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.
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.
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.
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.
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.