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

Juli Choi, Hye Jin Kwon, Jung Eun Lee, Yunjin Lee, Ju Young Seoh, Pyung Lim Han

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


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.

Original languageEnglish
Article numbere12888
JournalAging Cell
Issue number2
StatePublished - Apr 2019

Bibliographical note

Funding Information:
This research was supported by a grant (2018R1A2B2001535) from the Ministry of Science, ICT and Future Planning, Republic of Korea.

Publisher Copyright:
© 2019 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.


  • Alzheimer
  • BDNF
  • MeCP2
  • cognition
  • hyperoxygenation


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