Journal
JOURNAL OF NEUROSCIENCE RESEARCH
Volume 87, Issue 6, Pages 1283-1295Publisher
WILEY
DOI: 10.1002/jnr.21949
Keywords
Parkinson's disease; leucine-rich repeat kinase 2 (LRRK2); neurodegeneration; signal transduction
Categories
Funding
- National Institutes of Health [R21AG028797]
- National Parkinson Foundation (Mega Research Grants program)
- National Science Foundation (Advance Institutional Transformation Grant) [SBE-0245054]
- Johnson & Johnson Corporate Office of Science and Technology (Focused Funding program)
- NATIONAL INSTITUTE ON AGING [R21AG028797] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Parkinson's disease (PD) is the most common neurodegenerative movement disorder, with a prevalence of more than 1% after the age of 65 years. Mutations in the gene encoding leucine-rich repeat kinase-2 (LRRK2) have recently been linked to autosomal dominant, late-onset PD that is clinically indistinguishable from typical, idiopathic disease. LRRK2 is a multidomain protein containing several protein interaction motifs as well as dual enzymatic domains of GTPase and protein kinase activities. Disease-associated mutations are found throughout the multidomain structure of the protein. LRRK2, however, is unique among the PD-causing genes, because a missense mutation, G2019S, is a frequent determinant of not only familial but also sporadic PD. Thus, LRRK2 has emerged as a promising therapeutic target for combating PD. In this Mini-Review, we look at the current state of knowledge regarding the domain structure, amino acid substitutions, and potential functional roles of LRRK2. (C) 2008 Wiley-Liss, Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available