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Parkinson's disease.
Hum Mol Genet. 2007 Oct 15; 16 Spec No. 2:R183-94.HM

Abstract

Parkinson's disease (PD) is a chronic progressive neurodegenerative movement disorder characterized by a profound and selective loss of nigrostriatal dopaminergic neurons. Clinical manifestations of this complex disease include motor impairments involving resting tremor, bradykinesia, postural instability, gait difficulty and rigidity. Current medications only provide symptomatic relief and fail to halt the death of dopaminergic neurons. A major hurdle in development of neuroprotective therapies are due to limited understanding of disease processes leading to death of dopaminergic neurons. While the etiology of dopaminergic neuronal demise is elusive, a combination of genetic susceptibilities and environmental factors seems to play a critical role. The majority of PD cases are sporadic however, the discovery of genes linked to rare familial forms of disease (encoding alpha-synuclein, parkin, DJ-1, PINK-1 and LRRK2) and studies from experimental animal models has provided crucial insights into molecular mechanisms in disease pathogenesis and identified probable targets for therapeutic intervention. Recent findings implicate mitochondrial dysfunction, oxidative damage, abnormal protein accumulation and protein phosphorylation as key molecular mechanisms compromising dopamine neuronal function and survival as the underlying cause of pathogenesis in both sporadic and familial PD. In this review we provide an overview of the most relevant findings made by the PD research community in the last year and discuss how these significant findings improved our understanding of events leading to nigrostriatal dopaminergic degeneration, and identification of potential cell survival pathways that could serve as targets for neuroprotective therapies in preventing this disabling neurological illness.

Authors+Show Affiliations

Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, A-501, New York, NY 10021, USA. bot2003@med.cornell.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review

Language

eng

PubMed ID

17911161

Citation

Thomas, Bobby, and M Flint Beal. "Parkinson's Disease." Human Molecular Genetics, vol. 16 Spec No. 2, 2007, pp. R183-94.
Thomas B, Beal MF. Parkinson's disease. Hum Mol Genet. 2007;16 Spec No. 2:R183-94.
Thomas, B., & Beal, M. F. (2007). Parkinson's disease. Human Molecular Genetics, 16 Spec No. 2, R183-94.
Thomas B, Beal MF. Parkinson's Disease. Hum Mol Genet. 2007 Oct 15;16 Spec No. 2:R183-94. PubMed PMID: 17911161.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Parkinson's disease. AU - Thomas,Bobby, AU - Beal,M Flint, PY - 2007/10/4/pubmed PY - 2007/12/7/medline PY - 2007/10/4/entrez SP - R183 EP - 94 JF - Human molecular genetics JO - Hum Mol Genet VL - 16 Spec No. 2 N2 - Parkinson's disease (PD) is a chronic progressive neurodegenerative movement disorder characterized by a profound and selective loss of nigrostriatal dopaminergic neurons. Clinical manifestations of this complex disease include motor impairments involving resting tremor, bradykinesia, postural instability, gait difficulty and rigidity. Current medications only provide symptomatic relief and fail to halt the death of dopaminergic neurons. A major hurdle in development of neuroprotective therapies are due to limited understanding of disease processes leading to death of dopaminergic neurons. While the etiology of dopaminergic neuronal demise is elusive, a combination of genetic susceptibilities and environmental factors seems to play a critical role. The majority of PD cases are sporadic however, the discovery of genes linked to rare familial forms of disease (encoding alpha-synuclein, parkin, DJ-1, PINK-1 and LRRK2) and studies from experimental animal models has provided crucial insights into molecular mechanisms in disease pathogenesis and identified probable targets for therapeutic intervention. Recent findings implicate mitochondrial dysfunction, oxidative damage, abnormal protein accumulation and protein phosphorylation as key molecular mechanisms compromising dopamine neuronal function and survival as the underlying cause of pathogenesis in both sporadic and familial PD. In this review we provide an overview of the most relevant findings made by the PD research community in the last year and discuss how these significant findings improved our understanding of events leading to nigrostriatal dopaminergic degeneration, and identification of potential cell survival pathways that could serve as targets for neuroprotective therapies in preventing this disabling neurological illness. SN - 0964-6906 UR - https://www.unboundmedicine.com/medline/citation/17911161/Parkinson's_disease_ L2 - https://academic.oup.com/hmg/article-lookup/doi/10.1093/hmg/ddm159 DB - PRIME DP - Unbound Medicine ER -