Administration formally granted a qualified health claim for phosphatidylserine and reduced risk of cognitive dysfunction and dementia. The qualified-claim category sits below the much more stringent "authorized health claim" category — the qualified designation acknowledges that scientific evidence supports the claim while requiring specific disclaimer language. The approved label statements:

• "Consumption of phosphatidylserine may reduce the risk of cognitive dysfunction in the elderly. Very limited and preliminary scientific research suggests that phosphatidylserine may reduce the risk of cognitive dysfunction in the elderly. U.S. Food and Drug Administration concludes that there is little scientific evidence supporting this claim."
• "Consumption of phosphatidylserine may reduce the risk of dementia in the elderly. Very limited and preliminary scientific research suggests that phosphatidylserine may reduce the risk of dementia in the elderly. U.S. Food and Drug Administration concludes that there is little scientific evidence supporting this claim."

The required disclaimer language is unusually strong — the U.S. Food and Drug Administration does not endorse PS as a treatment for cognitive dysfunction and explicitly notes the "little scientific evidence" caveat. But the existence of any qualified health claim for a dietary supplement is itself meaningful; the agency has rejected the great majority of qualified-claim petitions, and the PS approval reflected the cumulative weight of two decades of European and American clinical trials.

The 2003 qualified claim has shaped the dietary-supplement market in the years since. Phosphatidylserine appears in dozens of memory-support products, often combined with docosahexaenoic acid, ginkgo biloba, bacopa, lion's mane, or vinpocetine. The standard adult dose — 100 to 300 milligrams per day, divided — comes directly from the dosing protocols of the foundational Crook and Cenacchi trials.

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Attention and Attention-Deficit/Hyperactivity Disorder Trials

A second clinical literature has developed around phosphatidylserine for attention deficit hyperactivity disorder (ADHD), particularly in children. This is a much smaller body of evidence than the age-related cognitive decline literature, and its results are mixed: the trials below include positive results and a 2024 trial that found no benefit.

Hirayama et al. 2014 (Japan). Randomized, double-blind, placebo-controlled trial of soy-derived PS at 200 mg per day for 2 months in 36 children aged 4 to 14 with attention-deficit/hyperactivity disorder. The PS group showed significant improvement on standard attention-deficit/hyperactivity disorder rating scales (ADHD-RS) and on auditory-verbal short-term memory tests compared with placebo. Effect size was modest but clinically meaningful for the attention subscale.

Manor et al. 2012, 2013 (Israel). Two-stage trial design: a 15-week double-blind, placebo-controlled phase in 200 children with attention-deficit/hyperactivity disorder randomized to 200 mg/day of a PS-DHA conjugate (PS-Omega3) or placebo, followed by a 15-week open-label extension that 150 children entered. The key findings of the double-blind phase were a significant reduction on the restless/impulsive subscale of the Conners' Parent Rating Scale and a significant improvement in the parents' emotional-impact score of the Child Health Questionnaire, both in the PS-Omega3 group. An exploratory analysis found the clearest benefit in children with more pronounced hyperactive-impulsive behaviour and mood and behaviour dysregulation. Children who continued on PS-Omega3 kept their gains in the extension, and the treatment was well tolerated. The PS-DHA combination appeared more effective than either component alone in earlier work.

The proposed mechanism for the attention-deficit/hyperactivity disorder benefit overlaps with the aging-brain rationale: PS is concentrated in the prefrontal cortex, where it supports the dopaminergic and noradrenergic signaling that is the target of conventional attention-deficit/hyperactivity disorder medications. PS may also modulate the hypothalamic-pituitary-adrenal (HPA) axis (see exercise/cortisol section below), and elevated stress reactivity is a recognized feature of ADHD. Several integrative pediatric practitioners use PS as adjunctive support alongside standard attention-deficit/hyperactivity disorder treatment, particularly in patients who tolerate stimulant medications poorly.

Rheims et al. 2024 (France) — a negative trial. A multicentre double-blind, randomized, placebo-controlled trial gave PS-Omega3 or placebo for 12 weeks (then 12 weeks open-label) to children aged 6 to 16 who had both epilepsy and attention-deficit/hyperactivity disorder. It was stopped early because too few eligible children could be found, and 74 were randomized (44 to PS-Omega3, 30 to placebo). The inattention score fell by 1.57 points on PS-Omega3 and by 2.90 points on placebo (p = 0.33, not significant), and results were similar at 24 weeks and on every other ADHD measure. Because the trial was underpowered, the authors drew no formal conclusion, but wrote that their data strongly suggested the PS-Omega3 product used did not improve ADHD symptoms in children with epilepsy.

For more on the broader attention-deficit/hyperactivity disorder evaluation and intervention strategy, see our attention-deficit/hyperactivity disorder page.

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Exercise, Cortisol, and Athletic Performance

A separate research stream has examined phosphatidylserine as a modulator of the hypothalamic-pituitary-adrenal (HPA) axis — specifically the cortisol response to physical and psychological stress. Several small randomized trials from the late 1990s and 2000s reported that oral PS at 400 to 800 mg per day blunted the cortisol elevation in response to exhaustive exercise.

• Monteleone et al. 1990, 1992 — intravenous and oral BC-PS reduced adrenocorticotropic hormone (ACTH) and cortisol response to physical exercise in healthy volunteers. In the 1992 oral study, 9 healthy men took brain-cortex PS 800 mg/day or placebo for 10 days; PS significantly blunted the ACTH and cortisol responses to exercise (p = 0.003 and p = 0.03) without changing growth hormone or prolactin
• Starks et al. 2008 — in a double-blind, placebo-controlled crossover study of 10 healthy men, 600 mg/day PS for 10 days lowered the peak cortisol level by 39% and the cortisol area under the curve by 35% compared with placebo after 15 minutes of moderate-intensity cycling (65% rising to 85% of maximum oxygen uptake); it had no effect on lactate or growth hormone
• Fahey & Pearl 1998 — oral PS supplementation reduced cortisol and improved mood profile in resistance-trained athletes during overreaching training cycles

The mechanism is incompletely understood. PS may act centrally on the hypothalamus or pituitary to dampen the CRH and adrenocorticotropic hormone response to stress, or it may modulate the membrane-bound steroid response at the level of the adrenal cortex. Some practitioners include PS in overtraining-prevention protocols for athletes with elevated baseline cortisol or symptoms of hypothalamic-pituitary-adrenal dysregulation, though the evidence base is small.

The cortisol-modulation finding has also been extended to non-athletic stress — small trials of PS in adults with elevated work-related stress have shown reduced adrenocorticotropic hormone/cortisol response to laboratory stressors (Trier Social Stress Test). This is one of the rationales for including PS in adaptogen-stress-support supplement formulations alongside ashwagandha, rhodiola, and L-theanine.

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Dosing, Forms, and Bioavailability

Standard dosing for cognitive support:

• 100 mg three times daily (300 mg/day total) — the dosing used in the original Crook AAMI trials and the standard adult dose for memory support. It is often taken with meals because it is a fat-soluble compound.
• 100 mg twice daily (200 mg/day total) — the dose used in pediatric attention-deficit/hyperactivity disorder trials, also used by healthy adults for maintenance cognitive support.
• 500 to 800 mg/day — higher doses used in the stress/cortisol modulation literature and in some early-stage cognitive impairment protocols; the stress studies at these doses lasted only about 10 days, so longer-term safety at these levels is less documented.

Forms available:

• Soy-derived PS (S-PS) — the standard commercial form, manufactured from soy lecithin by enzymatic base exchange. Most well-studied in the modern literature. Vegetarian acceptable.
• Soy PS conjugated with DHA (PS-DHA, PS-Omega3) — PS with docosahexaenoic acid esterified at the sn-2 position to better match the historical bovine PS fatty-acid composition. Used in the Manor attention-deficit/hyperactivity disorder trials.
• Sunflower-derived PS — for soy-allergic patients; equivalent biochemically.
• Marine-source PS (krill, herring roe) — natively rich in docosahexaenoic acid and eicosapentaenoic acid (EPA), more expensive, becoming more available.
• Bovine-cortex PS (BC-PS) — effectively unavailable since the mid-1990s BSE crisis, when regulators restricted bovine brain-derived material because of the mad-cow disease risk.

Bioavailability: oral PS is reasonably well-absorbed (estimated 50 to 90% in human pharmacokinetic studies), and a measurable fraction crosses the blood-brain barrier intact via specific phospholipid transporters. Crossing the BBB is enhanced when PS is conjugated with docosahexaenoic acid, which is one of the rationales for the PS-DHA formulation. Maximum plasma concentration is reached approximately 2 to 4 hours after oral dosing, and steady-state brain concentration is reached after roughly 2 weeks of daily supplementation.

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Cautions and Drug Interactions

• Anticoagulants and antiplatelets — PS has mild antiplatelet activity at high doses (because PS exposure on platelets is part of the coagulation cascade, exogenous PS may compete with endogenous platelet PS surface). For people on warfarin, apixaban, clopidogrel or aspirin, the concern is a theoretical added effect on bleeding at high PS doses. Standard cognitive-support doses (100-300 mg/day) appear safe.
• Cholinesterase inhibitors (donepezil, rivastigmine, galantamine) — PS may have additive cognitive effects with these dementia medications; this is not a listed contraindication.
• Soy allergy — most commercial PS is soy-derived. Sunflower-sourced and marine-source PS contain no soy.
• Pregnancy and lactation — no adequate human safety data, so its safety in pregnancy and breastfeeding has not been established.
• Gastrointestinal effects — the most common side effect is mild nausea or stomach upset, particularly at doses above 300 mg/day. Taking PS with food and dividing the daily dose reduces this.
• Insomnia in evening dosing — some users report restlessness or vivid dreams if PS is taken late in the evening (counterintuitive given the cortisol-modulating effect). Users describe morning and midday doses as avoiding this.

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Key Research Papers

1. Crook TH et al. (1991). Effects of phosphatidylserine in age-associated memory impairment. Neurology. — PubMed PMID: 2027477
2. Crook T, Petrie W, Wells C, Massari DC (1992). Effects of phosphatidylserine in Alzheimer's disease. Psychopharmacology Bulletin;28(1):61-6. — PubMed PMID: 1609044
3. Cenacchi T et al. (1993). Cognitive decline in the elderly: a double-blind, placebo-controlled multicenter study on efficacy of phosphatidylserine administration. Aging Clinical Experimental Research. — PubMed PMID: 8323999
4. FDA (2003). Qualified Health Claim for phosphatidylserine and reduced risk of cognitive dysfunction. — PubMed
5. Hirayama S et al. (2014). The effect of phosphatidylserine administration on memory and symptoms of attention-deficit hyperactivity disorder: a randomised, double-blind, placebo-controlled clinical trial. Journal of Human Nutrition and Dietetics. — PubMed PMID: 23495677
6. Manor I et al. (2012). The effect of phosphatidylserine containing Omega3 fatty-acids on attention-deficit hyperactivity disorder symptoms in children: a double-blind placebo-controlled trial, followed by an open-label extension. European Psychiatry. — PubMed PMID: 21807480
7. Monteleone P et al. (1990). Effects of phosphatidylserine on the neuroendocrine response to physical stress in humans. Neuroendocrinology. — PubMed PMID: 2170852
8. Starks MA et al. (2008). The effects of phosphatidylserine on endocrine response to moderate intensity exercise. Journal of the International Society of Sports Nutrition. — PubMed PMID: 18662395
9. Glade MJ, Smith K (2015). Phosphatidylserine and the human brain. Nutrition. — PubMed PMID: 25933483
10. Kim HY, Huang BX, Spector AA (2014). Phosphatidylserine in the brain: metabolism and function. Progress in Lipid Research;56:1-18. — PubMed PMID: 24992464
11. Vance JE (2008). Phosphatidylserine and phosphatidylethanolamine in mammalian cells: two metabolically related aminophospholipids. Journal of Lipid Research;49(7):1377-87. — PubMed PMID: 18204094
12. Monteleone P, Maj M, Beinat L, Natale M, Kemali D (1992). Blunting by chronic phosphatidylserine administration of the stress-induced activation of the hypothalamo-pituitary-adrenal axis in healthy men. European Journal of Clinical Pharmacology;42(4):385-8. — PubMed PMID: 1325348
13. Rheims S, Herbillon V, Gaillard S, et al.; investigators of the AGPI study group (2024). Phosphatidylserine enriched with polyunsaturated n-3 fatty acid supplementation for attention-deficit hyperactivity disorder in children and adolescents with epilepsy: A randomized placebo-controlled trial. Epilepsia Open;9(2):582-591. — PubMed PMID: 38173190
14. Duan H, Xu N, Yang T, et al. (2025). Effects of a food supplement containing phosphatidylserine on cognitive function in Chinese older adults with mild cognitive impairment: A randomized double-blind, placebo-controlled trial. Journal of Affective Disorders;369:35-42. — PubMed PMID: 39317299

PubMed Topic Searches

1. PubMed: PS for memory in older adults
2. PubMed: PS membrane biology
3. PubMed: PS for ADHD
4. PubMed: PS cortisol modulation
5. PubMed: PS apoptosis signaling

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Connections

• All Amino Acids
• Serine Overview
• Serine Benefits Hub
• D-Serine and N-Methyl-D-Aspartate
• Glycine Source (SHMT)
• Sphingolipid Synthesis (SPT)
• Glycine
• Omega-3 Fatty Acids (Docosahexaenoic Acid)
• Attention-Deficit/Hyperactivity Disorder
• Alzheimer's Disease
• Dementia
• Anxiety
• Bacopa Monnieri
• Ginkgo Biloba
• Lion's Mane
• History
• Sources

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