Acetyl-l-Carnitine

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Acetyl-l-Carnitine

Alternative A form of carnitine which may metabolise lipofuscin and age-related pigment deposits; it is claimed to attenuate age-associated memory loss and Alzheimer’s disease, and increase longevity.
Source Meats—beef, chicken, pork—dairy products, fruits, vegetables, grains
Physiology An acetylated metabolic byproduct of l-carnitine and acetyl-CoA, which is produced within mitochondria during strenuous exercise. ALCAR is a potent antioxidant and nutrient which helps transport fatty acids across lipid membranes into mitochondria, rejuvenating membranes and effete enzymes.
References in periodicals archive ?
62) The efficacy, tolerability, and safety of ALCAR were investigated during a 12-week, double-blind, placebo-controlled trial in patients with mild dementia caused by AD, and vascular dementia.
65) During the double-blind, placebo-controlled study, ALCAR was administered to 7 probable Alzheimer's disease patients who were compared using P magnetic resonance spectroscopic measures and clinical investigations to 5 placebo-treated probable AD patients and 21- ag matched health controls for a 1 year period (Pettegrew, Klunk, Panchalingam, Kanfer, & McClure, 1995).
He explains that brain cells require ALCAR as fuel to keep tiny energy generators called mitochondria humming along.
Boosting ALCAR in brain cells helps revive mitochondrial functioning, creating a surge in overall mental and physical energy, claims Dr.
Acetyl-L-carnitine is a naturally occurring substance that acts as a carrier of fatty acids from the cytosol into the mitochondrial matrix where they can be subjected to oxidation and it is freely exchanged across membranes and can provide acetyl groups, from which to regenerate acetyl-CoA, therefore facilitating the transport of metabolic energy In animal studies, ALCAR has been reported to protect central and peripheral nervous system synapses in neurodegenerative and aging models to elevate nerve growth factor levels.
The results suggest that the ALCAR treatment in old rats activates PGC-1alpha-dependent mitochondrial biogenesis, thus partially reverting the age-related mitochondrial decay.
03) in old versus young animals and also greater when compared with old rats fed ALCAR or LA alone.