Cited by 738Alzheimer's disease research and treatmentsMitochondrial Function and PathologyDementia and Cognitive Impairment Research

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Mitochondrial Aβ: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease

Caspersen, Casper, Wang, Ning, Yao, Jun, Sosunov, Alexander, Chen, Xi, Lustbader, Joyce W., Xu, Hong Wei, Stern, David, McKhann, Guy, Du Yan, Shi·2005·The FASEB Journal

DOI 10.1096/fj.05-3735fje

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Abstract

Although amyloid-beta peptide (Abeta) is the neurotoxic species implicated in the pathogenesis of Alzheimer's disease (AD), mechanisms through which intracellular Abeta impairs cellular properties, resulting in neuronal dysfunction, remain to be clarified. Here we demonstrate that intracellular Abeta is present in mitochondria from brains of transgenic mice with targeted neuronal overexpression of mutant human amyloid precursor protein and AD patients. Abeta progressively accumulates in mitochondria and is associated with diminished enzymatic activity of respiratory chain complexes (III and IV) and a reduction in the rate of oxygen consumption. Importantly, mitochondria-associated Abeta, principally Abeta42, was detected as early as 4 months, before extensive extracellular Abeta deposits. Our studies delineate a new means through which Abeta potentially impairs neuronal energetics, contributing to cellular dysfunction in AD.

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Authors: Caspersen, C., Wang, N., Yao, J., Sosunov, A., Chen, X., Lustbader, J. W., Xu, H. W., Stern, D., McKhann, G., & Du Yan, S.
Affiliations: Columbia University Irving Medical Center (US)
Fujian Medical University (CN)
University of Cincinnati (US)
Department of Surgery College of Physicians & Surgeons of Columbia University 630 West 168th Street New York NY 10032
ORCID: Wang, Ning
Yao, Jun
Xu, Hong Wei
McKhann, Guy
Venue: The FASEB Journal
Publisher: Wiley
Published: 2005-10-06
Volume: 19
Issue: 14
Pages: 2040-2041
ISSN: 0892-6638 (ISSN-L)
1530-6860
DOI: 10.1096/fj.05-3735fje
OpenAlex: W2103024032
Cited by: 738
References: 77
Citations by year: 2026: 12 · 2025: 22 · 2024: 23 · 2023: 29 · 2022: 31 · 2021: 43 · 2020: 46 · 2019: 41 · 2018: 32 · 2017: 38 · 2016: 39 · 2015: 26 · 2014: 40 · 2013: 54 · 2012: 58
FWCI: 13.84
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: The FASEB Journal (publishedVersion)
PubMed (publishedVersion)
Funders: Michael J. Fox Foundation for Parkinson's Research (P50 AG08702, AG16736, P01 AG17490, NS 042855)
Hørslev-Fonden
Sundhed og Sygdom, Det Frie Forskningsråd
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: amyloid-beta, Alzheimer's disease, respiratory chain complexes, cytochrome bc1 complex, cytochrome c oxidase, oxygen consumption, amyloid-beta 42, amyloid precursor protein, transgenic mice
MeSH terms: Alzheimer Disease, Animals, Brain, Cerebral Cortex, Cytosol, Energy Metabolism, Enzyme-Linked Immunosorbent Assay, Humans, Mice, Inbred C57BL, Mice, Transgenic, Mitochondria, Models, Biological, Mutation, Neurons, Oxygen Consumption, Peptide Fragments, Peptide Hydrolases, Protein Synthesis Inhibitors, Time Factors, Immunoblotting, Amyloid beta-Peptides, Microscopy, Immunoelectron, Oxidative Stress, Microscopy, Confocal, Brefeldin A, Electron Transport Chain Complex Proteins, Mice, Plaque, Amyloid

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Mitochondrial Aβ: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease

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