Mitochondria and Calcium in Alzheimer's Disease: From Cell Signaling to Neuronal Cell Death

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 beta 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.

Automated summary

Mitochondrial dysfunction plays a crucial role in the pathogenesis of neurological diseases, including AD. Besides the link between mitochondrial dynamics and amyloid beta toxicity, dysregulation of mitochondrial calcium homeostasis is also related to other risk factors in AD. Researchers have reviewed the latest literature on mitochondrial dysregulation in AD, highlighting the potential of mitochondrial calcium transporters as therapeutic candidates for developing neuroprotective drugs against AD.