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Related Experiment Video

Updated: Aug 25, 2025

Author Spotlight: Decoding Mitochondrial Aging

Author Spotlight: Decoding Mitochondrial Aging

Published on: June 30, 2023

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.

|October 14, 2022

Summary

This summary is machine-generated.

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 disease ERK signaling Willin/FRMD6 mitochondrial dysfunction neurodegeneration oxidative stress

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Quantitative Analysis of Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Stabilization in a Neural Model of Alzheimer's Disease (AD)

Quantitative Analysis of Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Stabilization in a Neural Model of Alzheimer's Disease (AD)

Published on: January 10, 2025

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.