Parkinson's disease: genetic versus toxin-induced rodent models.

作者: Mügen Terzioglu , Dagmar Galter

DOI: 10.1111/J.1742-4658.2008.06302.X

关键词:

摘要: Parkinson's disease (PD), a common progressive neurodegenerative disorder, is characterized by degeneration of dopamine neurons in the substantia nigra and neuronal proteinaceous aggregates called Lewy bodies (LBs). The etiology PD probably combination environmental genetic factors. Recent progress molecular genetics has identified several genes causing PD, including alpha-synuclein, leucine-rich repeat kinase 2 (LRRK2), Parkin, DJ-1 PTEN-induced 1 (PINK1), many them coding for proteins found LBs and/or implicated mitochondrial function. However, mechanism(s) leading to development have not been identified, despite intensive research. Animal models help us obtain insights into mechanisms symptoms allowing investigate new therapeutic strategies and, addition, provide an indispensable tool basic As does arise spontaneously animals, characteristic specific functional changes be induced administration toxins or manipulations. This review will focus on comparison three types rodent animal used study different aspects PD: (a) using neurotoxins; (b) genetically modified mouse reproducing findings from linkage studies based ablation necessary survival neurons; (c) tissue-specific knockouts mice targeting neurons. advantages disadvantages these are discussed.

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