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The same study Kathy posted came over Medscaper too....

Cerebral Hypoxia Implicated in Pathogenesis of Alzheimer's Disease

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NEW YORK (Reuters Health) Nov 20 - Cerebral hypoperfusion and consequent hypoxia may facilitate the pathogenesis of Alzheimer's disease, new research suggests, by increasing the expression of a certain cleavage enzyme.

While a number of histologic features for Alzheimer's disease have been described, the underlying mechanisms responsible for most sporadic cases of the disease are unclear. Previous reports linking a history of stroke and vascular risk factors with the neurodegenerative disease suggest that cerebral hypoperfusion with resultant hypoxia may play a role in the pathogenesis.

In an earlier study, Dr. Weihong Song, from the University of British Columbia in Vancouver, Canada, and colleagues had shown that upregulation of the gene for beta-site amyloid-beta precursor protein cleavage enzyme 1 (BACE1) seemed to facilitate the development of Alzheimer's disease in patients with Down's syndrome.

In the current study, reported in the November 20th Early Edition of the Proceedings of the National Academy of Sciences, the researchers show that the BACE1 gene has a promoter region that is responsive to hypoxia.

In vitro and in vivo testing showed that hypoxia caused increased expression of the gene, resulting in increased amyloid-beta protein production. In mice, hypoxia-related amyloid-beta protein deposition was associated with memory deficits.

"Taken together, our results clearly demonstrate that hypoxia can facilitate Alzheimer's disease pathogenesis and provide a molecular mechanism linking vascular factors to Alzheimer's disease. Our study suggests that interventions to improve cerebral perfusion may benefit Alzheimer's disease patients," the authors conclude.

Proc Natl Acad Sci USA 2006

Carol in IL

Mom to seven including , 6 with TOF, AVcanal, GERD, LS, Asthma, subglottal stenosis, chronic constipation ( cured now ) and DS.

My problem is not how I look. It's how you see me.

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