Abstract
The CST3 Thr25 allele of CST3, which encodes cystatin C, leads to reduced cystatin C secretion and conveys susceptibility to Alzheimer's disease. Here we show that overexpression of human cystatin C in brains of APP-transgenic mice reduces cerebral amyloid-beta deposition and that cystatin C binds amyloid-beta and inhibits its fibril formation. Our results suggest that cystatin C concentrations modulate cerebral amyloidosis risk and provide an opportunity for genetic risk assessment and therapeutic interventions.
Original language | English |
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Pages (from-to) | 1437-1439 |
Journal | Nature Genetics |
Volume | 39 |
Issue number | 12 |
DOIs | |
Publication status | Published - 2007 |
Subject classification (UKÄ)
- Pharmacology and Toxicology
- Medicinal Chemistry