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Researchers in Japan have found that a kind of longevity gene could prevent vascular dementia induced by cerebral infarction, which is likely to help develop new therapies to the disease.
In an experiment made by a research group comprised of researchers from National Cerebral and Cardiovascular Center, Nagoya University and Kyoto University, Sirtuin type 1 (SIRT1)- overexpressing mice driven by a prion promoter and their wild-type littermates were subjected to bilateral common carotid artery stenosis using external microcoils.
SIRT1 is a protein deacetylase that has been reported to suppress neurodegenerative and cardiovascular diseases in model organisms.
As a resulut, cerebral hypoperfusion induced by bilateral common carotid artery stenosis caused memory impairment and histological changes in wild-type littermates, said the researchers in the latest online edition of Stroke, a peer- reviewed medical journal published monthly by the American Heart Association.
However, these phenotypes were rescued in SIRT1-overexpressing mice, where cerebral blood flow maintained even poststenosis, they said.
"Brain endothelial nitric oxide synthase was acetylated after cerebral hypoperfusion in wild-type littermates but remained unacetylated in SIRT1-overexpressing mice," they said. "Moreover, treatment with SIRT1 inhibitors and endothelial nitric oxide synthase inhibitors abolished the vasculoprotective effects of SIRT1."
The results indicate that neurovascular endothelial SIRT1 potentiation upregulates the nitric oxide system and counters cerebral hypoperfusion injury. "This novel cerebral blood flow preserving mechanism offers potential molecular targets for future therapeutic intervention," they said.
In 2012, there were about 4.62 million people in Japan suffering from senile dementia, among which, vascular dementia accounted for about 30 percent.
