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Alteration in alpha-synuclein mRNA expression in Parkinson's disease.
Mov Disord. 2004 Feb; 19(2):162-70.MD

Abstract

The presynaptic protein alpha-synuclein is considered to play an important role in the pathophysiology of Parkinson's disease (PD). Point mutations in the alpha-synuclein gene have been demonstrated in familial PD and alpha-synuclein is a major component of Lewy bodies, the pathological hallmark of the sporadic disease. It is not clear whether abnormal accumulation of alpha-synuclein is the result of abnormal levels of expression of the gene in neurodegenerative conditions. Expression of alpha-synuclein mRNA was therefore studied in control and PD brain using semiquantitative in situ hybridization. alpha-synuclein was expressed widely and hybridization signal was seen in most cortical regions, hippocampus, cerebellum, and brain stem. There was little mRNA in the striatum and no hybridization signal was detected in glia. High levels of alpha-synuclein mRNA expression in neurons did not seem to be a marker for Lewy body formation. Abundant signal was seen both in regions in which Lewy body deposition occurs commonly in idiopathic PD (PD), such as substantia nigra and frontal and temporal cortex, as well as in less susceptible regions, e.g. visual cortex. Quantitative comparison of mRNA expression in regions of predilection for Lewy body formation showed that mRNA expression was reduced significantly in melanized substantia nigra neurons and frontal cortex neurons in Parkinson's disease. In substantia nigra neurons there seemed to be a negative correlation between cellular mRNA expression and disease duration. These findings are in broad agreement with other studies of the expression of alpha-synuclein mRNA in human brain and suggest that Lewy body formation is unlikely to be the result of overexpression of alpha-synuclein.

Authors+Show Affiliations

Queen Square Brain Bank for Neurological Disorders, Institute of Neurology, London, United Kingdom.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

14978671

Citation

Kingsbury, Ann E., et al. "Alteration in Alpha-synuclein mRNA Expression in Parkinson's Disease." Movement Disorders : Official Journal of the Movement Disorder Society, vol. 19, no. 2, 2004, pp. 162-70.
Kingsbury AE, Daniel SE, Sangha H, et al. Alteration in alpha-synuclein mRNA expression in Parkinson's disease. Mov Disord. 2004;19(2):162-70.
Kingsbury, A. E., Daniel, S. E., Sangha, H., Eisen, S., Lees, A. J., & Foster, O. J. (2004). Alteration in alpha-synuclein mRNA expression in Parkinson's disease. Movement Disorders : Official Journal of the Movement Disorder Society, 19(2), 162-70.
Kingsbury AE, et al. Alteration in Alpha-synuclein mRNA Expression in Parkinson's Disease. Mov Disord. 2004;19(2):162-70. PubMed PMID: 14978671.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Alteration in alpha-synuclein mRNA expression in Parkinson's disease. AU - Kingsbury,Ann E, AU - Daniel,Susan E, AU - Sangha,Hardev, AU - Eisen,Sarah, AU - Lees,Andrew J, AU - Foster,Oliver J F, PY - 2004/2/24/pubmed PY - 2004/8/3/medline PY - 2004/2/24/entrez SP - 162 EP - 70 JF - Movement disorders : official journal of the Movement Disorder Society JO - Mov Disord VL - 19 IS - 2 N2 - The presynaptic protein alpha-synuclein is considered to play an important role in the pathophysiology of Parkinson's disease (PD). Point mutations in the alpha-synuclein gene have been demonstrated in familial PD and alpha-synuclein is a major component of Lewy bodies, the pathological hallmark of the sporadic disease. It is not clear whether abnormal accumulation of alpha-synuclein is the result of abnormal levels of expression of the gene in neurodegenerative conditions. Expression of alpha-synuclein mRNA was therefore studied in control and PD brain using semiquantitative in situ hybridization. alpha-synuclein was expressed widely and hybridization signal was seen in most cortical regions, hippocampus, cerebellum, and brain stem. There was little mRNA in the striatum and no hybridization signal was detected in glia. High levels of alpha-synuclein mRNA expression in neurons did not seem to be a marker for Lewy body formation. Abundant signal was seen both in regions in which Lewy body deposition occurs commonly in idiopathic PD (PD), such as substantia nigra and frontal and temporal cortex, as well as in less susceptible regions, e.g. visual cortex. Quantitative comparison of mRNA expression in regions of predilection for Lewy body formation showed that mRNA expression was reduced significantly in melanized substantia nigra neurons and frontal cortex neurons in Parkinson's disease. In substantia nigra neurons there seemed to be a negative correlation between cellular mRNA expression and disease duration. These findings are in broad agreement with other studies of the expression of alpha-synuclein mRNA in human brain and suggest that Lewy body formation is unlikely to be the result of overexpression of alpha-synuclein. SN - 0885-3185 UR - https://www.unboundmedicine.com/medline/citation/14978671/Alteration_in_alpha_synuclein_mRNA_expression_in_Parkinson's_disease_ L2 - https://doi.org/10.1002/mds.10683 DB - PRIME DP - Unbound Medicine ER -