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Pathogenesis of Parkinson's disease.
Curr Opin Investig Drugs. 2001 May; 2(5):657-62.CO

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by degeneration of the nigrostriatal dopaminergic pathway and the appearance of cytoplasmic proteinaceous aggregates known as Lewy bodies. Studies of familial PD have uncovered rare causative mutations in genes, including alpha-synuclein. Mutations or oxidative modification of alpha-synuclein causes it to aggregate; alpha-synuclein is a major component of the Lewy body in both familial and sporadic PD. Biochemical analysis has implicated mitochondrial dysfunction in PD. Epidemiological studies indicate a role of exposure to pesticides, some of which are mitochondrial toxins. Mitochondrial dysfunction, resulting from genetic defects, environmental toxins, or a combination of the two, may cause alpha-synuclein aggregation and produce selective neurodegeneration through mechanisms involving oxidative stress and excitotoxicity. Efforts to better define PD pathogenesis should reveal novel therapeutic targets.

Authors+Show Affiliations

Department of Neurology, Emory University, Atlanta, GA 30322, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

11569943

Citation

Sherer, T B., et al. "Pathogenesis of Parkinson's Disease." Current Opinion in Investigational Drugs (London, England : 2000), vol. 2, no. 5, 2001, pp. 657-62.
Sherer TB, Betarbet R, Greenamyre JT. Pathogenesis of Parkinson's disease. Curr Opin Investig Drugs. 2001;2(5):657-62.
Sherer, T. B., Betarbet, R., & Greenamyre, J. T. (2001). Pathogenesis of Parkinson's disease. Current Opinion in Investigational Drugs (London, England : 2000), 2(5), 657-62.
Sherer TB, Betarbet R, Greenamyre JT. Pathogenesis of Parkinson's Disease. Curr Opin Investig Drugs. 2001;2(5):657-62. PubMed PMID: 11569943.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pathogenesis of Parkinson's disease. AU - Sherer,T B, AU - Betarbet,R, AU - Greenamyre,J T, PY - 2001/9/25/pubmed PY - 2001/11/3/medline PY - 2001/9/25/entrez SP - 657 EP - 62 JF - Current opinion in investigational drugs (London, England : 2000) JO - Curr Opin Investig Drugs VL - 2 IS - 5 N2 - Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by degeneration of the nigrostriatal dopaminergic pathway and the appearance of cytoplasmic proteinaceous aggregates known as Lewy bodies. Studies of familial PD have uncovered rare causative mutations in genes, including alpha-synuclein. Mutations or oxidative modification of alpha-synuclein causes it to aggregate; alpha-synuclein is a major component of the Lewy body in both familial and sporadic PD. Biochemical analysis has implicated mitochondrial dysfunction in PD. Epidemiological studies indicate a role of exposure to pesticides, some of which are mitochondrial toxins. Mitochondrial dysfunction, resulting from genetic defects, environmental toxins, or a combination of the two, may cause alpha-synuclein aggregation and produce selective neurodegeneration through mechanisms involving oxidative stress and excitotoxicity. Efforts to better define PD pathogenesis should reveal novel therapeutic targets. SN - 1472-4472 UR - https://www.unboundmedicine.com/medline/citation/11569943/Pathogenesis_of_Parkinson's_disease_ L2 - https://medlineplus.gov/parkinsonsdisease.html DB - PRIME DP - Unbound Medicine ER -