Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2009 Dec:15 Suppl 4:S24-7.
doi: 10.1016/S1353-8020(09)70830-2.

Does autophagy worsen or improve the survival of dopaminergic neurons?

Affiliations
Review

Does autophagy worsen or improve the survival of dopaminergic neurons?

Livia Pasquali et al. Parkinsonism Relat Disord. 2009 Dec.

Abstract

In eukaryotic cells intracellular components are mainly degraded by autophagy and the ubiquitin-proteasome system. Autophagy is more flexible compared with the ubiquitin-proteasome system and it is involved in the degradation of long-lived proteins and organelles, such as mitochondria, which cannot be degraded by the ubiquitin-proteasome. Although autophagy is able to compensate for ubiquitin-proteasome dysfunction, the opposite does not occur. Autophagy is frequently involved in neurodegeneration; however, there is no consensus on its role in cell survival, as it can be either neuroprotective or neurotoxic. With respect to dopaminergic neurons, there is evidence that autophagy occurs during damage to substantia nigra neurons such as in Parkinson's disease. Moreover, a variety of inherited forms of Parkinson's disease are characterized by mutated proteins that belong to the autophagy pathway. Inhibition of autophagy precipitates dopaminergic cell death, whereas autophagy activation rescues the death of nigral dopaminergic neurons induced by proteasome inhibitors. Taken together, this evidence suggests that autophagy improves the survival of dopaminergic cells.

PubMed Disclaimer

Similar articles

Cited by

LinkOut - more resources