In vivo silencing of alpha-synuclein using naked siRNA

Jada Lewis(Jacksonville College), Heather L. Melrose(Mayo Clinic in Florida), David Bumcrot(Alnylam Pharmaceuticals (United States)), Andrew Hope(University of Surrey), Cynthia Zehr(Mayo Clinic in Florida), Sarah Lincoln(Mayo Clinic in Florida), Adam Braithwaite(Mayo Clinic in Florida), Zhen He(Mayo Clinic in Florida), Sina Ogholikhan(Mayo Clinic in Florida), Kelly M. Hinkle(Mayo Clinic in Florida), Caroline Kent(Mayo Clinic in Florida), Ivanka Toudjarska(Alnylam Pharmaceuticals (United States)), Klaus Charissé(Alnylam Pharmaceuticals (United States)), Ravi Braich(Alnylam Pharmaceuticals (United States)), Rajendra K. Pandey(Alnylam Pharmaceuticals (United States)), Michael G. Heckman(Mayo Clinic in Florida), Demetrius M. Maraganore(Mayo Clinic), Julia E. Crook(Mayo Clinic in Florida), Matthew J. Farrer(Mayo Clinic in Florida)
Molecular Neurodegeneration
January 1, 2008
Cited by 145Open Access
Full Text

Abstract

BACKGROUND: Overexpression of alpha-synuclein (SNCA) in families with multiplication mutations causes parkinsonism and subsequent dementia, characterized by diffuse Lewy Body disease post-mortem. Genetic variability in SNCA contributes to risk of idiopathic Parkinson's disease (PD), possibly as a result of overexpression. SNCA downregulation is therefore a valid therapeutic target for PD. RESULTS: We have identified human and murine-specific siRNA molecules which reduce SNCA in vitro. As a proof of concept, we demonstrate that direct infusion of chemically modified (naked), murine-specific siRNA into the hippocampus significantly reduces SNCA levels. Reduction of SNCA in the hippocampus and cortex persists for a minimum of 1 week post-infusion with recovery nearing control levels by 3 weeks post-infusion. CONCLUSION: We have developed naked gene-specific siRNAs that silence expression of SNCA in vivo. This approach may prove beneficial toward our understanding of the endogenous functional equilibrium of SNCA, its role in disease, and eventually as a therapeutic strategy for alpha-synucleinopathies resulting from SNCA overexpression.


Related Papers