Promoting basal levels of autophagy in the nervous system enhances longevity and oxidant resistance in adult Drosophila
Open accessAbstract
Autophagy is involved with the turnover of intracellular components and the management of stress responses. Genetic studies in mice have shown that suppression of neuronal autophagy can lead to the accumulation of protein aggregates and neurodegeneration. However, no study has shown that increasing autophagic gene expression can be beneficial to an aging nervous system. Here we demonstrate that expression of several autophagy genes is reduced in Drosophila neural tissues as a normal part of aging. The age-dependent suppression of autophagy occurs concomitantly with the accumulation of insoluble ubiquitinated proteins (IUP), a marker of neuronal aging and degeneration. Mutations in the Atg8a gene (autophagy-related 8a) result in reduced lifespan, IUP accumulation and increased sensitivity to oxidative stress. In contrast, enhanced Atg8a expression in older fly brains extends the average adult lifespan by 56% and promotes resistance to oxidative stress and the accumulation of ubiquitinated and oxidized proteins. These data indicate that genetic or age-dependent suppression of autophagy is closely associated with the buildup of cellular damage in neurons and a reduced lifespan, while maintaining the expression of a rate-limiting autophagy gene prevents the age-dependent accumulation of damage in neurons and promotes longevity.
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In flies, increasing autophagy in neurons alone is sufficient to extend lifespan, and reducing autophagy shortens lifespan and gives rise to neurodegeneration.
“In flies, increasing autophagy in neurons alone is sufficient to extend lifespan (52), and reducing autophagy shortens lifespan and gives rise to neurodegeneration (52,53).”
From Neural mechanisms of ageing and cognitive decline (2010) · cites this paper as [52]
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- Authors
- Simonsen, A., Cumming, R. C., Brech, A., Isakson, P., Schubert, D. R., & Finley, K. D.
- Affiliations
- Salk Institute for Biological Studies (US)
- Western University (CA)
- Venue
- Autophagy
- Publisher
- Informa UK Limited
- Published
- 2008-02-16
- Volume
- 4
- Issue
- 2
- Pages
- 176-184
- ISSN
- 1554-8627 (ISSN-L)
- 1554-8635
- OpenAlex
- W1967809393
- Cited by
- 716
- References
- 35
- Citations by year
- 2026: 21 · 2025: 33 · 2024: 32 · 2023: 45 · 2022: 47 · 2021: 53 · 2020: 43 · 2019: 46 · 2018: 43 · 2017: 45 · 2016: 42 · 2015: 32 · 2014: 44 · 2013: 38 · 2012: 28
- FWCI
- 11.89
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Autophagy (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Norges Forskningsråd
- Canadian Institutes of Health Research
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurobiology and Insect Physiology Research
- Keywords
- neuronal aging, Atg8a, lifespan extension, oxidative stress resistance, protein aggregation, neurodegeneration, Drosophila, brain aging, oxidized proteins
- MeSH terms
- Aging, Amino Acid Sequence, Animals, Autophagy, Drosophila, Female, Gene Expression Regulation, Immunity, Innate, Longevity, Male, Membrane Proteins, Models, Biological, Molecular Sequence Data, Nerve Tissue Proteins, Nervous System Physiological Phenomena, Oxidants, Reactive Oxygen Species, Sequence Homology, Amino Acid, Oxidative Stress, Ubiquitin, Drosophila Proteins, Animals, Genetically Modified
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