Therapeutic strategies for Parkinson's disease based on data derived from genetic research

Olaf Riess*, Daniela Berg, Rejko Krüger, Jörg B. Schulz

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

6 Citations (Scopus)


Following the identification of mutations in α-synuclein as the cause of some rare forms of familial Parkinson's disease (PD), genetic research has uncovered numerous gene loci of PD. Meanwhile, several neurodegenerative diseases have been shown to accumulate α-synuclein in neuronal and glial cells summarizing this group of diseases as synucleinopathies. All currently known gene defects causing PD alter the ubiquitin-proteasomal pathway of protein degradation. Identification of these disease mutations allows studying the functional consequences which lead to cellular dysfunction and cell death in cell culture and transgenic animal models, to identify therapeutic targets and to test potential protective strategies in these models.

Original languageEnglish
Pages (from-to)I3-I10
JournalJournal of Neurology, Supplement
Issue number1
Publication statusPublished - Feb 2003
Externally publishedYes


  • Iron
  • Oxidative stress
  • Parkinson's disease
  • Protein aggregation
  • α-synuclein


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