ALCARvsMagnesium Glycinate

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.

Magnesium is required for over 300 enzymatic reactions including neurotransmitter synthesis (tyrosine hydroxylase, tryptophan hydroxylase), energy production (ATPases, kinases, glycolytic enzymes), and DNA repair (PARP, DNA polymerases). In the brain, magnesium blocks NMDA receptors at the voltage-dependent Mg2+ binding site within the channel pore (GluN1/GluN2 subunits), preventing excessive calcium influx and excitotoxicity — Mg2+ is displaced only upon depolarization and glycine/glutamate binding. The glycine component activates inhibitory glycine receptors (GlyR alpha1/alpha2) in the brainstem and spinal cord, and serves as an obligatory co-agonist at the GluN1 glycine site of NMDA receptors. Glycine also modulates NMDA receptor function. Together, magnesium and glycine produce calming effects through complementary inhibitory mechanisms: reduced glutamatergic excitability and enhanced inhibitory neurotransmission.