Parkin and 𝛂-Synuclein: Opponent Actions in The Pathogenesis of Parkinson’S Disease
| Autor: | David Miller, Mark R. Cookson, Melisa J. Baptista |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
0301 basic medicine
Parkinson's disease Ubiquitin-Protein Ligases Synucleins Nerve Tissue Proteins Biology Parkin Gene product 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals Humans Alpha-synuclein Genetics Mechanism (biology) General Neuroscience Parkinsonism Parkinson Disease medicine.disease nervous system diseases 030104 developmental biology nervous system chemistry Proteasome alpha-Synuclein Synuclein Neurology (clinical) Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | The Neuroscientist. 10:63-72 |
| ISSN: | 1089-4098 1073-8584 |
| DOI: | 10.1177/1073858403260392 |
| Popis: | Dominant mutations in the gene for •-synuclein, a small presynaptic protein, can cause Parkinson’s disease. Although there is still substantial debate about the precise mechanisms, •-synuclein is toxic to vulnerable neurons, probably as a result of its tendency to aggregate. Opposing this is another gene product that, when mutated, causes a recessive form of parkinsonism, parkin. Parkin has been recently shown to protect cells against •-synuclein toxicity. However, the precise details of the mechanism are unclear. This review will discuss the concept that there are multiple neuronal functions that are targeted by mutant •-synuclein, and in many cases, there is evidence that parkin can protect cells against damage to the same systems. The authors will also discuss ways in which to test some of these ideas, by using newly identified genes such as DJ-1 that cause similar phenotypes. |
| Databáze: | OpenAIRE |
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