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Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish
Author(s) -
Guiqi Ren,
Shengchang Xin,
Song Li,
Hanbing Zhong,
Shuo Lin
Publication year - 2011
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0020630
Subject(s) - lrrk2 , zebrafish , dopaminergic , loss function , phenotype , biology , parkinson's disease , neuroscience , microbiology and biotechnology , disease , genetics , dopamine , pathology , medicine , gene
Mutations in LRRK2 are genetically linked to Parkinson's disease (PD) but its normal biological function is largely unknown. Sheng et al. recently reported that deletion of the WD40 domain of LRRK2 in zebrafish specifically causes PD-like loss of neurons and behavior defect. However, our similar early study and recent confirming experiments using the same reagents reported by Sheng et al. failed to reproduce the phenotype of the loss of dopaminergic neurons, although the mRNA of LRRK2 was molecularly disrupted. Our study suggests that function of LRRK2 and its usefulness to generate zebrafish PD model needs further evaluation.

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