ALCARvsGinkgo Biloba

ALCAR crosses the blood-brain barrier via the organic cation transporter (OCTN2) more effectively than L-carnitine. In neurons, it is hydrolyzed by carnitine acetyltransferase to donate its acetyl group to coenzyme A, forming acetyl-CoA—which can then be used for acetylcholine synthesis via choline acetyltransferase, effectively providing raw material for the memory neurotransmitter. ALCAR also transports long-chain fatty acids across the inner mitochondrial membrane via the carnitine palmitoyltransferase system for beta-oxidation and ATP production. ALCAR activates nerve growth factor (NGF) signaling, possibly through modulation of NGF receptor (TrkA) expression or downstream MAPK/ERK pathways. It has antioxidant properties, reducing lipid peroxidation in mitochondrial membranes and scavenging free radicals. These mechanisms support cognitive function and neuroprotection.

Ginkgo biloba extract (EGb 761) contains flavonoids (quercetin, kaempferol, isorhamnetin) and terpenoids (ginkgolides A, B, C, J and bilobalide). The flavonoids are potent antioxidants that scavenge superoxide, hydroxyl radicals, and peroxynitrite, and protect neurons from oxidative damage; they may also chelate iron. The terpenoids (ginkgolides and bilobalide) improve blood flow by antagonizing platelet-activating factor (PAF) at the PAF receptor, which reduces platelet aggregation, blood viscosity, and improves microcirculation in the brain. Bilobalide protects mitochondria and reduces apoptosis. Ginkgo modulates nitric oxide (NO) availability via endothelial nitric oxide synthase (eNOS) for vasodilation. It inhibits monoamine oxidase A and B (MAO-A, MAO-B), mildly elevating dopamine and serotonin. It may enhance cholinergic transmission and reduce amyloid aggregation.