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Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils
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Mitochondrial function and Aβ in Alzheimer's disease postmortem brain.

Benjamin R Troutwine1, Taylor A Strope2, Edziu Franczak3

  • 1University of Kansas Alzheimer's Disease Center, Kansas City, KS, USA; Department of Neurology, University of Kansas Medical Center, Kansas City, KS, USA.

Neurobiology of Disease
|June 6, 2022
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease (AD) brains show impaired mitochondrial function and reduced electron transport chain (ETC) proteins. These deficits correlate with amyloid-beta (Aβ) pathology, suggesting a link between mitochondrial dysfunction and AD progression.

Keywords:
Alzheimer's diseaseAβBrainCytochrome oxidaseMitochondria

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Area of Science:

  • Neuroscience
  • Mitochondrial Biology
  • Alzheimer's Disease Research

Background:

  • Mitochondrial dysfunction is a known hallmark of Alzheimer's disease (AD).
  • The precise relationship between impaired mitochondrial function and AD pathologies in human subjects remains unclear.

Purpose of the Study:

  • To investigate the functional status of mitochondria in the brains of individuals with and without AD.
  • To explore the association between mitochondrial electron transport chain (ETC) function and AD neuropathology, including amyloid-beta (Aβ) and tau pathology.
  • To examine the impact of Apolipoprotein E (APOE) genotype on mitochondrial function in AD.

Main Methods:

  • Analysis of post-mortem human brain tissue from non-demented (ND) and AD subjects.
  • Assessment of mitochondrial electron transport chain (ETC) enzyme activity and protein expression.
  • Correlation analysis with neuropathological markers (Aβ, p-Tau) and APOE genotype.

Main Results:

  • AD subjects exhibited reduced cytochrome oxidase (COX) and complex II Vmax, indicating impaired ETC function.
  • APOE ε4 carriers displayed deficits in COX, complex II, and complex III.
  • AD brains showed decreased expression of Complex I-III ETC proteins, while APOE ε4 carriers did not.
  • No correlation was found between p-Tau Thr 181 and mitochondrial function, but non-demented brains showed a positive correlation between Aβ concentration and COX Vmax.

Conclusions:

  • Brain mitochondrial function is dysregulated in Alzheimer's disease.
  • A link exists between mitochondrial dysfunction and Aβ pathology in AD.
  • APOE genotype influences mitochondrial function in the context of AD.