Cocaine neurotoxicity and neurological damage stem from several mechanisms, including mitochondrial dysfunction (Poon et al., 2007), neuroinflammation (Moran et al., 2005), and autophagy ( 3.1 Vascular effects of cocaine Cocaine impairs vascular function by causing vasoconstriction, reducing cerebral blood flow, and decreasing tissue oxygenation
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Your body produces it on its own, but production declines significantly with age, from roughly 200 ng/mL at age 20 to around 80 ng/mL by age 60
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Both peptides have documented neuroprotective research activity: Epitalon demonstrated reduction of amyloid precursor protein (APP) processing markers in rodent brain models, improved behavioural performance in aged animals (Morris Water Maze, novel object recognition), and neuroprotective effects potentially mediated via melatonins anti-amyloidogenic and anti-tau hyperphosphorylation activity
