ALCARvsTaurine

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.

Taurine activates GABA-A receptors (particularly extrasynaptic δ-containing subtypes) and glycine receptors (GlyR) as a partial agonist, providing inhibitory modulation that reduces neural excitability and hyperexcitability. It acts as a powerful antioxidant, scavenging hypochlorous acid, hydroxyl radicals, and peroxynitrite in mitochondria and cytosol. Taurine regulates calcium homeostasis via modulation of ryanodine receptors and IP3 receptors, preventing excitotoxic calcium overload. It modulates osmotic balance through the taurine transporter (TauT/SLC6A6) to protect cells from swelling under stress. Taurine may enhance mitochondrial function and biogenesis. Recent research shows it maintains telomere length, reduces cellular senescence markers (p16, p21), and modulates the mTOR pathway.