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Alzheimer Disease
Regulation of glucose by HIF-1 protects neurons from amyloid beta peptide
September 1st, 2003
The regulation of glucose metabolism by HIF-1 mediates a neuroprotective response to amyloid beta peptide. According to recent research from the United States, "It is frequently argued that both amyloid beta (A-beta) and oxidative stress are involved in the pathogenesis of Alzheimer's disease (AD). We show here that clonal nerve cell lines and primary cortical neurons that are resistant to A-beta toxicity have an enhanced flux of glucose through both the glycolytic pathway and the hexose monophosphate shunt." "AD brain also has increased enzymatic activities in both pathways relative to age-matched controls," reported Thomas Soucek and colleagues at...
Source: Health & Medicine Week (2003-09-01)
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