The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Protein homeostasis and aging in neurodegeneration
Open accessAbstract
Genetic and environmental factors responsible for numerous neurodegenerative diseases vary between disorders, yet age remains a universal risk factor. Age-associated decline in protein homeostasis, or proteostasis, enables disease-linked proteins to adopt aberrant tertiary structures, accumulate as higher-ordered aggregates, and cause a myriad of cellular dysfunctions and neuronal death. However, recent findings suggest that the assembly of disease proteins into tightly ordered aggregates can significantly delay proteotoxic onset. Furthermore, manipulation of metabolic pathways through key signaling components extends lifespan, bolsters proteostasis networks, and delays the onset of proteotoxicity. Thus, understanding the relationship between proteostasis and aging has provided important insights into neurodegeneration.
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Cites
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Cited by
A chaperome subnetwork safeguards proteostasis in aging and neurodegenerative disease
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Widespread Proteome Remodeling and Aggregation in Aging C. elegans
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Aging, Rejuvenation, and Epigenetic Reprogramming: Resetting the Aging Clock
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Metadata
- Authors
- Douglas, P. M., & Dillin, A.
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2010-09-06
- Volume
- 190
- Issue
- 5
- Pages
- 719-729
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W2137209191
- Cited by
- 372
- References
- 37
- FWCI
- 6.52
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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