About this Research Topic
Over the last few years, new knowledge has enabled us to develop a better understanding of the brain metabolism and its energy requirements. This new knowledge calls for new metabolic/energy driven interventions that will facilitate the healing process in different types of brain injuries. One of the promising therapeutic interventions developed is the use of Hyperbaric oxygen therapy (HBOT). There is growing evidence from basic science, as well as from pre-clinical and clinical trials that HBOT can induce neuroplasticity in different types of brain injuries, even years after the acute insult. The neurotherapeutic effects have been demonstrated in stroke, traumatic brain injury, central sensitization syndrome, and age-related cognitive decline including vascular dementia and Alzheimer’s disease.
HBOT includes the inhalation of 100% oxygen at pressures exceeding one atmosphere absolute (1 ATA) to enhance the amount of oxygen dissolved in the body’s tissues. During HBOT, the arterial O2 tension typically exceeds 2000 mmHg, and levels of 200–400 mmHg occur in tissues. Historically, HBOT has been applied worldwide mostly for chronic non healing wounds. In recent years, there is growing evidence related to the regenerative effects of HBOT. It is now know that the combined action of both hyperoxia and hyperbaric pressure, leads to significant improvement in tissue oxygenation while targeting both oxygen and pressure sensitive genes, resulting in improved mitochondrial metabolism with anti-apoptotic and anti-inflammatory effects. Moreover, these genes induce stem cell proliferation, augmented circulating levels of endothelial progenitor cells (EPCs) and angiogenesis factors, which induce angiogenesis and improved blood flow in the ischemic area. In recent years there is growing evidence that HBOT can also induce brain regeneration and neuroplasticity.
The intermittent increase of oxygen concentration induces many of the mediators and cellular mechanism that are usually induced during hypoxia but without the hazardous hypoxia - termed hyperoxic-hypoxic paradoxes. The intermittent hyperoxic exposure during HBOT can affect HIF-1 levels, matrix metalloproteinases (MMP) activity, VEGF, induce stem cell proliferation, augment circulating levels of endothelial progenitor cells (EPCs) and angiogenesis factors, as well as induce angiogenesis and improved blood flow in the ischemic area. In addition to stimulation of EPCs, HBOT can decrease the inflammatory response in endothelial cells mediated by TNF-alpha, and thus, promote vascular recovery. Both animal and human studies have demonstrated the beneficial effects of HBOT on mitochondrial function.
This Research Topic will be dedicated to scientific publications that can shed additional light on the neurotherapeutic mechanisms induced by HBOT on the brain, the types of injuries and patients who might benefit from the treatment, and the effectiveness of the different protocols that can be used. The Topic will include basic science, pre-clinical, clinical, and translational Original Research, as well as Reviews that will summarize the data available today.
Topic Editor Shai Efrati is a co-founder and shareholder of AVIV Scientific Ltd. Topic Editor Amir Hadanny is a shareholder of AVIV Scientific Ltd. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
HBOT includes the inhalation of 100% oxygen at pressures exceeding one atmosphere absolute (1 ATA) to enhance the amount of oxygen dissolved in the body’s tissues. During HBOT, the arterial O2 tension typically exceeds 2000 mmHg, and levels of 200–400 mmHg occur in tissues. Historically, HBOT has been applied worldwide mostly for chronic non healing wounds. In recent years, there is growing evidence related to the regenerative effects of HBOT. It is now know that the combined action of both hyperoxia and hyperbaric pressure, leads to significant improvement in tissue oxygenation while targeting both oxygen and pressure sensitive genes, resulting in improved mitochondrial metabolism with anti-apoptotic and anti-inflammatory effects. Moreover, these genes induce stem cell proliferation, augmented circulating levels of endothelial progenitor cells (EPCs) and angiogenesis factors, which induce angiogenesis and improved blood flow in the ischemic area. In recent years there is growing evidence that HBOT can also induce brain regeneration and neuroplasticity.
The intermittent increase of oxygen concentration induces many of the mediators and cellular mechanism that are usually induced during hypoxia but without the hazardous hypoxia - termed hyperoxic-hypoxic paradoxes. The intermittent hyperoxic exposure during HBOT can affect HIF-1 levels, matrix metalloproteinases (MMP) activity, VEGF, induce stem cell proliferation, augment circulating levels of endothelial progenitor cells (EPCs) and angiogenesis factors, as well as induce angiogenesis and improved blood flow in the ischemic area. In addition to stimulation of EPCs, HBOT can decrease the inflammatory response in endothelial cells mediated by TNF-alpha, and thus, promote vascular recovery. Both animal and human studies have demonstrated the beneficial effects of HBOT on mitochondrial function.
This Research Topic will be dedicated to scientific publications that can shed additional light on the neurotherapeutic mechanisms induced by HBOT on the brain, the types of injuries and patients who might benefit from the treatment, and the effectiveness of the different protocols that can be used. The Topic will include basic science, pre-clinical, clinical, and translational Original Research, as well as Reviews that will summarize the data available today.
Topic Editor Shai Efrati is a co-founder and shareholder of AVIV Scientific Ltd. Topic Editor Amir Hadanny is a shareholder of AVIV Scientific Ltd. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
Keywords: Oxygen, Brain, Hyperbaric, Hypoxia, Hyperoxia, HIF, Mitochondria
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
