Genetic causes of Parkinson’s disease: extending the pathway

  • O. Riess
  • R. Krüger
  • H. Hochstrasser
  • A. S. Soehn
  • S. Nuber
  • T. Franck
  • D. Berg
Conference paper

DOI: 10.1007/978-3-211-45295-0_29

Part of the Journal of Neural Transmission. Supplementa book series (NEURALTRANS, volume 70)
Cite this paper as:
Riess O. et al. (2006) Genetic causes of Parkinson’s disease: extending the pathway. In: Riederer P., Reichmann H., Youdim M.B.H., Gerlach M. (eds) Parkinson’s Disease and Related Disorders. Journal of Neural Transmission. Supplementa, vol 70. Springer, Vienna

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.

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Copyright information

© Springer-Verlag 2006

Authors and Affiliations

  • O. Riess
    • 1
  • R. Krüger
    • 2
  • H. Hochstrasser
    • 1
  • A. S. Soehn
    • 1
  • S. Nuber
    • 1
  • T. Franck
    • 1
  • D. Berg
    • 1
    • 2
  1. 1.Department of Medical GeneticsUniversity of TuebingenTuebingenGermany
  2. 2.Hertie Institute, Department of NeurologyUniversity of TuebingenGermany

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