Antioxidants protect PINK1-dependent dopaminergic neurons in Drosophila.

Abstract

Parkinson's disease (PD) is the most frequent neurodegenerative movement disorder. Mutations in the PINK1 gene are linked to the autosomal recessive early onset familial form of PD. The physiological function of PINK1 and pathological abnormality of PD-associated PINK1 mutants are largely unknown. We here show that inactivation of Drosophila PINK1 (dPINK1) using RNAi results in progressive loss of dopaminergic neurons and in ommatidial degeneration of the compound eye, which is rescued by expression of human PINK1 (hPINK1). Expression of human SOD1 suppresses neurodegeneration induced by dPINK1 inactivation. Moreover, treatment of dPINK1 RNAi flies with the antioxidants SOD and vitamin E significantly inhibits ommatidial degeneration. Thus, dPINK1 plays an essential role in maintaining neuronal survival by preventing neurons from undergoing oxidative stress, thereby suggesting a potential mechanism by which a reduction in PINK1 function leads to PD-associated neurodegeneration.

4 Figures and Tables

050100'05'06'07'08'09'10'11'12'13'14'15'16'17
Citations per Year

490 Citations

Semantic Scholar estimates that this publication has 490 citations based on the available data.

See our FAQ for additional information.

Cite this paper

@article{Wang2006AntioxidantsPP, title={Antioxidants protect PINK1-dependent dopaminergic neurons in Drosophila.}, author={Danling L. Wang and L. F. Qian and Hui Xiong and Jiandong Liu and Wendi S. Neckameyer and Sean M Oldham and Kun Xia and Jianzhi Wang and Rolf Bodmer and Zhuohua Zhang}, journal={Proceedings of the National Academy of Sciences of the United States of America}, year={2006}, volume={103 36}, pages={13520-5} }