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  Indian J Med Microbiol
 

Figure 1: Schematic diagram describing effects of hypoxia and hypoxia mimetic agents on neurons in Alzheimer's disease (AD) process. Severe and/or chronic hypoxia can leads to amyloid beta (Aβ) peptide formation and aggregation, Ca2+ dyshomeostasis, reactive oxygen species (ROS) formation in neurons as well as neuroinflammation (Chen et al., 2018). While mild, moderate and/or intermittent hypoxia have been found to induce protective adaptations in the brain (Lall et al., 2019). Hypoxia inducible factor (HIF), a key mediator of oxygen homeostasis, generates numerous pleiotropic protective effects, but also participates in Aβ peptide formation and aggregation. Hypoxia mimetic agents, both iron chelators and HIF prolyl hydroxylase (PHD) inhibitors, can remove ROS and reduce neuroinflammation, in addition to activating HIF. Pharmacological stabilization of HIF can be neuroprotective and be explored as an adjunctive therapy for AD.

Figure 1: Schematic diagram describing effects of hypoxia and hypoxia mimetic agents on neurons in Alzheimer's disease (AD) process.
Severe and/or chronic hypoxia can leads to amyloid beta (Aβ) peptide formation and aggregation, Ca<sup>2+</sup> dyshomeostasis, reactive oxygen species (ROS) formation in neurons as well as neuroinflammation (Chen et al., 2018). While mild, moderate and/or intermittent hypoxia have been found to induce protective adaptations in the brain (Lall et al., 2019). Hypoxia inducible factor (HIF), a key mediator of oxygen homeostasis, generates numerous pleiotropic protective effects, but also participates in Aβ peptide formation and aggregation. Hypoxia mimetic agents, both iron chelators and HIF prolyl hydroxylase (PHD) inhibitors, can remove ROS and reduce neuroinflammation, in addition to activating HIF. Pharmacological stabilization of HIF can be neuroprotective and be explored as an adjunctive therapy for AD.