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Parkinson’s Disease and Related Disorders

Volume 70 of the series Journal of Neural Transmission. Supplementa pp 181-189

Genetic causes of Parkinson’s disease: extending the pathway

  • O. RiessAffiliated withDepartment of Medical Genetics, University of Tuebingen
  • , R. KrügerAffiliated withHertie Institute, Department of Neurology, University of Tuebingen
  • , H. HochstrasserAffiliated withDepartment of Medical Genetics, University of Tuebingen
  • , A. S. SoehnAffiliated withDepartment of Medical Genetics, University of Tuebingen
  • , S. NuberAffiliated withDepartment of Medical Genetics, University of Tuebingen
  • , T. FranckAffiliated withDepartment of Medical Genetics, University of Tuebingen
  • , D. BergAffiliated withDepartment of Medical Genetics, University of TuebingenHertie Institute, Department of Neurology, University of Tuebingen

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Summary

The functional characterization of identified disease genes in monogenic forms of Parkinson’s disease (PD) allows first insights into molecular pathways leading to neurodegeneration and dysfunction of the nigrostriatal system. There is increasing evidence that disturbance of the ubiquitin proteasome pathway is one important feature of this process underscoring the relevance of protein misfolding and accumulation in the neurodegenerative process of PD. Other genes are involved in mitochondrial homeostasis and still others link newly identified signalling pathways to the established paradigm of oxidative stress in PD. Additional factors are posttranslational modifications of key proteins such as phosphorylation. Also, molecular data support the role of altered iron metabolism in PD. Here we describe known genes and novel genetic susceptibility factors and define their role in neurodegeneration.