ALCARvsL-Theanine

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.

L-Theanine (gamma-glutamylethylamide) crosses the blood-brain barrier via the large neutral amino acid transporter (LAT1/SLC7A5) and exerts anxiolytic effects through multiple pathways. It increases GABA synthesis by serving as a substrate for glutamate decarboxylase (GAD), elevating inhibitory tone without directly binding GABA-A receptors — avoiding sedation. It modulates serotonin by increasing tryptophan hydroxylase (TPH2) activity and raises dopamine levels in the prefrontal cortex via inhibition of dopamine reuptake. L-Theanine antagonizes glutamate binding at AMPA and kainate receptor subtypes (GluA1-4, GluK1-5), reducing excitatory neurotransmission and excitotoxicity risk. This glutamate antagonism, combined with increased GABA, drives the characteristic increase in alpha brain wave power (8-14 Hz) in the posterior parietal and occipital cortex — the EEG signature of relaxed alertness. When co-administered with caffeine, L-theanine attenuates caffeine-induced increases in blood pressure and anxiety by modulating sympathetic nervous system activation through alpha-2 adrenergic receptor pathways, while caffeine's dopaminergic and adenosine-blocking effects on focus and attention are preserved.