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Mitochondrial Involvement in Brain Function and Dysfunction: Relevance to Aging, Neurodegenerative Disorders and Longevity
Open accessAbstract
It is becoming increasingly evident that the mitochondrial genome may play a key role in neurodegenerative diseases. Mitochondrial dysfunction is characteristic of several neurodegenerative disorders, and evidence for mitochondria being a site of damage in neurodegenerative disorders is partially based on decreases in respiratory chain complex activities in Parkinson's disease, Alzheimer's disease, and Huntington's disease. Such defects in respiratory complex activities, possibly associated with oxidant/antioxidant balance perturbation, are thought to underlie defects in energy metabolism and induce cellular degeneration. Efficient functioning of maintenance and repair process seems to be crucial for both survival and physical quality of life. This is accomplished by a complex network of the so-called longevity assurance processes, which are composed of genes termed vitagenes. A promising approach for the identification of critical gerontogenic processes is represented by the hormesis-like positive effect of stress. In the present review, we discuss the role of energy thresholds in brain mitochondria and their implications in neurodegeneration. We then review the evidence for the role of oxidative stress in modulating the effects of mitochondrial DNA mutations on brain age-related disorders and also discuss new approaches for investigating the mechanisms of lifetime survival and longevity.
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“AD has been related to genetic mutations, among them in the gene encoding the Aβ precursor protein peptide, mutations in the presenilins genes (Calabrese et al., 2001) and the presence of the APOE ε4 allele (Martínez-Lazcano et al., 2010).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Calabrese et al., 2001
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Self-citation
Metadata
- Authors
- Calabrese, V., Scapagnini, G., Giuffrida Stella, A. M., Bates, T. E., & Clark, J. B.
- Affiliations
- University of Catania (IT)
- UCL Queen Square Institute of Neurology (GB)
- Venue
- Neurochemical Research
- Published
- 2001-06
- Volume
- 26
- Issue
- 6
- Pages
- 739-764
- ISSN
- 0364-3190 (ISSN-L)
- 1573-6903
- OpenAlex
- W1595816980
- Cited by
- 263
- References
- 196
- Citations by year
- 2026: 4 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 9 · 2020: 8 · 2019: 1 · 2018: 5 · 2017: 13 · 2016: 9 · 2015: 8 · 2014: 9 · 2013: 14 · 2012: 16
- FWCI
- 5.31
- Type
- journal article
- Language
- en
- Open access
- green
- figshare.com
- Licence
- Locations
- Neurochemical Research (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- mitochondrial dysfunction, neurodegenerative diseases, brain aging, longevity, Parkinson's disease, Alzheimer's disease, Huntington's disease, respiratory chain complexes, oxidative stress, mitochondrial DNA mutations, energy metabolism, vitagenes, hormesis, stress response, brain mitochondria
- MeSH terms
- Aging, Animals, Brain, Humans, Longevity, Mitochondria, Neurodegenerative Diseases
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