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Hyperoxygenation revitalizes Alzheimer’s disease pathology through the upregulation of neurotrophic factors

Title
Hyperoxygenation revitalizes Alzheimer’s disease pathology through the upregulation of neurotrophic factors
Authors
Choi J.Kwon H.-J.Lee J.-E.Lee Y.Seoh J.-Y.Han P.-L.
Ewha Authors
서주영한평림
SCOPUS Author ID
서주영scopus; 한평림scopus
Issue Date
2019
Journal Title
Aging Cell
ISSN
1474-9718JCR Link
Citation
Aging Cell vol. 18, no. 2
Keywords
AlzheimerBDNFcognitionhyperoxygenationMeCP2
Publisher
Blackwell Publishing Ltd
Indexed
SCOPUS WOS scopus
Document Type
Article
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by Aβ-induced pathology and progressive cognitive decline. The incidence of AD is growing globally, yet a prompt and effective remedy is not available. Aging is the greatest risk factor for AD. Brain aging proceeds with reduced vascularization, which can cause low oxygen (O 2 ) availability. Accordingly, the question may be raised whether O 2 availability in the brain affects AD pathology. We found that Tg-APP/PS1 mice treated with 100% O 2 at increased atmospheric pressure in a chamber exhibited markedly reduced Aβ accumulation and hippocampal neuritic atrophy, increased hippocampal neurogenesis, and profoundly improved the cognitive deficits on the multiple behavioral test paradigms. Hyperoxygenation treatment increased the expression of BDNF, NT3, and NT4/5 through the upregulation of MeCP2/p-CREB activity in HT22 cells in vitro and in the hippocampus of mice. In contrast, siRNA-mediated inhibition of MeCP2 or TrkB neurotrophin receptors in the hippocampal subregion, which suppresses neurotrophin expression and neurotrophin action, respectively, blocked the therapeutic effects of hyperoxygenation on the cognitive impairments of Tg-APP/PS1 mice. Our results highlight the importance of the O 2 -related mechanisms in AD pathology, which can be revitalized by hyperoxygenation treatment, and the therapeutic potential of hyperoxygenation for AD. © 2019 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
DOI
10.1111/acel.12888
Appears in Collections:
의과대학 > 의학과 > Journal papers
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