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Mol Cell Neurosci. 2008 Dec;39(4):586-91. doi: 10.1016/j.mcn.2008.08.001. Epub 2008 Aug 27.

Lrrk2 and alpha-synuclein are co-regulated in rodent striatum.

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1
Department of Neuroscience, Karolinska Institutet, Retzius väg 8 B2:4, S-17177 Stockholm, Sweden.

Abstract

LRRK2, alpha-synuclein, UCH-L1 and DJ-1 are implicated in the etiology of Parkinson's disease. We show for the first time that increase in striatal alpha-synuclein levels induce increased Lrrk2 mRNA levels while Dj-1 and Uch-L1 are unchanged. We also demonstrate that a mouse strain lacking the dopamine signaling molecule DARPP-32 has significantly reduced levels of both Lrrk2 and alpha-synuclein, while mice carrying a disabling mutation of the DARPP-32 phosphorylation site T34A or lack alpha-synuclein do not show any changes. To test if striatal dopamine depletion influences Lrrk2 or alpha-synuclein expression, we used the neurotoxin 6-hydroxydopamine in rats and MitoPark mice in which there is progressive degeneration of dopamine neurons. Because striatal Lrrk2 and alpha-synuclein levels were not changed by dopamine depletion, we conclude that Lrrk2 and alpha-synuclein mRNA levels are possibly co-regulated, but they are not influenced by striatal dopamine levels.

PMID:
18790059
DOI:
10.1016/j.mcn.2008.08.001
[Indexed for MEDLINE]
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