只是一篇关于一项研究的快速帖子，该研究发现药物多奈哌齐 - 通常用于“治疗”阿尔茨海默病 (AD) - 可以改善肌肉中的线粒体功能。虽然有关多奈哌齐的研究结果存在争议且不是特别有趣，但在实际研究中发现 AD 患者的基础代谢率要低得多，脂肪酸氧化 (FAO) 显着上调，碳水化合物氧化减少。这一发现可以解释在动物模型中使用减少细胞脂肪供应（例如脂解）和/或直接抑制FAO的化学物质成功治疗AD的原因。阿司匹林、烟酰胺、孕酮、孕烯醇酮等是其中的一些干预措施，它们都对 AD 动物模型显示出疗效。
https://medicalxpress.com/news/2021-09-alzheimer-drug-mitochondial-function-muscles.html
https://academic.oup.com/function/advance-article/doi/10.1093/function/zqab045/6362606
“……我们特别发现，在 GXT 之前的安静休息期间，未服用药物的 MCI 和 MCI+med 受试者均表现出较低的空腹 RER 值。与认知健康的老年人相比，两组 MCI 受试者似乎更愿意使用脂肪酸底物，后者表现出更依赖碳水化合物使用的 RER. 有点令人惊讶的是，我们没有观察到组间血浆脂质谱或胰岛素抵抗的空腹标志物有任何差异。这可能是由于多种因素造成的，包括疾病的早期阶段、所有受试者的高强度体力活动、研究的横断面性质或其他已知影响脂质稳态的因素，例如遗传学。尽管如此，这表明线粒体生物能量差异可能存在于全身胰岛素抵抗和/或血脂异常之外，甚至先于全身胰岛素抵抗和/或血脂异常。”
Just a quick post in regards to a study that found the drug donepezil – commonly used to “treat” Alzheimer’s Disease (AD) – may improve mitochondrial function in muscles. While the findings of the study in regards to donepezil are debatable and not particularly interesting, buried inside the actual study is the finding that AD patients have much lower basal metabolic rate, significantly upregulated fatty acid oxidation (FAO), and decreased carbohydrate oxidation. This finding may explain the successful treatment of AD in animal models using chemicals that decrease fat supply to the cells (e.g. lipolysis) and/or inhibit FAO directly. Aspirin, niacinamide, progesterone, pregnenolone, etc are some of those interventions and they have all shown curative effects on animal models of AD.
https://medicalxpress.com/news/2021-09-alzheimer-drug-mitochondrial-function-muscles.html
https://academic.oup.com/function/advance-article/doi/10.1093/function/zqab045/6362606
“…We notably found that both unmedicated MCI and MCI+med subjects exhibited lower fasting RER values during quiet rest prior to the GXT. Both groups of MCI subjects appear to be more primed to use fatty acid substrates compared to cognitively healthy elderly adults, who exhibit an RER with a greater reliance on carbohydrate use. Somewhat surprisingly, we did not observe any differences in the plasma lipid profile or fasting markers of insulin resistance between groups. This may be due to a variety of factors, including the early disease stage, the high degree of physical activity in all the subjects, the cross-sectional nature of the study, or other factors known to affect lipid homeostasis, such as genetics. Nevertheless, this indicates that the mitochondrial bioenergetic differences can exist outside of or even precede whole-body insulin resistance and/or dyslipidemia.”
