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ShareScienceDaily (Apr. 26, 2009) — Researchers at the Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan have established the mechanism by which gangliosides may help treat Parkinson's disease.
These data are presented in the May 2009 issue of The American Journal of Pathology.
Parkinson's disease is caused by a loss of dopamine-secreting cells in the brain, which results in impaired motor skills, speech, and other functions. Abnormal accumulation of the protein α-synuclein may contribute to this neuronal cell death.
Gangliosides have been shown to inhibit a-synuclein aggregation. To discover the mechanism that drives ganglioside-mediated protection from a-synuclein-caused cell death, Wei et al treated cells with a molecule that disrupts the function of lysosomes, cell components responsible for digesting unneeded and excess material in cells. Treatment with gangliosides reversed the lysosomal disruption, which suggests that gangliosides protect against the lysosomal damage of a-synuclein accumulation.
Based on their present result, Wei et al "speculate that deregulation of the expression of gangliosides may underlie the process of axonal degeneration. If this is the case, it is naturally expected that restoration of the protective action of gangliosides might be a useful therapeutic strategy."
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The above story is reprinted from materials provided by American Journal of Pathology.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Wei J, Fujita M, Nakai M, Waragai M, Sekigawa A, Sugama S, Takenouchi T, Masliah M, Hashimoto M. Protective Role of Endogenous Gangliosides for Lysosomal Pathology in a Cellular Model of Synucleinopathies. American Journal Of Pathology, 2009; 174 (5): 1891 DOI: 10.2353/ajpath.2009.080680
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
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