Journal article
α-synuclein transgenic mice reveal compensatory increases in parkinson's disease-associated proteins dj-1 and parkin and have enhanced α-synuclein and pink1 levels after rotenone treatment
S George, SS Mok, M Nurjono, S Ayton, DI Finkelstein, CL Masters, QX Li, JG Culvenor
Journal of Molecular Neuroscience | Published : 2010
Abstract
Parkinson's disease (PD) is a severe neurodegenerative disorder characterised by loss of dopaminergic neurons of the substantia nigra. The pathological hallmarks are cytoplasmic inclusions termed Lewy bodies consisting primarily of aggregated α-synuclein (αSN). Different lines of transgenic mice have been developed to model PD but have failed to recapitulate the hallmarks of this disease. Since treatment of rodents with the pesticide rotenone can reproduce nigrostriatal cell loss and other features of PD, we aimed to test chronic oral administration of rotenone to transgenic mice over-expressing human αSN with the A53T mutation. Initial assessment of this transgenic line for compensatory mol..
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Funding Acknowledgements
We sincerely thank B. Etherton for gavaging the mice. We thank V. M. Lee and J.Q. Trojanowski for the transgenic mouse line. We thank J. Anderson for antibody 11A5, P. J. Kahle for Ab 7544 and T. Iwatsubo for mAb LB509. For assistance with immunohistochemistry, we thank L. Leone and J. George. These studies were supported by the National Health and Medical Research Council of Australia.