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Inflammation in Parkinson's disease: causative or epiphenomenal?
Subcell Biochem. 2007; 42:249-79.SB

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder characterized by a dramatic loss of dopaminergic neurons in the substantia nigra (SN). Several pathogenic mechanisms have been implicated in the demise of these cells, including dopamine-dependent oxidative stress, mitochondrial dysfunction, excitotoxicity, and proteasomal impairment. In recent years, the involvement of neuroinflammatory processes in nigral degeneration has gained increasing attention. Not only have activated microglia and increased levels of inflammatory mediators been detected in the striatum of PD patients, but a large body of animal studies points to a contributory role of inflammation in dopaminergic cell loss. For example, post-mortem examination of human subjects exposed to the parkinsonism-inducing toxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, revealed the presence of activated microglia decades after drug exposure, suggesting that even a brief pathogenic insult can induce an ongoing inflammatory response. Perhaps not surprisingly, nonsteroidal anti-inflammatory drugs have been shown to reduce the risk of developing PD. In the past few years, various pathways have come to light that could link neurodegeneration and microglial activation, finally ascribing a pathogenic trigger to the chronic inflammatory response characteristic of PD.

Authors+Show Affiliations

Department of Pharmacology and Pharmacotherapeutics, The Danish University of Pharmaceutical Sciences, Universitetsparken 2, 2100 Copenhagen, Denmark.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

17612055

Citation

Hald, Andreas, et al. "Inflammation in Parkinson's Disease: Causative or Epiphenomenal?" Sub-cellular Biochemistry, vol. 42, 2007, pp. 249-79.
Hald A, Van Beek J, Lotharius J. Inflammation in Parkinson's disease: causative or epiphenomenal? Subcell Biochem. 2007;42:249-79.
Hald, A., Van Beek, J., & Lotharius, J. (2007). Inflammation in Parkinson's disease: causative or epiphenomenal? Sub-cellular Biochemistry, 42, 249-79.
Hald A, Van Beek J, Lotharius J. Inflammation in Parkinson's Disease: Causative or Epiphenomenal. Subcell Biochem. 2007;42:249-79. PubMed PMID: 17612055.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inflammation in Parkinson's disease: causative or epiphenomenal? AU - Hald,Andreas, AU - Van Beek,Johan, AU - Lotharius,Julie, PY - 2007/7/7/pubmed PY - 2007/8/7/medline PY - 2007/7/7/entrez SP - 249 EP - 79 JF - Sub-cellular biochemistry JO - Subcell Biochem VL - 42 N2 - Parkinson's disease (PD) is a neurodegenerative disorder characterized by a dramatic loss of dopaminergic neurons in the substantia nigra (SN). Several pathogenic mechanisms have been implicated in the demise of these cells, including dopamine-dependent oxidative stress, mitochondrial dysfunction, excitotoxicity, and proteasomal impairment. In recent years, the involvement of neuroinflammatory processes in nigral degeneration has gained increasing attention. Not only have activated microglia and increased levels of inflammatory mediators been detected in the striatum of PD patients, but a large body of animal studies points to a contributory role of inflammation in dopaminergic cell loss. For example, post-mortem examination of human subjects exposed to the parkinsonism-inducing toxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, revealed the presence of activated microglia decades after drug exposure, suggesting that even a brief pathogenic insult can induce an ongoing inflammatory response. Perhaps not surprisingly, nonsteroidal anti-inflammatory drugs have been shown to reduce the risk of developing PD. In the past few years, various pathways have come to light that could link neurodegeneration and microglial activation, finally ascribing a pathogenic trigger to the chronic inflammatory response characteristic of PD. SN - 0306-0225 UR - https://www.unboundmedicine.com/medline/citation/17612055/Inflammation_in_Parkinson's_disease:_causative_or_epiphenomenal L2 - https://antibodies.cancer.gov/detail/CPTC-SIGLEC1-1 DB - PRIME DP - Unbound Medicine ER -