Role of mtDNA disturbances in the pathogenesis of Alzheimer’s and Parkinson’s disease
Abstract
Neurodegenerative diseases (e.g. Alzheimer's and Parkinson's disease) are becoming increasingly problematic to healthcare systems. Therefore, their underlying mechanisms are trending topics of study in medicinal research. Numerous studies have evidenced a strong association between mitochondrial DNA disturbances (e.g. oxidative damage, mutations, and methylation shifts) and the initiation and progression of neurodegenerative diseases. Therefore, this review discusses the risk and development of neurodegenerative diseases in terms of disturbances in mitochondrial DNA and as a part of a complex ecosystem that includes other important mechanisms (e.g. neuroinflammation and the misfolding and aggregation of amyloid-β peptides, α-synuclein, and tau proteins). In addition, the influence of individual mitochondrial DNA haplogroups on the risk and development of neurodegenerative diseases is also described and discussed.
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Mitochondrial genome homeostasis is essential for mitochondrial function, and deleterious mutations in the mitochondrial genome are implicated in metabolic disorders, aging, and neurodegenerative disorders.
“The mitochondrial genome homeostasis is essential for mitochondrial function, and its deleterious mutations are implicated in metabolic disorders, aging, and neurodegenerative disorders (Antonyova et al, 2020; Sanchez-Contreras et al, 2023).”
From The mitochondrial long non-coding RNA lncMtloop regulates mitochondrial transcription and suppresses Alzheimer’s disease (2024) · cites this paper as Antonyova et al, 2020
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References 171 · Cited by 45
- Authors
- Antonyová, V., Kejík, Z., Brogyányi, T., Kaplánek, R., Pajková, M., Talianová, V., Hromádka, R., Masařík, M., Sýkora, D., Mikšátková, L., Martásek, P., & Jakubek, M.
- Affiliations
- Charles University (CZ)
- Corresponding author
- Jakubek, Milan
- Venue
- DNA Repair
- Publisher
- Elsevier BV
- Published
- 2020-07
- Volume
- 91-92
- Pages
- 102871
- ISSN
- 1568-7856 (ISSN-L)
- 1568-7864
- OpenAlex
- W3027522526
- Cited by
- 45
- References
- 171
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 10 · 2023: 5 · 2022: 8 · 2021: 10 · 2020: 4
- FWCI
- 0.65
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- DNA repair (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministerstvo Průmyslu a Obchodu (FV20572)
- Ministerstvo Školství, Mládeže a Tělovýchovy (EATRIS-CZ LM2018133, LQ1604, CZ.1.05/1.1.00/02.0109)
- Univerzita Karlova v Praze (Q27/LF1, UNCE 204064, SVV260521)
- Technologická Agentura České Republiky (TN01000013)
- Ministerstvo Zdravotnictví Ceské Republiky (17-32727A, RVO-VFN-64165/2012)
- Technology Agency of the Czech Republic
- Grantová Agentura České Republiky (GACR 18-09296S)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- mitochondrial DNA, Alzheimer's disease, Parkinson's disease, neurodegenerative diseases, oxidative damage, mitochondrial DNA mutations, mtDNA methylation, neuroinflammation, amyloid-beta, alpha-synuclein, tau protein, protein aggregation, mtDNA haplogroups, disease risk
- MeSH terms
- Alzheimer Disease, DNA Damage, DNA, Mitochondrial, Humans, Inflammation, Mutation, Parkinson Disease, Amyloid beta-Peptides, tau Proteins, alpha-Synuclein, Protein Aggregation, Pathological
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