Kramer Peter
Department of General Psychology, University of Padua, Padua, Italy.
Front Aging Neurosci. 2021 Dec 23;13:776936. doi: 10.3389/fnagi.2021.776936. eCollection 2021.
Alzheimer's and Parkinson's are the two best-known neurodegenerative diseases. Each is associated with the excessive aggregation in the brain and elsewhere of its own characteristic amyloid proteins. Yet the two afflictions have much in common and often the same amyloids play a role in both. These amyloids need not be toxic and can help regulate bile secretion, synaptic plasticity, and immune defense. Moreover, when they do form toxic aggregates, amyloids typically harm not just patients but their pathogens too. A major port of entry for pathogens is the gut. Keeping the gut's microbe community (microbiota) healthy and under control requires that our cells' main energy producers (mitochondria) support the gut-blood barrier and immune system. As we age, these mitochondria eventually succumb to the corrosive byproducts they themselves release, our defenses break down, pathogens or their toxins break through, and the side effects of inflammation and amyloid aggregation become problematic. Although it gets most of the attention, local amyloid aggregation in the brain merely points to a bigger problem: the systemic breakdown of the entire human superorganism, exemplified by an interaction turning bad between mitochondria and microbiota.
阿尔茨海默病和帕金森病是两种最广为人知的神经退行性疾病。每种疾病都与自身特征性淀粉样蛋白在大脑及其他部位的过度聚集有关。然而,这两种疾病有许多共同之处,而且往往相同的淀粉样蛋白在两者中都起作用。这些淀粉样蛋白不一定有毒,还可以帮助调节胆汁分泌、突触可塑性和免疫防御。此外,当它们形成有毒聚集体时,淀粉样蛋白通常不仅会伤害患者,也会伤害其病原体。病原体的一个主要进入途径是肠道。保持肠道微生物群落(微生物群)的健康并加以控制,需要我们细胞的主要能量产生者(线粒体)支持肠血屏障和免疫系统。随着年龄的增长,这些线粒体最终会屈服于它们自身释放的腐蚀性副产品,我们的防御系统会崩溃,病原体或其毒素会突破防线,炎症和淀粉样蛋白聚集的副作用就会成为问题。尽管大脑中的局部淀粉样蛋白聚集受到了最多关注,但它仅仅指向了一个更大的问题:整个人类超级生物体的系统性崩溃,线粒体与微生物群之间的不良相互作用就是例证。