Display Settings:

Format

Send to:

Choose Destination
Exp Neurol. 2008 Jan;209(1):22-7. Epub 2007 Aug 23.

In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?

Author information

  • Department of Neurology and Neurobiology, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA. mchesselet@mednet.ucla.edu

Abstract

Mutations in alpha-synuclein were the first genetic defect linked to Parkinson's disease (PD). The relevance of alpha-synuclein to sporadic PD is strongly supported by the presence of alpha-synuclein aggregates in neurons of patients. This has prompted the development of numerous animal models based on alpha-synuclein overexpression, primarily through genetic methods in mice and viral transduction in rats. In mice, different promoters and transgenes lead to a wide variety of phenotypes accompanied by non-existent, late onset, or non-specific neurodegeneration. Rapid neurodegeneration, in contrast, is observed after viral transduction but is limited to the targeted region and does not mimic the broad pathology observed in the disease. Overall, each model reproduces a subset of features of PD and can be used to identify therapeutic targets and test disease-modifying therapies. The predictive value of all models of the disease, however, remains speculative in the absence of effective neuroprotective treatments for PD in humans.

PMID:
17949715
[PubMed - indexed for MEDLINE]
PMCID:
PMC2262051
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk