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Background: Missense mutations and multiplications of the alpha-synuclein gene cause autosomal dominant familial Parkinson's disease (PD). alpha-Synuclein protein is also a major component of Lewy bodies, the hallmark pathological inclusions of PD. Therefore, alpha-synuclein plays an important role in the pathogenesis of familial and sporadic PD. To model alpha-synuclein-linked disease in vivo, transgenic mouse models have been developed that express wild-type or mutant human alpha-synuclein from a variety of neuronal-selective heterologous promoter elements. These models exhibit a variety of behavioral and neuropathological features resembling some aspects of PD. However, an important deficiency of these models is the observed lack of robust or progressive nigrostriatal dopaminergic neuronal degeneration that is characteristic of PD.
Henning Paul-Julius Stahlberg, Amanda Jennifer Lewis, Marta Di Fabrizio, Domenic Burger, Carolin Böing
Hilal Lashuel, Johannes Burtscher, Melek Firat Altay, Somanath Jagannath
Olaf Blanke, Fosco Bernasconi, Jevita Potheegadoo