The Role of Hypoxia-Inducible Factor 1 in Mild Cognitive Impairment

被引:0
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作者
Osigbemhe Iyalomhe
Sabina Swierczek
Ngozi Enwerem
Yuanxiu Chen
Monica O. Adedeji
Joanne Allard
Oyonumo Ntekim
Sheree Johnson
Kakra Hughes
Philip Kurian
Thomas O. Obisesan
机构
[1] Howard University Hospital,Geriatrics Division, Department of Medicine
[2] University of Utah School of Medicine,Department of Hematology/BMT
[3] Howard University Hospital,Division of Endovascular Surgery
[4] Howard University,Human Genome Center
[5] Howard University Clinical Research Unit (GHUCCTS CTSA),undefined
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关键词
Mild cognitive impairment; Hypoxia-inducible factor 1; Glucose; Glycolysis; Alzheimer’s disease; Reactive oxygen species; Inflammation;
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摘要
Neuroinflammation and reactive oxygen species are thought to mediate the pathogenesis of Alzheimer’s disease (AD), suggesting that mild cognitive impairment (MCI), a prodromal stage of AD, may be driven by similar insults. Several studies document that hypoxia-inducible factor 1 (HIF-1) is neuroprotective in the setting of neuronal insults, since this transcription factor drives the expression of critical genes that diminish neuronal cell death. HIF-1 facilitates glycolysis and glucose metabolism, thus helping to generate reductive equivalents of NADH/NADPH that counter oxidative stress. HIF-1 also improves cerebral blood flow which opposes the toxicity of hypoxia. Increased HIF-1 activity and/or expression of HIF-1 target genes, such as those involved in glycolysis or vascular flow, may be an early adaptation to the oxidative stressors that characterize MCI pathology. The molecular events that constitute this early adaptation are likely neuroprotective, and might mitigate cognitive decline or the onset of full-blown AD. On the other hand, prolonged or overwhelming stressors can convert HIF-1 into an activator of cell death through agents such as Bnip3, an event that is more likely to occur in late MCI or advanced Alzheimer’s dementia.
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页码:969 / 977
页数:8
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