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Cited by 1,274Alzheimer's disease research and treatmentsMitochondrial Function and PathologyAutophagy in Disease and Therapy

Mitochondria dysfunction in the pathogenesis of Alzheimer’s disease: Recent advances.

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Wang, Wenzhang, Zhao, Fanpeng, Ma, Xiaopin, Perry, George, Zhu, Xiongwei·2020·Molecular Neurodegeneration
DOI 10.1186/s13024-020-00376-6PMC PMC7257174
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Abstract

Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative diseases, characterized by impaired cognitive function due to progressive loss of neurons in the brain. Under the microscope, neuronal accumulation of abnormal tau proteins and amyloid plaques are two pathological hallmarks in affected brain regions. Although the detailed mechanism of the pathogenesis of AD is still elusive, a large body of evidence suggests that damaged mitochondria likely play fundamental roles in the pathogenesis of AD. It is believed that a healthy pool of mitochondria not only supports neuronal activity by providing enough energy supply and other related mitochondrial functions to neurons, but also guards neurons by minimizing mitochondrial related oxidative damage. In this regard, exploration of the multitude of mitochondrial mechanisms altered in the pathogenesis of AD constitutes novel promising therapeutic targets for the disease. In this review, we will summarize recent progress that underscores the essential role of mitochondria dysfunction in the pathogenesis of AD and discuss mechanisms underlying mitochondrial dysfunction with a focus on the loss of mitochondrial structural and functional integrity in AD including mitochondrial biogenesis and dynamics, axonal transport, ER-mitochondria interaction, mitophagy and mitochondrial proteostasis.

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  • In neurodegenerative diseases such as Alzheimer's and Parkinson's, mitochondrial fragmentation is often observed in affected neurons.

    “In the context of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, mitochondrial fragmentation is often observed in affected neurons (Wang et al., 2017; Wang et al., 2020).”

    From Aging promotes an increase in mitochondrial fragmentation in astrocytes (2024) · cites this paper as Wang et al., 2020

    The section “Abnormal mitochondrial fusion and fission in AD” (page unavailable) describes evidence of fragmented mitochondria in susceptible neurons from Alzheimer’s disease brain tissue. The paper mentions Parkinson’s disease in connection with ER–mitochondria tethering, but does not report mitochondrial fragmentation in affected Parkinson’s neurons. (LLM, conf=0.87)

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Authors
Wang, W., Zhao, F., Ma, X., Perry, G., & Zhu, X.
Affiliations
  • Case Western Reserve University (US)
  • The University of Texas at San Antonio (US)
Corresponding author
  • Wang, Wenzhang
  • Perry, George
  • Zhu, Xiongwei
ORCID
Venue
Molecular Neurodegeneration
Publisher
Springer Science and Business Media LLC
Published
2020-05-29
Volume
15
Issue
1
Pages
30-30
ISSN
1750-1326 (ISSN-L)
DOI
10.1186/s13024-020-00376-6
PMC
PMC7257174
OpenAlex
W3029234273
Cited by
1,274
References
29
Citations by year
2026: 213 · 2025: 287 · 2024: 249 · 2023: 215 · 2022: 161 · 2021: 124 · 2020: 24
FWCI
16.90
Type
journal article
Language
en
Open access
Licence
Locations
  • Molecular Neurodegeneration (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Dr. Robert M. Kohrman Memorial Fund
  • National Institutes of Health (NS083385, AG049179, AG056363, AG058015)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
Alzheimer's disease, mitochondrial dysfunction, neurodegeneration, mitochondrial biogenesis, mitochondrial dynamics, axonal transport, ER-mitochondria communication, mitophagy, mitochondrial proteostasis, oxidative stress, tau protein, amyloid plaques, therapeutic target
MeSH terms
Alzheimer Disease, Animals, Brain, Humans, Mitochondria, Neurons, Amyloid beta-Peptides, tau Proteins

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