Cited by 112Mitochondrial Function and PathologyGenetics, Aging, and Longevity in Model OrganismsCell death mechanisms and regulation

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Lifespan and mitochondrial control of neurodegeneration

Wright, Alan F, Jacobson, Samuel G, Cideciyan, Artur V, Roman, Alejandro J, Shu, Xinhua, Vlachantoni, Dafni, McInnes, Roderick R, Riemersma, Rudolph A·2004·Nature Genetics

DOI 10.1038/ng1448

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Abstract

We examine the allometric (comparative scaling) relationships between rates of neurodegeneration resulting from equivalent mutations in a diverse group of genes from five mammalian species with different maximum lifespan potentials. In both retina and brain, rates of neurodegeneration vary by as much as two orders of magnitude and are strongly correlated with maximum lifespan potential and rates of formation of mitochondrial reactive oxygen and nitrogen species (RONS). Cell death in these disorders is directly or indirectly regulated by the intrinsic mitochondrial cell death pathway. Mitochondria are the main source of RONS production and integrate cellular stress signals to coordinate the intrinsic pathway. We propose that these two functions are intimately related and that steady-state RONS-mediated signaling or damage to the mitochondrial stress-integration machinery is the principal factor setting the probability of cell death in response to a diverse range of cellular stressors. This provides a new and unifying framework for investigating neurodegenerative disorders.

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Authors: Wright, A. F., Jacobson, S. G., Cideciyan, A. V., Roman, A. J., Shu, X., Vlachantoni, D., McInnes, R. R., & Riemersma, R. A.
Affiliations: Western General Hospital (GB)
University of Pennsylvania (US)
University of Toronto (CA)
UiT The Arctic University of Norway (NO)
Corresponding author: Wright, Alan F
ORCID: Jacobson, Samuel G
Cideciyan, Artur V
Shu, Xinhua
Venue: Nature Genetics
Publisher: Springer Science and Business Media LLC
Published: 2004-10-28
Volume: 36
Issue: 11
Pages: 1153-1158
ISSN: 1061-4036 (ISSN-L)
1546-1718
DOI: 10.1038/ng1448
OpenAlex: W2050863429
Cited by: 111
References: 53
Citations by year: 2026: 4 · 2025: 3 · 2024: 2 · 2023: 5 · 2022: 4 · 2021: 6 · 2020: 8 · 2019: 3 · 2018: 7 · 2017: 5 · 2016: 3 · 2015: 5 · 2014: 5 · 2013: 3 · 2012: 3
FWCI: 0.46
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Genetics (publishedVersion)
PubMed (publishedVersion)
ResearchOnline (Glasgow Caledonian University) (acceptedVersion)
Funders: Macula Vision Research Foundation
National Institutes of Health
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 › Molecular Biology › Cell death mechanisms and regulation
Keywords: neurodegeneration, lifespan, allometric scaling, retina, brain, mammalian species comparison, genetic mutations
MeSH terms: Animals, Brain, Humans, Life Expectancy, Mitochondria, Nerve Degeneration, Retina, Species Specificity, Cell Death, Reactive Oxygen Species, Oxidative Stress, Neurodegenerative Diseases, Reactive Nitrogen Species

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