, Volume 21, Issue 7, pp 699–702 | Cite as

Der Beitrag der Gene beim Parkinson-Syndrom

  • Katja Lohmann
Wissenschaft Genetische Medizin


In the past two decades, a number of genetic causes of Parkinson disease (PD) have been elucidated. This includes both monogenic forms in which a single mutation is sufficient to cause PD and genetic risk factors. The latter only increase the susceptibility for PD and additional, likely environmental hits are necessary to develop the disease. PD genes such as LRRK2 and Parkin often encode proteins involved in mitochondrial function, protein degradation, or response to oxidative stress.


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  1. [1]
    Seeman P, Tinazzi M (2013) Loss of dopamine neuron terminals in antipsychotic-treated schizophrenia; relation to tardive dyskinesia. Prog Neuropsychopharmacol Biol Psychiatry 44:178–183CrossRefPubMedGoogle Scholar
  2. [2]
    Dickson DW (2012) Parkinson’s disease and parkinsonism: neuropathology. Cold Spring Harb Perspect Med 2, doi: 10.1101/cshperspect.a009258Google Scholar
  3. [3]
    Bach JP, Ziegler U, Deuschl G et al. (2011) Projected numbers of people with movement disorders in the years 2030 and 2050. Mov Disord 26:2286–2290CrossRefPubMedGoogle Scholar
  4. [4]
    Polymeropoulos MH, Lavedan C, Leroy E et al. (1997) Mutation in the alpha-synuclein gene identified in families with Parkinson’s disease. Science 276:2045–2047CrossRefPubMedGoogle Scholar
  5. [5]
    Trinh J, Farrer M (2013) Advances in the genetics of Parkinson disease. Nat Rev Neurol 9:445–454CrossRefPubMedGoogle Scholar
  6. [6]
    Verstraeten A, Theuns J, Van Broeckhoven C (2015) Progress in unraveling the genetic etiology of Parkinson disease in a genomic era. Trends Genet 31:140–149CrossRefPubMedGoogle Scholar
  7. [7]
    Lohmann K, Klein C (2014) Next generation sequencing and the future of genetic diagnosis. Neurotherapeutics 11:699–707PubMedCentralCrossRefPubMedGoogle Scholar
  8. [8]
    Nalls MA, Pankratz N, Lill CM et al. (2014) Large-scale meta-analysis of genome-wide association data identifies six new risk loci for Parkinson’s disease. Nat Genet 46:989–993PubMedCentralCrossRefPubMedGoogle Scholar
  9. [9]
    Haelterman NA, Yoon WH, Sandoval H et al. (2014) A mitocentric view of Parkinson’s disease. Annu Rev Neurosci 37:137–159CrossRefPubMedGoogle Scholar
  10. [10]
    Rakovic A, Grünewald A, Kottwitz J et al. (2011) Mutations in PINK1 and Parkin impair ubiquitination of Mitofusins in human fibroblasts. PLoS One 6:e16746CrossRefGoogle Scholar
  11. [11]
    Zavodszky E, Seaman MN, Moreau K et al. (2014) Mutation in VPS35 associated with Parkinson’s disease impairs WASH complex association and inhibits autophagy. Nat Commun 5:3828PubMedCentralCrossRefPubMedGoogle Scholar
  12. [12]
    Langston JW, Ballard P, Tetrud JW et al. (1983) Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis. Science 219:979–980CrossRefPubMedGoogle Scholar
  13. [13]
    Marras C, Lohmann K, Lang A et al. (2012) Fixing the broken system of genetic locus symbols: Parkinson disease and dystonia as examples. Neurology 78:1016–1024PubMedCentralCrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  1. 1.Institut für NeurogenetikUniversität zu LübeckLübeckDeutschland

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