The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
All-you-can-eat: autophagy in neurodegeneration and neuroprotection
Open accessAbstract
Autophagy is the major pathway involved in the degradation of proteins and organelles, cellular remodeling, and survival during nutrient starvation. Autophagosomal dysfunction has been implicated in an increasing number of diseases from cancer to bacterial and viral infections and more recently in neurodegeneration. While a decrease in autophagic activity appears to interfere with protein degradation and possibly organelle turnover, increased autophagy has been shown to facilitate the clearance of aggregation-prone proteins and promote neuronal survival in a number of disease models. On the other hand, too much autophagic activity can be detrimental as well and lead to cell death, suggesting the regulation of autophagy has an important role in cell fate decisions. An increasing number of model systems are now available to study the role of autophagy in the central nervous system and how it might be exploited to treat disease. We will review here the current knowledge of autophagy in the central nervous system and provide an overview of the various models that have been used to study acute and chronic neurodegeneration.
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Citations
Cites
Autophagy fights disease through cellular self-digestion
Mizushima, N., Levine, B., Cuervo, A. M., & Klionsky, D. J. (2008) · Nature · doi:10.1038/nature06639 · Cited by 6,452
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Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
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TSC2 Mediates Cellular Energy Response to Control Cell Growth and Survival
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Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice
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Loss of autophagy in the central nervous system causes neurodegeneration in mice
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Impairment of starvation-induced and constitutive autophagy in Atg7 -deficient mice
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Cited by
Spilman, P., Podlutskaya, N., Hart, M. J., Debnath, J., Gorostiza, O., Bredesen, D., Richardson, A., Strong, R., & Galvan, V. (2010) · PLoS ONE · doi:10.1371/journal.pone.0009979 · Cited by 1,033
“Autophagy is a key pathway for the clearance of aggregationprone proteins and may have a protective role in proteinopathies[20,39].”
BackgroundImmune activation in brain aging and neurodegeneration: too much or too little?
Lucin, K. M., & Wyss-Coray, T. (2009) · Neuron · doi:10.1016/j.neuron.2009.08.039 · Cited by 679
Self-citationBraak, H., & Del Tredici, K. (2017) · Journal of Parkinson’s Disease · doi:10.3233/jpd-179001 · Cited by 372
Regulation of the autophagy protein LC3 by phosphorylation
Cherra, S. J., Kulich, S. M., Uechi, G., Balasubramani, M., Mountzouris, J., Day, B. W., & Chu, C. T. (2010) · Journal of Cell Biology · doi:10.1083/jcb.201002108 · Cited by 304
Vingtdeux, V., Davies, P., Dickson, D. W., & Marambaud, P. (2011) · Acta Neuropathologica · doi:10.1007/s00401-010-0759-x · Cited by 296
Metadata
- Authors
- Jaeger, P. A., & Wyss-Coray, T.
- Venue
- Molecular Neurodegeneration
- Published
- 2009
- Volume
- 4
- Issue
- 1
- Pages
- 16
- ISSN
- 1750-1326 (ISSN-L)
- OpenAlex
- W2053103401
- Cited by
- 175
- References
- 61
- FWCI
- 10.49
- Type
- journal article
- Language
- en
- Open access
- gold
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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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