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

Abstract

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.

• Authors: Maria Calvo-Rodriguez, Brian J Bacskai
• Journal: Trends in neurosciences (Trends Neurosci) Vol. 44 Issue 2 Pg. 136-151 (02 2021) ISSN: 1878-108X [Electronic] England
• PMID: 33160650 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2020 Elsevier Ltd. All rights reserved.

Chemical References

• Amyloid beta-Peptides
• Calcium

Topics

• Alzheimer Disease
• Amyloid beta-Peptides
• Animals
• Calcium
• Cell Death
• Humans
• Mitochondria
• Signal Transduction