The DOI matches its Crossref record; 24 of the 26 references it cites were found in a registry or an index.
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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“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]
In the citing paper
“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]
Citations
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Oxidative damage to mitochondrial DNA shows marked age-dependent increases in human brain
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Cited by
Sorted by citations
The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives
Swerdlow, R. H., Burns, J. M., & Khan, S. M. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2013.09.010 · Cited by 786
“Existing data suggest mitochondrial function declines throughout much of adulthood and that adaptive changes, at least initially, mitigate this decline [47, 80-82].”
BackgroundMitochondrial biogenesis and mitochondrial DNA maintenance of mammalian cells under oxidative stress
Lee, H., & Wei, Y. (2004) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2004.09.010 · Cited by 678
Gureev, A. P., Shaforostova, E. A., & Popov, V. N. (2019) · Frontiers in Genetics · doi:10.3389/fgene.2019.00435 · Cited by 670
Oxidative Stress, Mitochondrial DNA Mutation, and Impairment of Antioxidant Enzymes in Aging
Wei, Y., & Lee, H. (2002) · Experimental Biology and Medicine · doi:10.1177/153537020222700901 · Cited by 600
Increase of mitochondria and mitochondrial DNA in response to oxidative stress in human cells
LEE, H.-C., YIN, P.-H., LU, C.-Y., CHI, C.-W., & WEI, Y.-H. (2000) · Biochemical Journal · doi:10.1042/bj3480425 · Cited by 551
Metadata
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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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