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Salama SA, Arab HH, Omar HA, Gad HS, Abd-Allah GM, Maghrabi IA, et al

Cellular levels of adenosine triphosphate, a molecule essential in the transport of calcium from the cytosol back into the sarcoplasmic reticulum during muscle relaxation, are reduced as a result of carnitine deficiency

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(Level 11b, Grade B) Surgical decompression at the site of anatomic narrowing has been promoted as an alternative treatment for patients with symptomatic DSPN

In preclinical studies, ALCAR reduced oxidative damage markers (lipid peroxidation, oxidized nucleotides, nitrotyrosine) in aged rat brains, while LCAR did not, despite both compounds similarly increasing ambulatory activity and tissue carnitine levels.[5] ALCAR also decreased infarction size in stroke models, whereas LCAR showed no protective effect in vivo, though both were neuroprotective in vitro.[6] These differences likely reflect ALCARs ability to donate acetyl groups for acetylcholine synthesis, energy production, and neurotransmitter metabolism.[2][7] For cardiovascular and metabolic applications, the compounds appear more comparable