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  Exploiting moderate hypoxia to benefit patients with brain disease: Molecular mechanisms and translational research in progress

Ehrenreich, H., Gassmann, M., Poustka, L., Burtscher, M., Hammermann, P., Sirén, A.-L., et al. (2023). Exploiting moderate hypoxia to benefit patients with brain disease: Molecular mechanisms and translational research in progress. Neuroprotection, 1(1), 9-19. doi:10.1002/nep3.15.

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Item Permalink: https://hdl.handle.net/21.11116/0000-000C-A864-6 Version Permalink: https://hdl.handle.net/21.11116/0000-000D-C044-D
Genre: Journal Article

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Neuroprotection - 2023 - Ehrenreich.pdf (Postprint), 909KB
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 Creators:
Ehrenreich, Hannelore1, Author           
Gassmann, Max, Author
Poustka, Luise, Author
Burtscher, Martin, Author
Hammermann, Peter, Author
Sirén, Anna-Leena, Author
Nave, Klaus-Armin2, Author           
Miskowiak, Kamilla, Author
Affiliations:
1Research Group of Clinical Neuroscience, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society, ou_3350303              
2Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society, ou_3350301              

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 Abstract: Hypoxia is increasingly recognized as an important physiological driving force. A specific transcriptional program, induced by a decrease in oxygen (O2) availability, for example, inspiratory hypoxia at high altitude, allows cells to adapt to lower O2 and limited energy metabolism. This transcriptional program is partly controlled by and partly independent of hypoxia-inducible factors. Remarkably, this same transcriptional program is stimulated in the brain by extensive motor-cognitive exercise, leading to a relative decrease in O2 supply, compared to the acutely augmented O2 requirement. We have coined the term “functional hypoxia” for this important demand-responsive, relative reduction in O2 availability. Functional hypoxia seems to be critical for enduring adaptation to higher physiological challenge that includes substantial “brain hardware upgrade,” underlying advanced performance. Hypoxia-induced erythropoietin expression in the brain likely plays a decisive role in these processes, which can be imitated by recombinant human erythropoietin treatment. This article review presents hints of how inspiratory O2 manipulations can potentially contribute to enhanced brain function. It thereby provides the ground for exploiting moderate inspiratory plus functional hypoxia to treat individuals with brain disease. Finally, it sketches a planned multistep pilot study in healthy volunteers and first patients, about to start, aiming at improved performance upon motor-cognitive training under inspiratory hypoxia.

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Language(s): eng - English
 Dates: 2023-02-212023-09
 Publication Status: Issued
 Pages: -
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 Rev. Type: Peer
 Identifiers: DOI: 10.1002/nep3.15
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Project name : This work has been supported by the Max Planck Society, the Max Planck Förderstiftung, the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation), via DFG-Center for Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB), and DFG-TRR 274/1 2020—408885537. M. G. acknowledges the Swiss National Science Foundation for the support of this project. In 2022, H. E. received a European Research Council (ERC) Advanced Grant under the European Union's Horizon Europe research and innovation programme (BREPOCI; grant agreement no. 101054369) and K. M. an ERC Consolidator Grant (ALTIBRAIN). Moreover, H. E. holds at present a grant from Roche Pharma AG, Grenzach-Wyhlen, enabling the continuation and extension of the GRAS (Göttingen Research Association for Schizophrenia) Data Collection in direction of Multiple Sclerosis (GRAMS, Göttingen Research Association for MS). The GRAMS project has also received support through a donation from Merck Serono GmbH.
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Project name : BREPOCI
Grant ID : 101054369
Funding program : Horizon 2020 (H2020)
Funding organization : European Commission (EC)
Project name : ALTIBRAIN
Grant ID : 101043416
Funding program : Horizon Europe (HE)
Funding organization : European Commission (EC)

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Title: Neuroprotection
Source Genre: Journal
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Pages: - Volume / Issue: 1 (1) Sequence Number: - Start / End Page: 9 - 19 Identifier: ISSN: 2770-730X