TY - JOUR
T1 - Pathological impacts of chronic hypoxia on alzheimer's disease
AU - Zhang, Feng
AU - Niu, Long
AU - Li, Song
AU - Le, Weidong
N1 - Funding Information:
*E-mail: [email protected]. Tel/Fax: +86-411-8813-5850. ORCID Weidong Le: 0000-0001-7459-2705 Author Contributions W.L. conceived the structure of the review. F.Z., L.N., and S.L. performed literature searches and wrote the manuscript. F.Z., L.N., S.L., and W.L. revised the manuscript. Funding This work was supported in part by funding from the National Natural Sciences Foundation of China (NSFC 81430021 and 81771521). Notes The authors declare no competing financial interest.
Publisher Copyright:
© 2018 American Chemical Society.
PY - 2019/2/20
Y1 - 2019/2/20
N2 - Chronic hypoxia is considered as one of the important environmental factors contributing to the pathogenesis of Alzheimer's disease (AD). Many chronic hypoxia-causing comorbidities, such as obstructive sleep apnea syndrome (OSAS) and chronic obstructive pulmonary disease (COPD), have been reported to be closely associated with AD. Increasing evidence has documented that chronic hypoxia may affect many pathological aspects of AD including amyloid β (Aβ) metabolism, tau phosphorylation, autophagy, neuroinflammation, oxidative stress, endoplasmic reticulum (ER) stress, and mitochondrial and synaptic dysfunction, which may collectively result in neurodegeneration in the brain. In this Review, we briefly summarize the effects of chronic hypoxia on AD pathogenesis and discuss the underlying mechanisms. Since chronic hypoxia is common in the elderly and may contribute to the pathogenesis of AD, prospective prevention and treatment targeting hypoxia may be helpful to delay or alleviate AD.
AB - Chronic hypoxia is considered as one of the important environmental factors contributing to the pathogenesis of Alzheimer's disease (AD). Many chronic hypoxia-causing comorbidities, such as obstructive sleep apnea syndrome (OSAS) and chronic obstructive pulmonary disease (COPD), have been reported to be closely associated with AD. Increasing evidence has documented that chronic hypoxia may affect many pathological aspects of AD including amyloid β (Aβ) metabolism, tau phosphorylation, autophagy, neuroinflammation, oxidative stress, endoplasmic reticulum (ER) stress, and mitochondrial and synaptic dysfunction, which may collectively result in neurodegeneration in the brain. In this Review, we briefly summarize the effects of chronic hypoxia on AD pathogenesis and discuss the underlying mechanisms. Since chronic hypoxia is common in the elderly and may contribute to the pathogenesis of AD, prospective prevention and treatment targeting hypoxia may be helpful to delay or alleviate AD.
KW - Alzheimer's disease
KW - Chronic hypoxia
KW - amyloid β
KW - autophagy
KW - neuroinflammation
KW - tau
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U2 - 10.1021/acschemneuro.8b00442
DO - 10.1021/acschemneuro.8b00442
M3 - Review article
C2 - 30412668
AN - SCOPUS:85057529926
SN - 1948-7193
VL - 10
SP - 902
EP - 909
JO - ACS Chemical Neuroscience
JF - ACS Chemical Neuroscience
IS - 2
ER -