Mitochondrial dysfunction in neurodegenerative disorders
Open accessAbstract
Recent advances in understanding the role of mitochondrial dysfunction in neurodegenerative diseases have expanded the opportunities for neurotherapeutics targeting mitochondria to alleviate symptoms and slow disease progression. In this review, we offer a historical account of advances in mitochondrial biology and neurodegenerative disease. Additionally, we summarize current knowledge of the normal physiology of mitochondria and the pathogenesis of mitochondrial dysfunction, the role of mitochondrial dysfunction in neurodegenerative disease, current therapeutics and recent therapeutic advances, as well as future directions for neurotherapeutics targeting mitochondrial function. A focus is placed on reactive oxygen species and their role in the disruption of telomeres and their effects on the epigenome. The effects of mitochondrial dysfunction in the etiology and progression of Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and Huntington's disease are discussed in depth. Current clinical trials for mitochondria-targeting neurotherapeutics are discussed.
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Mitochondrial dysfunction is not merely a downstream consequence of Aβ and tau pathology but may act as an initiating factor in the pathogenesis of sporadic AD.
“The mitochondrial cascade hypothesis proposes that mitochondrial dysfunction is not merely a downstream consequence of Aβ and tau pathology but may act as an initiating factor in the pathogenesis of sporadic AD [53].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [53]
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References 192 · Cited by 396
Research works printed but not linked: 3
- [122]Doerfler W. Böhm P. 1 ed DNA Methylation: Basic Mechanisms 2006 Springer Berlin, Heidelberg
- [159][press release] FDA approves treatment of amyotrophic lateral sclerosis associated with a mutation in the SOD1 gene 2023
- [162][press release] Wave Life Sciences Announces Topline Results from Phase 1b/2a FOCUS-C9 Study of WVE-004 for C9orf72-associated Amyotrophic Lateral Sclerosis and Frontotemporal Dementia 23 May 2023
- Authors
- Klemmensen, M. M., Borrowman, S. H., Pearce, C., Pyles, B., & Chandra, B.
- Affiliations
- University of Iowa (US)
- University of Iowa Hospitals and Clinics (US)
- Corresponding author
- Chandra, Bharatendu
- Venue
- Neurotherapeutics
- Publisher
- Elsevier BV
- Published
- 2024-01
- Volume
- 21
- Issue
- 1
- Pages
- e00292
- ISSN
- 1878-7479 (ISSN-L)
- PMC
- PMC10903104
- OpenAlex
- W4389937124
- Cited by
- 396
- References
- 192
- Citations by year
- 2026: 192 · 2025: 158 · 2024: 46
- FWCI
- 10.19
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Neurotherapeutics (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Roy J. and Lucille A. Carver College of Medicine, University of Iowa
- University of Iowa
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial dysfunction, neurodegenerative diseases, reactive oxygen species, telomere shortening, epigenome, Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, Huntington's disease, mitochondrial biology, clinical trials
- MeSH terms
- Alzheimer Disease, Humans, Mitochondria, Reactive Oxygen Species, Neurodegenerative Diseases, Mitochondrial Diseases
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