Reduced steady-state levels of mitochondrial RNA and increased mitochondrial DNA amount in human brain with aging
Abstract
The contribution of the mitochondrial genetic system in the degenerative processes of senescence remains unclear. This study deals with age-related changes in brain mtDNA expression in humans. Brain tissue from the frontal lobe cortex was obtained from autopsy of 13 humans aged between 21 and 84 years. No structural changes were detected in mtDNA, increased mtDNA content and reduced steady-state level of mitochondrial transcripts and transcription ratio (mtRNA/mtDNA) were associated with aging. These findings suggest that the increase of the mtDNA levels could be considered as an inefficient compensatory mechanism to maintain the normal levels of mtRNA transcripts. This unbalanced mitochondrial condition could play a role in the process of senescence in human brain.
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Mitochondrial function declines throughout much of adulthood, and adaptive changes at least initially mitigate this decline.
“Existing data suggest mitochondrial function declines throughout much of adulthood and that adaptive changes, at least initially, mitigate this decline [47, 80-82].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [82]
Mitochondrial mass, or parameters related to it, appear to change during brain aging; overall studies suggest that with advancing age mitochondrial mass increases or attempts to increase.
“Mitochondrial mass, or at least parameters related to it, also appear to change during brain aging. Studies are limited, but overall suggest that with advancing age mitochondrial mass increases or attempts to increase.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [116]
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- Authors
- Barrientos, A., Casademont, J., Cardellach, F., Estivill, X., Urbano-Marquez, A., & Nunes, V.
- Affiliations
- Hospital Clínic de Barcelona (ES)
- Corresponding author
- Nunes, Virginia
- Venue
- Molecular Brain Research
- Publisher
- Elsevier BV
- Published
- 1997-12
- Volume
- 52
- Issue
- 2
- Pages
- 284-289
- ISSN
- 0169-328X (ISSN-L)
- OpenAlex
- W2018590086
- Cited by
- 149
- References
- 26
- Citations by year
- 2024: 5 · 2023: 2 · 2022: 5 · 2021: 1 · 2020: 3 · 2019: 2 · 2018: 7 · 2017: 4 · 2016: 9 · 2015: 8 · 2014: 5 · 2013: 11 · 2012: 8
- FWCI
- 0.71
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Generalitat de Catalunya
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial DNA, mitochondrial RNA, brain aging, mitochondrial transcription, senescence, compensatory mechanisms, human brain
- MeSH terms
- RNA, Mitochondrial, Adult, Aged, Aged, 80 and over, Aging, DNA, Mitochondrial, DNA, Ribosomal, Frontal Lobe, Humans, Middle Aged, Reference Values, Regression Analysis, RNA, RNA, Ribosomal, 18S, Transcription, Genetic
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