ALCARvsCordyceps

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.

Cordycepin (3'-deoxyadenosine), the primary bioactive compound, increases ATP production by enhancing mitochondrial electron transport chain efficiency — it may act as an alternative substrate or modulator of Complex I and Complex III. Cordycepin activates AMPK (AMP-activated protein kinase) via increased AMP/ATP ratio or direct activation of the alpha subunit, promoting glucose uptake through GLUT4 translocation and fatty acid oxidation via CPT-1 and ACC inhibition. Cordyceps increases erythropoietin (EPO) production, likely through HIF-1alpha stabilization in hypoxic-sensitive tissues, improving oxygen-carrying capacity. Cordycepin has adenosine-like activity, modulating purinergic P1 (A1, A2A, A2B, A3) and P2 receptors. Anti-inflammatory effects occur through inhibition of NF-kB (reducing IKK degradation of IkB and nuclear translocation) and reduction of pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha). Adenosine deaminase-resistant cordycepin may also affect RNA polyadenylation.