The role of cell type-specific mitochondrial dysfunction in the pathogenesis of Alzheimer's disease

BMB Rep. 2019 Dec;52(12):679-688. doi: 10.5483/BMBRep.2019.52.12.282.


The decrease of metabolism in the brain has been observed as the important lesions of Alzheimer's disease (AD) from the early stages of diagnosis. The cumulative evidence has reported that the failure of mitochondria, an organelle involved in diverse biological processes as well as energy production, maybe the cause or effect of the pathogenesis of AD. Both amyloid and tau pathologies have an impact upon mitochondria through physical interaction or indirect signaling pathways, resulting in the disruption of mitochondrial function and dynamics which can trigger AD. In addition, mitochondria are involved in different biological processes depending on the specific functions of each cell type in the brain. Thus, it is necessary to understand mitochondrial dysfunction as part of the pathological phenotypes of AD according to each cell type. In this review, we summarize that 1) the effects of AD pathology inducing mitochondrial dysfunction and 2) the contribution of mitochondrial dysfunction in each cell type to AD pathogenesis. [BMB Reports 2019; 52(12): 679-688].

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / etiology
  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Astrocytes / pathology
  • Brain / pathology
  • Humans
  • Microglia / pathology
  • Mitochondria / metabolism*
  • Mitochondria / pathology
  • Mitochondrial Dynamics
  • Neurons / pathology
  • Oxidative Phosphorylation
  • tau Proteins / metabolism


  • Amyloid beta-Peptides
  • tau Proteins