Amyloid beta, mitochondrial structural and functional dynamics in Alzheimer's disease

P. Hemachandra Reddy

Research output: Contribution to journalReview articlepeer-review

207 Scopus citations

Abstract

Mitochondria are the major source of energy for the normal functioning of brain cells. Increasing evidence suggests that the amyloid precursor protein (APP) and amyloid beta (Aβ) accumulate in mitochondrial membranes, cause mitochondrial structural and functional damage, and prevent neurons from functioning normally. Oligomeric Aβ is reported to induce intracellular Ca2+ levels and to promote the excess accumulation of intracellular Ca2+ into mitochondria, to induce the mitochondrial permeability transition pore to open, and to damage mitochondrial structure. Based on recent gene expression studies of APP transgenic mice and AD postmortem brains, and APP/Aβ and mitochondrial structural studies, we propose that the overexpression of APP and the increased production of Aβ may cause structural changes of mitochondria, including an increase in the production of defective mitochondria, a decrease in mitochondrial trafficking, and the alteration of mitochondrial dynamics in neurons affected by AD. This article discusses some critical issues of APP/Aβ associated with mitochondria, mitochondrial structural and functional damage, and abnormal intracellular calcium regulation in neurons from AD patients. This article also discusses the link between Aβ and impaired mitochondrial dynamics in AD.

Original languageEnglish (US)
Pages (from-to)286-292
Number of pages7
JournalExperimental Neurology
Volume218
Issue number2
DOIs
StatePublished - Aug 2009
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Amyloid beta
  • Amyloid precursor protein
  • Mitochondria

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience

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