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Synodinou, K

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

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Activity-dependent NMDA receptor degradation mediated by retrotranslocation and ubiquitination

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