Journal
NATURE GENETICS
Volume 39, Issue 12, Pages 1440-1442Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ng.2007.29
Keywords
`
Categories
Funding
- NIA NIH HHS [AG017617] Funding Source: Medline
- NINDS NIH HHS [NS42029] Funding Source: Medline
Ask authors/readers for more resources
Using transgenic mice expressing human cystatin C ( encoded by CST3), we show that cystatin C binds soluble amyloid-beta peptide and inhibits cerebral amyloid deposition in amyloid-beta precursor protein ( APP) transgenic mice. Cystatin C expression twice that of the endogenous mouse cystatin C was sufficient to substantially diminish amyloid-beta deposition. Thus, cystatin C has a protective role in Alzheimer's disease pathogenesis, and modulation of cystatin C concentrations may have therapeutic implications for the disease.
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