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Hyperbaric Oxygen Therapy

Brain Scan

Neurological Disorders

A traumatic brain injury, or TBI, is an injury to the brain that affects how it works. TBIs vary in severity, and can be mild or severe, open or closed. Brain trauma disrupts the flow of oxygen to injured part(s) of the brain, often leading to cell damage and improper functioning.

Post concussion syndrome (PCS) occurs in 25 % of mild traumatic brain injuries, and it can cause symptoms such as headache, dizziness, neuropsychiatric symptoms, and cognitive impairments.

HBOT provides the body with an abundance of oxygen, which allows the oxygen to pass to brain tissue that has had the blood supply interrupted. HBOT had proved to increase tissue oxygenation, decrease swelling and inflammation, reduce the chance of cell death, reduce intracranial pressure, and assist with the growth of new tissue and new blood vessels.

Dementia/Alzheimer’s Disease result from abnormalities in the brain, caused by buildups between nerve cells and/or inside cells. which disrupt normal communication in the nerve cells. HBOT reduces oxygen starvation and inflammation in the brain. It also reduces the buildups between/in the nerve cells, allowing for reduction of symptoms and improvement in behavior.

Studies on Neurological Disorders and HBOT

Hyperbaric oxygen ameliorates cognitive impairment in patients with Alzheimer's disease and amnestic mild cognitive impairment.

Chen J, Zhang F, Zhao L, Cheng C, Zhong R, Dong C, Le W. Hyperbaric oxygen ameliorates cognitive impairment in patients with Alzheimer's disease and amnestic mild cognitive impairment. Alzheimers Dement (N Y). 2020 Jun 14;6(1):e12030. doi: 10.1002/trc2.12030. PMID: 32548235; PMCID: PMC7293997.

Introduction

It has been reported that environmental factors such as hypoxia could contribute to the pathogenesis of Alzheimer's disease (AD). Therapeutics like hyperbaric oxygen treatment, which improves tissue oxygen supply and ameliorates hypoxic conditions in the brain, may be an alternative therapy for AD and amnestic mild cognitive impairment (aMCI). The present work aims to investigate the potential therapeutic effect of hyperbaric oxygen treatment for AD and aMCI.

Results

In self‐comparison study, one course of hyperbaric oxygen treatment significantly improved the cognitive function assessed by MMSE and MoCA in AD patients after 1‐month follow‐up; such treatment also significantly improved MMSE score at 3‐month follow‐up and MoCA score at 1‐ and 3‐month follow‐up in aMCI patients. The ADL scale was significantly improved in AD patients after 1‐ and 3‐month follow‐up. Compared to the control AD patients, the MMSE and MoCA in hyperbaric oxygen treated AD patients were significantly improved after 1‐month follow‐up. Hyperbaric oxygen treatment also ameliorated the reduced brain glucose metabolism in some of the AD and aMCI patients.

Conclusion

Based on previous studies and our recent findings, we propose that hyperbaric oxygen treatment may be a promising alternative therapy for AD and aMCI.

The neuroprotective effects of oxygen therapy in Alzheimer's disease: a narrative review

Yang C, Yang Q, Xiang Y, Zeng XR, Xiao J, Le WD. The neuroprotective effects of oxygen therapy in Alzheimer's disease: a narrative review. Neural Regen Res. 2023 Jan;18(1):57-63. doi: 10.4103/1673-5374.343897. PMID: 35799509; PMCID: PMC9241400.

Abstract

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.

Hypoxia and HBOT in Alzheimer's

Hyperbaric oxygen therapy alleviates vascular dysfunction and amyloid burden in an Alzheimer’s disease mouse model and in elderly patients

Shapira R, Gdalyahu A, Gottfried I, Sasson E, Hadanny A, Efrati S, Blinder P, Ashery U. Hyperbaric oxygen therapy alleviates vascular dysfunction and amyloid burden in an Alzheimer’s disease mouse model and in elderly patients. Aging (Albany NY). 2021 Sep 9; 13:20935-20961 . https://doi.org/10.18632/aging.203485

Abstract

Vascular dysfunction is entwined with aging and in the pathogenesis of Alzheimer’s disease (AD) and contributes to reduced cerebral blood flow (CBF) and consequently, hypoxia. Hyperbaric oxygen therapy (HBOT) is in clinical use for a wide range of medical conditions. In the current study, we exposed 5XFAD mice, a well-studied AD model that presents impaired cognitive abilities, to HBOT and then investigated the therapeutical effects using two-photon live animal imaging, behavioral tasks, and biochemical and histological analysis. HBOT increased arteriolar luminal diameter and elevated CBF, thus contributing to reduced hypoxia. Furthermore, HBOT reduced amyloid burden by reducing the volume of pre-existing plaques and attenuating the formation of new ones. This was associated with changes in amyloid precursor protein processing, elevated degradation and clearance of Aß protein and improved behavior of 5XFAD mice. Hence, our findings are consistent with the effects of HBOT being mediated partially through a persistent structural change in blood vessels that reduces brain hypoxia. Motivated by these findings, we exposed elderly patients with significant memory loss at baseline to HBOT and observed an increase in CBF and improvement in cognitive performances. This study demonstrates HBOT efficacy in hypoxia-related neurological conditions, particularly in AD and aging.

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