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Is the mitochondrial outermembrane protein VDAC1 therapeutic target for Alzheimer's disease?

P Hemachandra Reddy1

  • 1Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, OR 97006, USA. reddyh@ohsu.edu

Biochimica Et Biophysica Acta
|September 22, 2012
PubMed

Insights

Voltage-dependent anion channel 1 (VDAC1) is elevated in Alzheimer's disease (AD), contributing to mitochondrial dysfunction and synaptic damage by interacting with amyloid beta and tau. This review explores VDAC1's role in regulating mitochondrial pores in AD progression.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Mitochondrial dysfunction and synaptic damage are early indicators of Alzheimer's disease (AD) pathogenesis.
  • Amyloid beta (Aβ) and hyperphosphorylated tau are implicated in these early AD events.
  • Elevated levels of voltage-dependent anion channel 1 (VDAC1) are observed in AD brains and models.

Purpose of the Study:

  • To review research on the relationship between VDAC1 and mitochondrial permeability transition (MPT) pore regulation in AD.
  • To elucidate VDAC1's role in AD pathogenesis.

Main Methods:

  • Review of existing literature on AD postmortem brains, AD mouse models, and cell models.
  • Analysis of research linking VDAC1 to Aβ and phosphorylated tau.
  • Examination of VDAC1's impact on mitochondrial function.

Main Results:

  • VDAC1 is elevated in affected regions of AD brains and APP transgenic mouse cortices.
  • VDAC1 interacts with Aβ and phosphorylated tau in AD.
  • VDAC1 dysregulates MPT pores, mitochondrial transport, and oxidative phosphorylation, causing mitochondrial dysfunction.

Conclusions:

  • VDAC1 plays a significant role in AD pathogenesis by disrupting mitochondrial function.
  • Targeting VDAC1 may offer a therapeutic strategy for Alzheimer's disease.

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