Role of mtDNA disturbances in the pathogenesis of Alzheimer's and Parkinson's disease
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
32502755
DOI
10.1016/j.dnarep.2020.102871
PII: S1568-7864(20)30119-1
Knihovny.cz E-resources
- Keywords
- Alzheimer’s disease, Mitochondrial DNA disturbances, Neuroinflammation, Oxidative stress, Parkinson’s disease, Peptide and protein aggregation,
- MeSH
- alpha-Synuclein metabolism MeSH
- Alzheimer Disease etiology genetics MeSH
- Amyloid beta-Peptides metabolism MeSH
- Humans MeSH
- DNA, Mitochondrial * MeSH
- Mutation * MeSH
- Parkinson Disease etiology genetics MeSH
- Protein Aggregation, Pathological MeSH
- DNA Damage * MeSH
- tau Proteins metabolism MeSH
- Inflammation MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- alpha-Synuclein MeSH
- Amyloid beta-Peptides MeSH
- DNA, Mitochondrial * MeSH
- tau Proteins MeSH
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.
References provided by Crossref.org
Mitochondria in human reproduction: novel paradigm in the onset of neurodegenerative disorders
Targeting of the Mitochondrial TET1 Protein by Pyrrolo[3,2-b]pyrrole Chelators
Iron Complexes of Flavonoids-Antioxidant Capacity and Beyond
