The benefits of phosphatidylserine for the brain

I. Cerebral Physiological Basis of Phosphatidylserine

Phosphatidylserine (PS) is a phospholipid compound present in cell membranes, particularly abundant in the cell membranes of brain neurons (accounting for 15%-20% of total brain phospholipids). Its unique molecular structure—glycerol backbone linked to serine and two fatty acid chains—makes it a key component for maintaining neuronal membrane fluidity, signal transduction, and synaptic plasticity. In the human body, phosphatidylserine can be synthesized from serine and phosphatidylcholine under enzymatic catalysis. However, with age (especially after 50 years old), synthesis efficiency declines, necessitating supplementation through diet (e.g., fish, nuts) or exogenous preparations.

II. Core Mechanisms for Enhancing Memory

1. Enhancing Synaptic Transmission Efficiency

Phosphatidylserine is a vital component of synaptic vesicle membranes, maintaining the stability of presynaptic membranes and promoting the release of neurotransmitters (such as acetylcholine and dopamine). Studies show that after PS supplementation, the concentration of acetylcholine in the synaptic cleft of the hippocampus (a key brain region for memory formation) increases by 10%-15%, significantly improving the conversion of short-term memory to long-term memory. For example, a clinical trial in 60-80-year-olds with mild cognitive impairment found that 300 mg daily PS supplementation for 12 weeks improved visual memory test scores by 22% compared to the placebo group.

2. Protecting Neuronal Membrane Integrity

Oxidative stress is a primary cause of neuronal damage during aging. The fatty acid chains of phosphatidylserine (mostly unsaturated fatty acids) act as antioxidants, neutralizing free radical damage to membrane structures. Additionally, it activates the calcium pump (Ca²⁺-ATPase) on cell membranes, preventing neuronal apoptosis caused by intracellular calcium overload, thus maintaining hippocampal neuron count and avoiding degenerative changes in memory-related brain regions.

3. Regulating Neuroplasticity-Related Proteins

Phosphatidylserine promotes the expression of brain-derived neurotrophic factor (BDNF), a key regulator of neuronal survival, differentiation, and synaptic plasticity. BDNF enhances long-term potentiation (LTP—the cellular basis of learning and memory) by activating the TrkB receptor, enabling more efficient signal transmission between neurons. Animal experiments show that PS-supplemented rats shorten platform-finding time by 30% in the Morris water maze test, with a 40% increase in hippocampal BDNF protein levels.

III. Multidimensional Pathways for Improving Cognitive Function

1. Regulating Cerebral Energy Metabolism

Cognitive activities (e.g., attention, logical reasoning) require substantial energy. Phosphatidylserine optimizes neuronal mitochondrial function: as a component of mitochondrial membranes, it maintains respiratory chain complex activity; it also enhances neuronal glucose uptake efficiency by promoting the migration of glucose transporter GLUT3 to the cell membrane. Clinical studies find that elderly subjects show an 18% increase in prefrontal cortex glucose metabolism rate after PS supplementation, positively correlated with improved performance in cognitive tasks (e.g., digit symbol substitution tests).

2. Alleviating Neuroinflammation and Oxidative Damage

Neuroinflammation is a key pathological basis of cognitive disorders like Alzheimer's disease (AD). Phosphatidylserine inhibits excessive activation of microglia, reducing the release of pro-inflammatory factors (TNF-α, IL-6). Furthermore, it binds to β-amyloid (Aβ), inhibiting its aggregation into toxic fibrils and lowering AD risk. A study in early AD patients showed that combined PS and cholinesterase inhibitor treatment for 6 months improved MMSE scores by 3 points and increased cerebrospinal fluid Aβ42 levels by 12% compared to monotherapy.

3. Improving Neurotransmitter System Balance

Beyond acetylcholine, phosphatidylserine regulates neurotransmitter systems like dopamine and 5-hydroxytryptamine:

Promotes dopamine synthesis and release in dopaminergic neurons, enhancing attention and executive function;

Increases sensitivity of 5-hydroxytryptamine receptors (e.g., 5-HT1A), improving mood and indirectly reducing anxiety-related interference with cognitive function. For instance, student groups supplementing PS before exams showed a 15% reduction in anxiety scores and a 10% increase in logical reasoning test accuracy.

IV. Clinical Evidence and Target Populations

Age-related Cognitive Decline: Multiple double-blind controlled trials confirm that 200-300 mg daily PS supplementation for 3-6 months improves memory scores by 15%-20% in adults over 65, delaying memory decline.

Childhood Cognitive Development: Studies in 8-12-year-olds with attention deficits show PS supplements improve visuospatial memory and verbal fluency, with significant effects after 8 weeks.

Athletes and Mental Workers: Short-term PS supplementation (100-200 mg/day) relieves cognitive fatigue from high-intensity training/work, shortens reaction time, and enhances decision-making efficiency.

V. Supplementation Methods and Precautions

Sources and Dosage: Natural phosphatidylserine mainly exists in deep-sea fish (mackerel, sardines, ~100-200 mg/100g) and nuts (e.g., sunflower seeds). Preparations are mostly soybean-extracted or synthetic, with a recommended daily dose of 100-300 mg taken 2-3 times.

Synergy with Other Nutrients: Combining phosphatidylserine with Omega-3 fatty acids (e.g., DHA) enhances membrane repair, while 合用 phosphatidylcholine promotes acetylcholine synthesis for improved memory effects.

Safety: No significant side effects at normal doses, but individuals with renal insufficiency should control dosage (excess may increase phosphorus load). Pregnant and lactating women are advised to use under medical guidance.

VI. Future Research Directions

At present, there are still unsolved mysteries about the mechanism of phosphatidylserine in the brain, such as whether it indirectly affects cognition by regulating the gut-brain axis or its associations with other neurodegenerative diseases (e.g., Parkinson's disease).