TY - JOUR
T1 - The neuroprotective effects of oxygen therapy in Alzheimer's disease
T2 - a narrative review
AU - Yang, Cui
AU - Yang, Qiu
AU - Xiang, Yang
AU - Zeng, Xian Rong
AU - Xiao, Jun
AU - Le, Wei Dong
N1 - Funding Information:
This work was supported by the Key Research and Development Support Project of Chengdu Science and Technology Bureau, No. 2019-YF05-00655-SN (to WDL) and the Key Project of the Medical Science Department, University of Electronic Science and Technology of China, No. ZYGX2020ZB035 (to WDL).
Publisher Copyright:
© 2023 Wolters Kluwer Medknow Publications. All rights reserved.
PY - 2023/1
Y1 - 2023/1
N2 - Alzheimer's disease (AD) is a degenerative neurological disease that primarily affects the elderly. Drug therapy is the main strategy for AD treatment, but current treatments suffer from poor efficacy and a number of side effects. Non-drug therapy is attracting more attention and may be a better strategy for treatment of AD. Hypoxia is one of the important factors that contribute to the pathogenesis of AD. Multiple cellular processes synergistically promote hypoxia, including aging, hypertension, diabetes, hypoxia/obstructive sleep apnea, obesity, and traumatic brain injury. Increasing evidence has shown that hypoxia may affect multiple pathological aspects of AD, such as amyloid-beta metabolism, tau phosphorylation, autophagy, neuroinflammation, oxidative stress, endoplasmic reticulum stress, and mitochondrial and synaptic dysfunction. Treatments targeting hypoxia may delay or mitigate the progression of AD. Numerous studies have shown that oxygen therapy could improve the risk factors and clinical symptoms of AD. Increasing evidence also suggests that oxygen therapy may improve many pathological aspects of AD including amyloid-beta metabolism, tau phosphorylation, neuroinflammation, neuronal apoptosis, oxidative stress, neurotrophic factors, mitochondrial function, cerebral blood volume, and protein synthesis. In this review, we summarized the effects of oxygen therapy on AD pathogenesis and the mechanisms underlying these alterations. We expect that this review can benefit future clinical applications and therapy strategies on oxygen therapy for AD.
AB - Alzheimer's disease (AD) is a degenerative neurological disease that primarily affects the elderly. Drug therapy is the main strategy for AD treatment, but current treatments suffer from poor efficacy and a number of side effects. Non-drug therapy is attracting more attention and may be a better strategy for treatment of AD. Hypoxia is one of the important factors that contribute to the pathogenesis of AD. Multiple cellular processes synergistically promote hypoxia, including aging, hypertension, diabetes, hypoxia/obstructive sleep apnea, obesity, and traumatic brain injury. Increasing evidence has shown that hypoxia may affect multiple pathological aspects of AD, such as amyloid-beta metabolism, tau phosphorylation, autophagy, neuroinflammation, oxidative stress, endoplasmic reticulum stress, and mitochondrial and synaptic dysfunction. Treatments targeting hypoxia may delay or mitigate the progression of AD. Numerous studies have shown that oxygen therapy could improve the risk factors and clinical symptoms of AD. Increasing evidence also suggests that oxygen therapy may improve many pathological aspects of AD including amyloid-beta metabolism, tau phosphorylation, neuroinflammation, neuronal apoptosis, oxidative stress, neurotrophic factors, mitochondrial function, cerebral blood volume, and protein synthesis. In this review, we summarized the effects of oxygen therapy on AD pathogenesis and the mechanisms underlying these alterations. We expect that this review can benefit future clinical applications and therapy strategies on oxygen therapy for AD.
KW - Alzheimer's disease
KW - amyloid-beta metabolism
KW - clinical symptoms
KW - hypoxia
KW - neuroinflammation
KW - neuronal apoptosis
KW - oxygen therapy
KW - pathogenesis
KW - risk factor
KW - tau phosphorylation
UR - http://www.scopus.com/inward/record.url?scp=85143064960&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85143064960&partnerID=8YFLogxK
U2 - 10.4103/1673-5374.343897
DO - 10.4103/1673-5374.343897
M3 - Review article
AN - SCOPUS:85143064960
VL - 18
SP - 57
EP - 63
JO - Neural Regeneration Research
JF - Neural Regeneration Research
SN - 1673-5374
IS - 1
ER -