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The Role of Mitochondria in Neurodegenerative Diseases: the Lesson from Alzheimer’s Disease and Parkinson’s Disease
Open accessAbstract
Although the pathogenesis of neurodegenerative diseases is still widely unclear, various mechanisms have been proposed and several pieces of evidence are supportive for an important role of mitochondrial dysfunction. The present review provides a comprehensive and up-to-date overview about the role of mitochondria in the two most common neurodegenerative disorders: Alzheimer's disease (AD) and Parkinson's disease (PD). Mitochondrial involvement in AD is supported by clinical features like reduced glucose and oxygen brain metabolism and by numerous microscopic and molecular findings, including altered mitochondrial morphology, impaired respiratory chain function, and altered mitochondrial DNA. Furthermore, amyloid pathology and mitochondrial dysfunction seem to be bi-directionally correlated. Mitochondria have an even more remarkable role in PD. Several hints show that respiratory chain activity, in particular complex I, is impaired in the disease. Mitochondrial DNA alterations, involving deletions, point mutations, depletion, and altered maintenance, have been described. Mutations in genes directly implicated in mitochondrial functioning (like Parkin and PINK1) are responsible for rare genetic forms of the disease. A close connection between alpha-synuclein accumulation and mitochondrial dysfunction has been observed. Finally, mitochondria are involved also in atypical parkinsonisms, in particular multiple system atrophy. The available knowledge is still not sufficient to clearly state whether mitochondrial dysfunction plays a primary role in the very initial stages of these diseases or is secondary to other phenomena. However, the presented data strongly support the hypothesis that whatever the initial cause of neurodegeneration is, mitochondrial impairment has a critical role in maintaining and fostering the neurodegenerative process.
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“Mitochondrial dysfunction has been reported in a number of neurodegenerative diseases [3–6] and correlates with dendritic pathology and synapse disassembly [7–10].”
From AMPK hyperactivation promotes dendrite retraction, synaptic loss, and neuronal dysfunction in glaucoma (2021) · cites this paper as [4]
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Metadata
- Authors
- Monzio Compagnoni, G., Di Fonzo, A., Corti, S., Comi, G. P., Bresolin, N., & Masliah, E.
- Affiliations
- University of Milan (IT)
- National Institutes of Health (US)
- Venue
- Molecular Neurobiology
- Published
- 2020-05-22
- Volume
- 57
- Issue
- 7
- Pages
- 2959-2980
- ISSN
- 0893-7648 (ISSN-L)
- 1559-1182
- PMC
- PMC9047992
- OpenAlex
- W3027900078
- Cited by
- 378
- References
- 309
- Citations by year
- 2026: 44 · 2025: 71 · 2024: 96 · 2023: 61 · 2022: 57 · 2021: 38 · 2020: 11
- FWCI
- 4.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- Funders
- Fresco Institute for Parkinson's and Movement Disorders (not available)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Keywords
- mitochondria, mitochondrial dysfunction, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, mitochondrial DNA, electron transport chain, complex I, Parkin, PINK1, alpha-synuclein, amyloid pathology, multiple system atrophy, atypical parkinsonism, brain metabolism
- MeSH terms
- Alzheimer Disease, Animals, Brain, DNA, Mitochondrial, Humans, Mitochondria, Parkinson Disease, Electron Transport Complex I
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