Parkinson's disease: One biochemical pathway to fit all genes?

Rejko Krüger, Olaf Eberhardt, Olaf Riess, Jörg B. Schulz*, Olaf Riess

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

61 Citations (Scopus)


Although originally discounted, hereditary factors have emerged as the focus of research in Parkinson's disease (PD). Genetic studies have identified mutations in α-synuclein and ubiquitin C-terminal hydrolase as rare causes of autosomal dominant PD and mutations in parkin as a cause of autosomal recessive PD. Functional characterization of the identified disease genes implicates the ubiquitin-mediated protein degradation pathway in these hereditary forms of PD and also in the more common sporadic forms of PD. Subsequent identification of further loci in familial PD and diverse genetic factors modulating the risk for sporadic PD point to substantial genetic heterogeneity in the disease. Thus, new candidate genes are expected to encode proteins either involved in ubiquitin-mediated protein degradation or sequestrated in intracytoplasmic protein aggregations. Future identification of disease genes is required to confirm this hypothesis, thereby unifying the clinical and genetic heterogeneity of PD, including the common sporadic form of the disease, by one biochemical pathway.

Original languageEnglish
Pages (from-to)236-240
Number of pages5
JournalTrends in Molecular Medicine
Issue number5
Publication statusPublished - 2002
Externally publishedYes


Dive into the research topics of 'Parkinson's disease: One biochemical pathway to fit all genes?'. Together they form a unique fingerprint.

Cite this