Cited by 150Mitochondrial Function and PathologyGenetics, Aging, and Longevity in Model OrganismsAutophagy in Disease and Therapy

Reduced steady-state levels of mitochondrial RNA and increased mitochondrial DNA amount in human brain with aging

Barrientos, Antoni, Casademont, Jordi, Cardellach, Francesc, Estivill, Xavier, Urbano-Marquez, Alvaro, Nunes, Virginia·1997·Molecular Brain Research

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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Crossref · 10.1016/s0169-328x(97)00278-7

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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].”
  • 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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