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Ganglioside Metabolism and Parkinson's Disease
- Source :
- Frontiers in Neuroscience, Vol 12 (2018)
- Publication Year :
- 2018
- Publisher :
- Frontiers Media S.A., 2018.
-
Abstract
- Here we advance the hypothesis that Parkinson's disease (PD) is fundamentally a failure of trophic support for specific classes of neurons, primarily catecholaminergic. Evidence from our laboratory provides a framework into which a broad array of findings from many quarters can be integrated into a general theory that offers testable hypotheses to new and established investigators. Mice deficient in the ability to synthesize series-a gangliosides, specifically GM1 ganglioside, develop parkinsonism. We found that this seems to be due to a failure in signaling efficiency by the important catecholaminergic growth factor, GDNF. Interestingly, these mice accumulate alpha-synuclein in nigral neurons. Striatal over-expression of GDNF eliminates these aggregates and also restores normal motor function. These findings bring into question common beliefs about alpha-synuclein pathology and may help us to reinterpret other experimental findings in a new light. The purpose of this article is to provoke new thinking about PD and hopefully encourage younger scientists to explore some of the ideas presented below.
Details
- Language :
- English
- ISSN :
- 1662453X
- Volume :
- 12
- Database :
- Directory of Open Access Journals
- Journal :
- Frontiers in Neuroscience
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.328da69787ce4689b5a3f097fda82f93
- Document Type :
- article
- Full Text :
- https://doi.org/10.3389/fnins.2018.00045