Alzheimer’s Disease

Alzheimer’s Disease is progressive, neurodegenerative disease. It is most common in people ages 60-85, and the risk increases significantly as age increases. Memory impairment is typically the first symptom of Alzheimer’s, while problems with thinking, decision-making, simple task execution, and motor movements increase as the disease progresses. Patients also experience behavior changes and personality changes(1,2).  The symptoms of Alzheimer’s are thought to be caused by amyloid plaques and tau aggregates, which result in brain tissue inflammation, disrupted synapses, and nerve cell degeneration(3). This causes brain tissue degeneration, primarily in the hippocampus (responsible for memory) and the cortex (executive functioning)(4). While current drugs aim to treat the symptoms of Alzheimer’s, HBOT may be an effective treatment in that it directly affects Alzheimer’s disease pathology, with very few potential side effects(5). HBOT has been shown to decrease the formation, size, and number of amyloid plaques as well as reduce the formation of tau aggregates. Additionally, HBOT increases the level of anti-inflammatory cytokines while decreasing the level of inflammatory cytokines(6). Together, HBOT has been shown to improve the behavioral as well as biological changes that are caused by Alzheimer’s (6).

HBOT Research Shows Improvement to:

  • Improved cognition
  • Improved behavior
  • Decreased harmful disease pathology
  • Decreased brain tissue death
  • Decreased inflammation

Benefits of HBOT for Alzheimer’s Disease:

Prevents Further Cellular Damage

Preserves the integrity of blood vessel cells. This cellular protection helps improve blood flow to tissues and organs when damaged by conditions such as heart attack or stroke.

Reduces Inflammation & Swelling

Suppresses the cellular activity of the immune system which triggers swelling when an injury or damage to the body occurs.  While this reaction is meant to start healing and protect from injury it can result in secondary injury, pain, and prolonged recovery time.

Preserves, Repairs, & Enhances Cellular Functions

Boosts cellular metabolism, promotes rapid cell reproduction, and enhances collagen synthesis. Collagen is a protein in connective tissues like skin.

Maximizes Oxygen Transport

Allows for 100% saturation of hemoglobin molecules. Additional O2 molecules then dissolve directly into the plasma (the fluid component of blood) for transport.

Key Research on Hyperbaric Oxygen Treatment for Alzheimer’s Disease

Hyperbaric oxygen therapy for Alzheimer’s dementia with positron emission tomography imaging: a case report.

A 58-year-old female was diagnosed with Alzheimer’s dementia (AD) which was rapidly progressive in the 8 months prior to initiation of hyperbaric oxygen therapy (HBOT). Fluorodeoxyglucose (FDG) positron emission tomography (PET) brain imaging demonstrated global and typical metabolic deficits in AD (posterior temporal-parietal watershed and cingulate areas). An 8-week course of HBOT reversed the patient’s symptomatic decline. Repeat PET imaging demonstrated a corresponding 6.5-38% regional and global increase in brain metabolism, including increased metabolism in the typical AD diagnostic areas of the brain. Continued HBOT in conjunction with standard pharmacotherapy maintained the patient’s symptomatic level of function over an ensuing 22 months. This is the first reported case of simultaneous HBOT-induced symptomatic and FDG PET documented improvement of brain metabolism in AD and suggests an effect on global pathology in AD.

Hyperbaric oxygen therapy ameliorates pathophysiology of 3xTg-AD mouse model by attenuating neuroinflammation.

There is a real need for new interventions for Alzheimer’s disease (AD). Hyperbaric oxygen therapy (HBOT), the medical administration of 100% oxygen at conditions greater than 1 atmosphere absolute, has been used successfully to treat several neurological conditions, but its effects on AD pathology have never been thoroughly examined. Therefore, we exposed old triple-transgenic (3xTg) and non-transgenic mice to HBOT followed by behavioral, histological, and biochemical analyses. HBOT attenuated neuroinflammatory processes by reducing astrogliosis, microgliosis, and the secretion of proinflammatory cytokines (IL-1β and TNFα) and increasing expression of scavenger receptor A, arginase1, and antiinflammatory cytokines (IL-4 and IL-10). Moreover, HBOT reduced hypoxia, amyloid burden, and tau phosphorylation in 3xTg mice and ameliorated their behavioral deficits. Therefore, we suggest that HBOT has multifaceted effects that reduce AD pathologies, even in old mice. Given that HBOT is used in the clinic to treat various indications, including neurological conditions, these results suggest HBOT as a novel therapeutic intervention for AD.

Recent News on Hyberbaric Oxygen Treatment for Alzheimer’s Disease

Additional Research

Hyperbaric oxygen therapy for Alzheimer’s dementia with positron emission tomography imaging: a case report.

A 58-year-old female was diagnosed with Alzheimer’s dementia (AD) which was rapidly progressive in the 8 months prior to initiation of hyperbaric oxygen therapy (HBOT). Fluorodeoxyglucose (FDG) positron emission tomography (PET) brain imaging demonstrated global and typical metabolic deficits in AD (posterior temporal-parietal watershed and cingulate areas). An 8-week course of HBOT reversed the patient’s symptomatic decline. Repeat PET imaging demonstrated a corresponding 6.5-38% regional and global increase in brain metabolism, including increased metabolism in the typical AD diagnostic areas of the brain. Continued HBOT in conjunction with standard pharmacotherapy maintained the patient’s symptomatic level of function over an ensuing 22 months. This is the first reported case of simultaneous HBOT-induced symptomatic and FDG PET documented improvement of brain metabolism in AD and suggests an effect on global pathology in AD.

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The treatment of cognitive dysfunction in dementia: a multiple treatments meta-analysis.

No cure is currently available for dementia; however, various treatments and interventions have been reported to be effective. The factors influencing the efficacy of dementia treatment have not been comprehensively evaluated. This study evaluated the factors influencing treatment effects on cognitive dysfunction in dementia by comparing the results obtained from a meta-analysis based on meta-regression. The most effective intervention for dementia available is symptomatic treatment for vascular dementia. Antipsychotic treatment for dementia alleviates cognitive dysfunction less effectively than does symptomatic treatment. Alternative therapies are also effective at present. Further research on causes and very early diagnosis of Alzheimer disease is warranted.

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Hyperbaric Oxygen Therapy for Alzheimer’s Disease.

Recent studies indicate that hyperbaric oxygen therapy (HBOT), a well-established therapy for decompression illness, could be a potential therapy for Alzheimer’s disease (AD). However, due to oxygen toxicity i.e., increased oxidative stress implicated in HBOT, the risk and benefit of HBOT for AD patients need to be further assessed clinically.

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Hyperbaric oxygen therapy ameliorates pathophysiology of 3xTg-AD mouse model by attenuating neuroinflammation.

There is a real need for new interventions for Alzheimer’s disease (AD). Hyperbaric oxygen therapy (HBOT), the medical administration of 100% oxygen at conditions greater than 1 atmosphere absolute, has been used successfully to treat several neurological conditions, but its effects on AD pathology have never been thoroughly examined. Therefore, we exposed old triple-transgenic (3xTg) and non-transgenic mice to HBOT followed by behavioral, histological, and biochemical analyses. HBOT attenuated neuroinflammatory processes by reducing astrogliosis, microgliosis, and the secretion of proinflammatory cytokines (IL-1β and TNFα) and increasing expression of scavenger receptor A, arginase1, and antiinflammatory cytokines (IL-4 and IL-10). Moreover, HBOT reduced hypoxia, amyloid burden, and tau phosphorylation in 3xTg mice and ameliorated their behavioral deficits. Therefore, we suggest that HBOT has multifaceted effects that reduce AD pathologies, even in old mice. Given that HBOT is used in the clinic to treat various indications, including neurological conditions, these results suggest HBOT as a novel therapeutic intervention for AD.

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Hyperbaric Oxygen Pretreatment Improves Cognition and Reduces Hippocampal Damage Via p38 Mitogen-Activated Protein Kinase in a Rat Model.

To investigate the effects of hyperbaric oxygen (HBO) pretreatment on cognitive decline and neuronal damage in an Alzheimer’s disease (AD) rat model. Rats were divided into three groups: normal saline (NS), AD, and HBO+AD. In the AD group, amyloid β peptide (Aβ)₁₋₄₀ was injected into the hippocampal CA1 region of the brain. NS rats received NS injection. In the HBO+AD group, rats received 5 days of daily HBO therapy following Aβ₁₋₄₀ injection. Learning and memory capabilities were examined using the Morris water maze task. Neuronal damage and astrocyte activation were evaluated by hematoxylin-eosin staining and immunohistochemistry, respectively. Dendritic spine density was determined by Golgi-Cox staining. Tumor necrosis factor-α, interleukin-1β, and interleukin-10 production was assessed by enzyme-linked immunosorbent assay. Neuron apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling. Protein expression was examined by western blotting. HBO pretreatment improves cognition and reduces hippocampal damage via p38 MAPK in AD rats.

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Hyperbaric Oxygen and Ginkgo Biloba Extract Ameliorate Cognitive and Memory Impairment via Nuclear Factor Kappa-B Pathway in Rat Model of Alzheimer’s Disease.

Hyperbaric oxygen (HBO) and Ginkgo biloba extract (e.g., EGB 761) were shown to ameliorate cognitive and memory impairment in Alzheimer’s disease (AD). However, the exact mechanism remains elusive. The aim of the present study was to investigate the possible mechanisms of HBO and EGB 761 via the function of nuclear factor kappa-B (NF-κB) pathway. AD rats were induced by injecting β-amyloid 25-35 into the hippocampus. All animals were divided into six groups: Normal, sham, AD model, HBO (2 atmosphere absolute; 60 min/d), EGB 761 (20 mg·kg-1·d-1 ), and HBO/EGB 761 groups. Morris water maze tests were used to assess cognitive, and memory capacities of rats; TdT-mediated dUTP Nick-End Labeling staining and Western blotting were used to analyze apoptosis and NF-κB pathway-related proteins in hippocampus tissues. orris water maze tests revealed that EGB 761 and HBO significantly improved the cognitive and memory ability of AD rats. In addition, the protective effect of combinational therapy (HBO/EGB 761) was superior to either HBO or EGB 761 alone. In line, reduced apoptosis with NF-κB pathway activation was observed in hippocampus neurons treated by HBO and EGB 761. ur results suggested that HBO and EGB 761 improve cognitive and memory capacity in a rat model of AD. The protective effects are associated with the reduced apoptosis with NF-κB pathway activation in hippocampus neurons.

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The protective effect of hyperbaric oxygen and Ginkgo biloba extract on Aβ25-35-induced oxidative stress and neuronal apoptosis in rats.

Alzheimer’s disease (AD) is characterized by accumulation and deposition of Aβ peptides in human brains. The present study aimed to determine the protective effect of HBO and EGB761 on Aβ25-35 peptides induced cognitive impairment and neuronal toxicity in rats. Characteristics of AD were induced in rats by the administration of Aβ25-35 in hippocampus. Rats were treated with HBO (2ATA 60min/day), EGB761 (20mg/kg/day), and the combination of HBO+EGB761 (20mg/kg/day+2ATA). The Morris water maze was used to detect the protective effects of HBO and EGB761 against cognitive impairment. The activities of SOD and GSH, the apoptosis-related genes and proteins and the apoptosis rate of hippocampus were detected. Compared to the model group, EGB761 and HBO treatments synergistically improved the escape latency. Furthermore, the activities of SOD and GSH in rat hippocampal tissue were found to have increased with a concomitant reduction in MDA levels, Bax expression, cytochrome c release, and the activity of caspase-9/3.

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Hyperbaric oxygen and Ginkgo Biloba extract inhibit Aβ25-35-induced toxicity and oxidative stress in vivo: a potential role in Alzheimer’s disease.

Alzheimer’s disease is characterized by the accumulation and deposition of Aβ peptides in human brains and Aβ induced free radical-mediated damage is one of the hypotheses. In the present study, we explored the protective effects of hyperbaric oxygen (HBO) and Ginkgo Biloba extract (EGB761) on Aβ25-35-induced brain toxicity. Our results demonstrated that EGB761, HBO, and the combination HBO and EGB761, could significantly improve the cognitive function in AD rats’ model, especially the combination group. What’s more, the activities of superoxide dismutase (SOD) in rat hippocampal tissue were obviously enhanced followed by evidently reduced malondialdehyde (MDA) levels in the same treatment groups mentioned earlier. There were no differences of nitric oxide (NO) productions in the group of EGB761, HBO, and HBO and EGB761, but they were all lower than that of model group. These findings suggest that both HBO and EGB761 may relieve cell toxicity and oxidative stress in AD and thus play a potential protective role in AD. Furthermore, the combination could have better effects compared with single one.

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Hyperbaric oxygen therapy for vascular dementia.

Hyperbaric oxygen therapy (HBOT) has been used to treat a variety of conditions and has shown possible efficacy for treating vascular dementia (VaD) in experimental and preliminary clinical studies. To assess the efficacy and safety of HBOT for VaD, used alone or as an adjuvant treatment. We searched ALOIS: the Cochrane Dementia and Cognitive Improvement Group Specialised Register on 20 December 2011 using the terms: hyperbaric OR oxygen OR HBO OR HBOT. ALOIS contains records of clinical trials identified from monthly searches of a number of major healthcare databases, numerous trial registries and grey literature sources. We also searched the Chinese Biomedical Database (CBM), the Chinese National Knowledge Infrastructure (CNKI) and the VIP Chinese Science and Technique Journals Database on 10 November 2011 using the terms ‘gaoyayang’, ‘xueguanxingchidai’ and ‘chidai’. In addition, we contacted authors of included studies for additional information.

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References
  1. 2019. https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/symptoms-causes/syc-20350447.
  2. “Stages of Alzheimer’s.” Alzheimer’s Disease and Dementia. Accessed August 7, 2019. https://alz.org/alzheimers-dementia/stages.
  3. Selkoe, Dennis J, and John Hardy. “The Amyloid Hypothesis of Alzheimer’s Disease at 25 Years.” EMBO Molecular Medicine 8, no. 6 (June 2016): 595–608. https://doi.org/10.15252/emmm.201606210.
  4. “The Progression of Alzheimer’s Disease.” BrightFocus Foundation, July 2, 2015. https://www.brightfocus.org/alzheimers-disease/infographic/progression-alzheimers-disease.
  5. “How Is Alzheimer’s Disease Treated?” National Institute on Aging. Accessed August 8, 2019. https://www.nia.nih.gov/health/how-alzheimers-disease-treated.
  6. Shapira, Ronit, Beka Solomon, Shai Efrati, Dan Frenkel, and Uri Ashery. “Hyperbaric Oxygen Therapy Ameliorates Pathophysiology of 3xTg-AD Mouse Model by Attenuating Neuroinflammation.” Neurobiology of Aging 62 (2018): 105–19. https://doi.org/10.1016/j.neurobiolaging.2017.10.007.

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