The DOI matches its Crossref record; 76 of the 77 references it cites were found in a registry or an index.
Mitochondrial Aβ: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease
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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“accumulating data certainly do suggest APP and Aβ, as well as the entire γ-secretase complex, physically associate with mitochondria and can effect changes in mitochondrial function [58-67].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [58]
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Metadata
- 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
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2005-10-06
- Volume
- 19
- Issue
- 14
- Pages
- 2040-2041
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- 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
- 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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