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Tytuł:
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Mitochondria in Parkinson disease: back in fashion with a little help from genetics.
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Autorzy:
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Muqit MM; Department of Molecular Neuroscience, Institute of Neurology, University College London, Queen Square, London WC1N 3BG, England.
Gandhi S
Wood NW
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Źródło:
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Archives of neurology [Arch Neurol] 2006 May; Vol. 63 (5), pp. 649-54.
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Typ publikacji:
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Journal Article; Research Support, Non-U.S. Gov't
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Język:
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English
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Imprint Name(s):
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Original Publication: Chicago, American Medical Assn.
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MeSH Terms:
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Mitochondrial Diseases*/complications
Mitochondrial Diseases*/genetics
Mitochondrial Diseases*/pathology
Mitochondria/*pathology
Parkinson Disease/*pathology
Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Mitochondria/genetics ; Models, Biological ; Oncogene Proteins/genetics ; Parkinson Disease/etiology ; Parkinson Disease/genetics ; Protein Deglycase DJ-1 ; Protein Kinases/genetics
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Substance Nomenclature:
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0 (Intracellular Signaling Peptides and Proteins)
0 (Oncogene Proteins)
EC 2.7.- (Protein Kinases)
EC 2.7.11.1 (PTEN-induced putative kinase)
EC 3.1.2.- (PARK7 protein, human)
EC 3.1.2.- (Protein Deglycase DJ-1)
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Entry Date(s):
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Date Created: 20060510 Date Completed: 20060628 Latest Revision: 20161128
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Update Code:
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20240104
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DOI:
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10.1001/archneur.63.5.649
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PMID:
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16682534
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Parkinson disease is a devastating neurodegenerative disorder with no known cure. Impairment in mitochondrial dysfunction is thought to play a major role in the pathogenesis. Recent genetic advances suggest that mitochondrial dysfunction may be the primary defect. Drugs that target the mitochondria may therefore represent the best hope for disease-modifying therapies in Parkinson disease.