Hyperbaric Oxygen Therapy Alleviates Carbon Monoxide Poisoning–Induced Delayed Memory Impairment by Preserving Brain-Derived Neurotrophic Factor–Dependent Hippocampal Neurogenesis

Liu, Wen‐Chung; Yang, Shyh‐Chyun; Wu, Chun Ying; Chen, Lee Wei; Chan, Julie Y.H.

doi:10.1097/ccm.0000000000001299

Cited by 21 publications

(12 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…They found no improvement in the patients' states, and they reported a worse outcome in learning tests. (Liu et al, 2016) 10 rats after acute carbon monoxide poisoning 7 sessions for 60 min at 2.5 ATA Eight arm maze test Improvement in memory (Bi et al, 2017) 80 rats after CO intoxication; divided in two groups HBOT and HBOT + N-butylphthalide…”

Section: Hbot and Cognitive Dysfunctions After Co Intoxicationmentioning

confidence: 99%

Impact of Hyperbaric Oxygen Therapy on Cognitive Functions: a Systematic Review

et al. 2021

View full text Add to dashboard Cite

Hyperbaric oxygen therapy (HBOT) is a modality of treatment in which patients inhale 100% oxygen inside a hyperbaric chamber pressurised to greater than 1 atmosphere. The aim of this review is to discuss neuropsychological findings in various neurological disorders treated with HBOT and to open new perspectives for therapeutic improvement. A literature search was conducted in the MEDLINE (via PubMed) database from the inception up 10 May 2020. Eligibility criteria included original articles published in English. Case studies were excluded. Full-text articles were obtained from the selected studies and were reviewed on the following inclusion criteria (1) performed cognitive processes assessment (2) performed HBOT with described protocol. Two neuropsychologists independently reviewed titles, abstracts, full texts and extracted data. The initial search retrieved 1024 articles, and a total of 42 studies were finally included after applying inclusion and exclusion criteria. The search yielded controversial results with regard to the efficiency of HBOT in various neurological conditions with cognitive disturbance outcome. To the best of our knowledge this is the first state-of-the art, systematic review in the field. More objective and precise neuropsychological assessment methods are needed to exact evaluation of the efficacy of HBOT for neuropsychological deficits. Future studies should widen the assessment of HBOT effects on different cognitive domains because most of the existing studies have focussed on a single process. Finally, there is a need for further longitudinal studies.

show abstract

Section: Hbot and Cognitive Dysfunctions After Co Intoxicationmentioning

confidence: 99%

Impact of Hyperbaric Oxygen Therapy on Cognitive Functions: a Systematic Review

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Hyperbaric oxygen (HBO) therapy is the clinical application of pure oxygen at a higher pressure (usually 2–3 times atmospheric pressure) in a chamber to treat ischemia- or hypoxia-associated diseases, such as coronary heart disease, cerebral infarction and carbon monoxide poisoning ( 31 – 34 ). HBO therapy has been widely agreed by major hyperbaric craft groups, such as the Undersea and Hyperbaric Medical Society or the U.S. Food and Drug Administration ( 35 ).…”

Section: Introductionmentioning

confidence: 99%

Hyperbaric oxygen protects against myocardial ischemia‑reperfusion injury through inhibiting mitochondria dysfunction and autophagy

Chen

Nong

et al. 2020

Mol Med Rep

View full text Add to dashboard Cite

our previous study demonstrated that hyperbaric oxygen (HBo) improves heart function predominantly through reducing oxygen stress, modulating energy metabolism and inhibiting cell apoptosis. The present study aimed to investigate the protective effects of HBo on mitochondrial function and autophagy using rats with a ligated left anterior descending artery. The cardioprotective effects of HBo were mainly evaluated using ELISA, fluorescent probes, transmission electron microscopy and reverse transcription-quantitative Pcr (rT-qPcr). HBo pretreatment for 14 days (once a day) using a 0.25 MPa chamber improved mitochondrial morphology and decreased the number of autophagic vesicles, as observed using a transmission electron microscope. HBO pretreatment significantly increased the levels of aTP, adP, energy charge and the opening of the mitochondrial permeability transition pore, but decreased the levels of aMP, cytochrome c and reactive oxygen species. Moreover, HBo pretreatment significantly increased the gene or protein expression levels of eiF4e-binding protein 1, mammalian target of rapamycin (mTor), mitochondrial dna, nadH dehydrogenase subunit 1, mitofusin 1 and mitofusin 2, whereas it decreased the gene or protein expression levels of autophagy-related 5 (atg5), cytochrome c, dynamin-related protein 1 and p53, as determined using rT-qPcr or immunohistochemistry. in conclusion, HBo treatment was observed to protect cardiomyocytes during myocardial ischemia-reperfusion injury (Miri) by preventing mitochondrial dysfunction and inhibiting autophagy. Thus, these results provide novel evidence to support the use of HBo as a potential agent for the mitigation of Miri.

show abstract

“…Hyperbaric Oxygen (HBO) treatment significantly reduces the half-life of carboxyhemoglobin [33]. Several evidences have showed the benefits from hyperbaric-oxygen therapy on memory [34,35], delayed neuropsychological sequelae [36,37] and lowing mortality [38], but evidences supporting the use of hyperbaric oxygen in patients with CO poisoning come from randomized trials with significant limitations and observational studies. So identifying patients who will benefit from HBO treatment remains uncertain.…”

Section: Discussionmentioning

confidence: 99%

Increased long-term risk of dementia in patients with carbon monoxide poisoning: A systematic review and meta-analysis of cohort studies

Zhang¹,

Wei²,

Chien³

et al. 2019

Preprint

View full text Add to dashboard Cite

Background It has long been known that carbon monoxide poisoning is associated with cognitive dysfunction but whether carbon monoxide poisoning is a risk factor for incident dementia is still inconclusive. Our objective was to assess whether carbon monoxide poisoning increases the incidence of dementia. Methods We conducted a systematic review and meta analysis of cohort studies examining the risk of dementia in people with carbon monoxide poisoning. We searched the Cochrane Library, PubMed, and EMBASE from inception to 31 March 2019. Two authors independently selected studies, assessed the quality of included studies, and extracted data. Any disagreement was resolved by discussion with a third author. Only cohort study with an enough follow-up period was included, which reported the association between carbon monoxide poisoning and incidence of dementia in adults. Exposure was carbon monoxide poisoning; primary outcomes were incident all-cause dementia, Alzheimer’s disease and cognitive disorder. Summary estimates were obtained using random effects meta-analysis. Results Thirty-three full texts were initially searched, but only three studies met our inclusion criteria, and they were comprised of 134,563 participants who were initially free of dementia. The follow-up period ranged from 9 to 12 years. We found that CO poisoning increased the risk of dementia incidence [adjusted hazard ratio 2.61, 95% confidence interval (CI) 1.56 to 4.36, P = 0.0003]. Subgroup analysis showed that the increased dementia risk was significant in males but not in females, and the highest risk was in young age group, followed by in middle age group, but not in the old one (P > 0.05). Conclusions This meta-analysis suggests that overall the evidence from prospective cohort studies supported a link between carbon monoxide exposure and an increased dementia risk, although all the included studies were limited to Taiwanese population. Further studies that provide data for different ethnic groups are needed to clarify whether a subgroup of patients with carbon monoxide exposure has an elevated risk of dementia.

show abstract

Hyperbaric Oxygen Therapy Alleviates Carbon Monoxide Poisoning–Induced Delayed Memory Impairment by Preserving Brain-Derived Neurotrophic Factor–Dependent Hippocampal Neurogenesis

Abstract: The early hyperbaric oxygen treatment may alleviate delayed memory impairment after acute carbon monoxide poisoning by preserving adult neurogenesis via an increase in hippocampal brain-derived neurotrophic factor content.

Cited by 21 publications

References 66 publications

Impact of Hyperbaric Oxygen Therapy on Cognitive Functions: a Systematic Review

Impact of Hyperbaric Oxygen Therapy on Cognitive Functions: a Systematic Review

Hyperbaric oxygen protects against myocardial ischemia‑reperfusion injury through inhibiting mitochondria dysfunction and autophagy

Increased long-term risk of dementia in patients with carbon monoxide poisoning: A systematic review and meta-analysis of cohort studies

Contact Info

Product

Resources

About