https://transhumanist.ru/index.php?action=history&feed=atom&title=MCAT 2026-04-08T11:55:01Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=MCAT&diff=4457&oldid=prev 2021-04-29T19:19:09Z

<p>Новая страница: «Malonyl-CoA-acyl carrier protein transacylase, mitochondrial precursor (EC 2.3.1.39) (MCT) (Mitochondrial malonyl CoA:ACP acyltransferase) (Mitochondrial malonylt...»</p> <p><b>Новая страница</b></p><div>Malonyl-CoA-acyl carrier protein transacylase, mitochondrial precursor (EC 2.3.1.39) (MCT) (Mitochondrial malonyl CoA:ACP acyltransferase) (Mitochondrial malonyltransferase) ([Acyl-carrier-protein] malonyltransferase) [MT]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Small molecules as therapeutic drugs for Alzheimer&#039;s disease.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30877034<br /> |abstract=Mitochondrial dysfunction is a central protagonist of Alzheimer&#039;s disease (AD) pathogenesis. Mitochondrial dysfunction stems from various factors including mitochondrial DNA damage and oxidative stress from reactive oxygen species, membrane and ionic gradient destabilization, and interaction with toxic proteins such as amyloid beta (Aβ). Therapeutic drugs such as cholinesterase and glutamate inhibitors have proven to improve synaptic neurotransmitters, but do not address mitochondrial dysfunction. Researchers have demonstrated that oxidative damage may be reduced by increasing endogenous antioxidants, and/or increasing exogenous antioxidants such as vitamin C</div>

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