Mitochondrial Perturbation in Alzheimer's Disease and Diabetes

Prog Mol Biol Transl Sci. 2017;146:341-361. doi: 10.1016/bs.pmbts.2016.12.019. Epub 2017 Feb 4.

Abstract

Mitochondria are well-known cellular organelles that play a vital role in cellular bioenergetics, heme biosynthesis, thermogenesis, calcium homeostasis, lipid catabolism, and other metabolic activities. Given the extensive role of mitochondria in cell function, mitochondrial dysfunction plays a part in many diseases, including diabetes and Alzheimer's disease (AD). In most cases, there is overwhelming evidence that impaired mitochondrial function is a causative factor in these diseases. Studying mitochondrial function in diseased cells vs healthy cells may reveal the modified mechanisms and molecular components involved in specific disease states. In this chapter, we provide a concise overview of the major recent findings on mitochondrial abnormalities and their link to synaptic dysfunction relevant to neurodegeneration and cognitive decline in AD and diabetes. Our increased understanding of the role of mitochondrial perturbation indicates that the development of specific small molecules targeting aberrant mitochondrial function could provide therapeutic benefits for the brain in combating aging-related dementia and neurodegenerative diseases by powering up brain energy and improving synaptic function and transmission.

Keywords: Alzheimer disease; Diabetes; Mitochondrial dysfunction; Neuronal toxicity; Synaptic degeneration aging.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / metabolism*
  • Amyloid beta-Peptides / metabolism
  • Animals
  • Diabetes Mellitus / metabolism*
  • Humans
  • Mitochondria / metabolism
  • Mitochondria / pathology*
  • Neurons / metabolism
  • Neurons / pathology
  • Synapses / pathology

Substances

  • Amyloid beta-Peptides