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Related Experiment Video

Updated: Sep 15, 2025

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome

Published on: November 30, 2022

Amyloid-β protein precursor modulates mitophagy and mitochondrial function through its cellular localization.

Taylor A Strope^1,2, Benjamin Troutwine^2,3, Brittany M Hauger^2,3

¹Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, KS, USA.

Journal of Alzheimer'S Disease : JAD

|July 17, 2025

Summary

Altered amyloid-β protein precursor (AβPP) in mitochondria disrupts cellular energy production and function. This study reveals AβPP

Keywords:

Alzheimer's disease amyloid-β amyloid-β protein precursor mitochondria mitophagy

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Area of Science:

Mitochondrial biology
Neurodegenerative diseases
Cellular physiology

Background:

Amyloid-β protein precursor (AβPP) processing is known, but its mitochondrial function remains unclear.
AβPP's presence in mitochondria suggests a role in mitochondrial physiology.
Mitochondrial dysfunction is implicated in Alzheimer's disease (AD).

Purpose of the Study:

To investigate the consequences of altered mitochondrial AβPP content on mitochondrial function.
To examine the relationship between AβPP localization and mitochondrial dynamics, mitophagy, and biogenesis.

Main Methods:

Quantified mitochondrial AβPP in postmortem human brain tissue from non-demented and AD subjects.
Utilized wild-type and modified AβPP constructs with altered mitochondrial localization (D23A, 3 M).
Assessed mitochondrial function, including electron transport chain (ETC) activity, ATP levels, superoxide production, membrane potential, calcium content, dynamics, mitophagy, and biogenesis.

Main Results:

Increased mitochondrial AβPP localization observed in sporadic AD brains.
Modulating mitochondrial AβPP content (increased or decreased) impaired ETC activity, reduced ATP, increased superoxide, and altered mitochondrial calcium.
Altered AβPP levels differentially affected mitophagy flux and reduced mitochondrial biogenesis; C-terminus of AβPP is implicated in mitophagy induction.

Conclusions:

AβPP plays a critical role in maintaining mitochondrial physiology.
Dysregulation of AβPP mitochondrial content leads to significant mitochondrial dysfunction.
Findings suggest AβPP's involvement in mitophagy and potential implications for Alzheimer's disease pathogenesis.