Mitochondrial calcium signaling in non-neuronal cells: Implications for Alzheimer's disease pathogenesis

Biochim Biophys Acta Mol Basis Dis. 2024 Jun;1870(5):167169. doi: 10.1016/j.bbadis.2024.167169. Epub 2024 Apr 15.

Abstract

Mitochondrial dysregulation is pivotal in Alzheimer's disease (AD) pathogenesis. Calcium governs vital mitochondrial processes impacting energy conversion, oxidative stress, and cell death signaling. Disruptions in mitochondrial calcium (mCa2+) handling induce calcium overload and trigger the opening of mitochondrial permeability transition pore, ensuing energy deprivation and resulting in AD-related neuronal cell death. However, the role of mCa2+ in non-neuronal cells (microglia, astrocytes, oligodendrocytes, endothelial cells, and pericytes) remains elusive. This review provides a comprehensive exploration of mitochondrial heterogeneity and calcium signaling, offering insights into specific differences among various brain cell types in AD.

Keywords: Alzheimer's disease; Brain cells; Calcium; Heterogeneity; Mitochondria.

Publication types

  • Review
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease* / metabolism
  • Alzheimer Disease* / pathology
  • Animals
  • Astrocytes / metabolism
  • Astrocytes / pathology
  • Calcium Signaling* / physiology
  • Calcium* / metabolism
  • Endothelial Cells / metabolism
  • Endothelial Cells / pathology
  • Humans
  • Microglia / metabolism
  • Microglia / pathology
  • Mitochondria* / metabolism
  • Mitochondria* / pathology
  • Mitochondrial Permeability Transition Pore / metabolism
  • Neurons / metabolism
  • Neurons / pathology
  • Oligodendroglia / metabolism
  • Oligodendroglia / pathology
  • Oxidative Stress
  • Pericytes / metabolism
  • Pericytes / pathology