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Related Experiment Video

Updated: Aug 25, 2025

Author Spotlight: Decoding Mitochondrial Aging
08:48

Author Spotlight: Decoding Mitochondrial Aging

Published on: June 30, 2023

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Willin/FRMD6 Mediates Mitochondrial Dysfunction Relevant to Neuronal Aβ Toxicity.

Doris Chen1, Wanjia Yu1, Laura Aitken1

  • 1School of Biology, University of St Andrews, St Andrews KY16 9TF, UK.

Cells
|October 14, 2022
PubMed
Summary

Willin/FRMD6 may protect against Alzheimer's disease (AD) by preventing Aβ-induced mitochondrial dysfunction. Enhancing Willin/FRMD6 expression could be a therapeutic strategy for AD.

Keywords:
Alzheimer’s diseaseERK signalingWillin/FRMD6mitochondrial dysfunctionneurodegenerationoxidative stress

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Area of Science:

  • Neuroscience
  • Genetics
  • Cell Biology

Background:

  • Willin/FRMD6 is a potential Alzheimer's disease (AD) risk gene.
  • Mechanisms linking Willin/FRMD6 to AD pathogenesis are not fully understood.

Purpose of the Study:

  • Investigate the direct effects of amyloid-beta (Aβ) on Willin/FRMD6 expression.
  • Elucidate the role of mitochondrial oxidative stress in Willin/FRMD6's function in AD.

Main Methods:

  • Utilized mouse hippocampal HT-22 cells and primary mouse neurons.
  • Assessed Willin/FRMD6 protein expression levels.
  • Examined mitochondrial morphology, function, and energetics.
  • Analyzed ERK1/2 signaling pathway activation.

Main Results:

  • Aβ exposure led to decreased Willin/FRMD6 protein levels.
  • Willin/FRMD6 knockdown resulted in mitochondrial dysfunction and fragmentation.
  • Knockdown also caused upregulation of ERK1/2 signaling.
  • Increased Willin/FRMD6 expression ameliorated Aβ-induced mitochondrial abnormalities.

Conclusions:

  • Mitochondrial oxidative stress is a potential mechanism for Willin/FRMD6's role in AD.
  • Enhancing Willin/FRMD6 expression may offer a therapeutic approach for AD by protecting against mitochondrial and neuronal dysfunction.