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Alzheimer's disease (AD) is characterized by an adverse cellular environment and pathological alterations in distinct brain regions. The development is triggered or facilitated by a condition such as hypoxia or ischemia, or inflammation and is associated with disruptions of fundamental cellular functions, including metabolic and ion homeostasis. Increasing evidence suggests that hypoxia may affect many pathological aspects of AD, including oxidative stress, mitochondrial dysfunction, ER stress, amyloidogenic processing of APP, and Aβ accumulation, which may collectively result in neurodegeneration. Further investigation into the relationship between hypoxia and AD may provide an avenue for the effective preservation and pharmacological treatment of this neurodegenerative disease. This review summarizes the effects of normoxia and hypoxia on AD pathogenesis and discusses the underlying mechanisms. Regulation of HIF-1α and the role of its key players, including P53, VEGF, and GLUT1, are also discussed. • Hypoxia is one detrimental aspect of ischemia and stroke and also leads to AD development. • Hypoxia leads to Mitophagy and ER stress, which ultimately increase the chances of AD. • HIF-1 is known to maintained oxygen homeostasis, cellular energy metabolism, and tumor expression. • HIF-1α has been elucidated the representative transcription factor of hypoxic condition. • Signalling pathways plays a vital role in the induction of endogenous anti-oxidant enzymes against oxidative stress. [ABSTRACT FROM AUTHOR]