期刊
MOLECULAR AND CELLULAR NEUROSCIENCE
卷 24, 期 2, 页码 419-429出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S1044-7431(03)00198-2
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Alpha-synuclein was implicated in Parkinson's disease when missense mutations in the a-synuclein gene were found in autosomal dominant Parkinson's disease and a-synuclein was shown to be a major constituent of protein aggregates in sporadic Parkinson's disease and other synucleinopathies. We have generated transgenic mice expressing A53T mutant and wild-type human a-synuclein. The mutant transgenic protein was distributed abnormally to the axons, perikarya, and dendrites of neurons in many brain areas. In electron microscopic immunogold studies, no aggregation of alpha-synuclein was found in these mice. However, behavior analysis showed a progressive reduction of spontaneous vertical motor activity in both mutant lines correlating with the dosage of overexpression. In addition, deficits of grip strength, rotarod performance, and gait were observed in homozygous PrPmtB mice. Transgenic animals expressing mutant a-synuclein may be a valuable model to assess specific aspects of the pathogenesis of synucleinopathies. (C) 2003 Elsevier Inc. All rights reserved.
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