Mitochondrial dysfunction has been implicated in the pathogenesis of almost all neurological diseases, including Alzheimer's disease (AD). Historically, a primary focus in this context has been the link between mitochondrial dynamics and amyloid β toxicity. Recent evidence suggests that dysregulation of mitochondrial calcium homeostasis is also related to tau and other risk factors in AD, although an ongoing challenge in the field is that data collected from different models or experimental settings have not always been consistent. We examine recent literature on mitochondrial dysregulation in AD, with special emphasis on mitochondrial calcium. We include data from in vitro systems, genetic animal models, and AD-derived human tissue, and discuss whether mitochondrial calcium transporters should be proposed as therapeutic candidates for the development of neuroprotective drugs against AD.

中文翻译：

---

阿尔茨海默病中的线粒体和钙：从细胞信号传导到神经元细胞死亡

线粒体功能障碍与几乎所有神经系统疾病的发病机制有关，包括阿尔茨海默病 (AD)。从历史上看，这方面的主要关注点是线粒体动力学和淀粉样蛋白 β 毒性之间的联系。最近的证据表明，线粒体钙稳态失调也与 AD 中的 tau 和其他危险因素有关，尽管该领域的一个持续挑战是从不同模型或实验环境收集的数据并不总是一致的。我们检查了有关 AD 中线粒体失调的最新文献，特别强调线粒体钙。我们包括来自体外系统、遗传动物模型和 AD 衍生的人体组织的数据，