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Synuclein, dopamine and oxidative stress: co-conspirators in Parkinson's disease?
Brain Res Mol Brain Res. 2005 Mar 24; 134(1):18-23.BR

Abstract

The etiology of Parkinson's disease (PD) is presently unknown. The unifying hallmark of disease is depletion of dopamine and loss of nigrostriatal dopamine neurons. Familial and sporadic forms of the disease are described. The familial mutations occur within alpha-synuclein and molecules involved in protein degradation and mitochondrial function. Sporadic PD is thought to involve the interplay of genetic and environmental factors. Despite disparate initiating triggers, a convergent pathobiologic model for this common neurodegenerative disease has been proposed. Likely players have emerged that may form the basis for this common pathway model of disease. In this review, we examine the role of three most implicated PD pathogenic conspirators: synuclein, dopamine and oxidative stress.

Authors+Show Affiliations

Department of Neurology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

15790526

Citation

Maguire-Zeiss, Kathleen A., et al. "Synuclein, Dopamine and Oxidative Stress: Co-conspirators in Parkinson's Disease?" Brain Research. Molecular Brain Research, vol. 134, no. 1, 2005, pp. 18-23.
Maguire-Zeiss KA, Short DW, Federoff HJ. Synuclein, dopamine and oxidative stress: co-conspirators in Parkinson's disease? Brain Res Mol Brain Res. 2005;134(1):18-23.
Maguire-Zeiss, K. A., Short, D. W., & Federoff, H. J. (2005). Synuclein, dopamine and oxidative stress: co-conspirators in Parkinson's disease? Brain Research. Molecular Brain Research, 134(1), 18-23.
Maguire-Zeiss KA, Short DW, Federoff HJ. Synuclein, Dopamine and Oxidative Stress: Co-conspirators in Parkinson's Disease. Brain Res Mol Brain Res. 2005 Mar 24;134(1):18-23. PubMed PMID: 15790526.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Synuclein, dopamine and oxidative stress: co-conspirators in Parkinson's disease? AU - Maguire-Zeiss,Kathleen A, AU - Short,Douglas W, AU - Federoff,Howard J, PY - 2004/09/09/received PY - 2004/09/20/revised PY - 2004/09/26/accepted PY - 2005/3/26/pubmed PY - 2005/6/14/medline PY - 2005/3/26/entrez SP - 18 EP - 23 JF - Brain research. Molecular brain research JO - Brain Res Mol Brain Res VL - 134 IS - 1 N2 - The etiology of Parkinson's disease (PD) is presently unknown. The unifying hallmark of disease is depletion of dopamine and loss of nigrostriatal dopamine neurons. Familial and sporadic forms of the disease are described. The familial mutations occur within alpha-synuclein and molecules involved in protein degradation and mitochondrial function. Sporadic PD is thought to involve the interplay of genetic and environmental factors. Despite disparate initiating triggers, a convergent pathobiologic model for this common neurodegenerative disease has been proposed. Likely players have emerged that may form the basis for this common pathway model of disease. In this review, we examine the role of three most implicated PD pathogenic conspirators: synuclein, dopamine and oxidative stress. SN - 0169-328X UR - https://www.unboundmedicine.com/medline/citation/15790526/Synuclein_dopamine_and_oxidative_stress:_co_conspirators_in_Parkinson's_disease L2 - https://linkinghub.elsevier.com/retrieve/pii/S0169-328X(04)00452-8 DB - PRIME DP - Unbound Medicine ER -