Black Seed OilvsCDP-Choline

Thymoquinone is the primary bioactive, providing neuroprotection through multiple mechanisms: it scavenges reactive oxygen species (superoxide, hydroxyl radical, peroxynitrite) and upregulates Nrf2/ARE pathway, increasing glutathione (via GCLC, GSS), superoxide dismutase (SOD1/SOD2), and catalase. It inhibits NF-kB by preventing IkB-alpha degradation and blocking p65 nuclear translocation, reducing neuroinflammation and pro-inflammatory cytokine release. Thymoquinone inhibits acetylcholinesterase (AChE) at the peripheral anionic site, increasing synaptic acetylcholine. It modulates GABA-A receptors (positive allosteric modulation at benzodiazepine site), providing anxiolytic effects. Thymoquinone protects neurons from amyloid-beta toxicity by reducing oxidative stress and inhibiting beta-secretase (BACE1). It reduces tau hyperphosphorylation by inhibiting GSK-3beta and CDK5.

CDP-Choline is hydrolyzed by nucleotidases and phosphatases into choline and cytidine after oral ingestion. Choline enters the acetylcholine synthesis pathway via choline acetyltransferase. Cytidine is phosphorylated to CTP and converted to uridine monophosphate (UMP), which enters the Kennedy pathway and stimulates the synthesis of phosphatidylcholine via the enzyme CTP:phosphocholine cytidylyltransferase — phosphatidylcholine is a critical component of neuronal cell membranes and synaptic vesicles. This dual mechanism simultaneously boosts neurotransmitter production and repairs membrane damage from oxidative stress or ischemia. CDP-Choline also increases dopamine D2 receptor density in the striatum and enhances dopamine release. It may modulate glutamate excitotoxicity and support mitochondrial function.