Role of Hypoxiа Inducible (HIF) in Аlzheimer’s Disease

Abstract

Pathological assurances in Alzheimer's (AD), β amyloid (Aβ)-42 peptide & phosphorylate tau protein has been reported. As per an explanation for hypometabolism, there has been a sharp decline in the supply of oxygen & glucose to the human brain by ageing or oxygen deprivation. Hippocampus, entorhinal cortex, & adult neurogenesis-supplementary neocortical areas, such as parietal cortex, temporal cortex, & frontal cortex, are vulnerable to hypometabolism in the brain. In Alzheimer persons, brain sections through hypometabolism may cause over-expression of the APP and reduce the clearance of Amyloid β peptide. Amyloid β & lack of oxygen may induce swelling and, consequently, neuronal cell destroy. HIF-Iα has a leading part in cell adaptation by persuading the production of another proteins, including vascular endothelial growth hormone(VEGH) , erythropoietin(EPO) , and inducible (NO) nitric oxide synthase, among the transcription factors involved in the countervailing cycle. The HIF-1α stage, retaining it, was effective in alleviating nerve destruction during oxygen deprivation & delaying occurrance of AD by the stimulation of 4-hydroxylase propyl. In the preservation of nerve volumes of HIF-1α in agents such as Fe+(iron) chelator, heavy metals such as cobalt(CO), nickel(ni), etc.