AI Article Synopsis
- - Alzheimer's disease (AD) is linked to negative changes in brain cells caused by issues like low oxygen (hypoxia), inflammation, and other disruptions that affect cell functions and lead to neuron damage.
- - Hypoxia is shown to contribute to several harmful factors in AD, such as oxidative stress, problems with energy production, and the buildup of toxic proteins, which all play a role in neurodegeneration.
- - The review explores how oxygen levels impact the development of AD and examines important regulatory proteins involved in the disease, offering insights into potential treatments.
Article Abstract
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.
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| http://dx.doi.org/10.1016/j.arr.2023.102022 | DOI Listing |
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