Psychological and cognitive impairment of long‐term migrators to high altitudes and the relationship to physiological and biochemical changes

Gao, Yixing; Li, P.; Jiang, Chunhua; Liu, C.; Chen, Y.; Chen, L.; Ruan, Huai Zhen; Gao, Yuqi

doi:10.1111/ene.12507

Cited by 39 publications

(30 citation statements)

References 25 publications

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“…Sustained exposure to hypoxia is well known to induce brain damage [25] and cognitive impairment [60], [61], [62], [63], [64]. Remarkably, the processes associated to cell death and cognitive impairment are beginning to be appreciated in hyperoxia too [65], [66].…”

Section: Discussionmentioning

confidence: 99%

Brain adaptation to hypoxia and hyperoxia in mice

et al. 2017

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AimsHyperoxic breathing might lead to redox imbalance and signaling changes that affect cerebral function. Paradoxically, hypoxic breathing is also believed to cause oxidative stress. Our aim is to dissect the cerebral tissue responses to altered O2 fractions in breathed air by assessing the redox imbalance and the recruitment of the hypoxia signaling pathways.ResultsMice were exposed to mild hypoxia (10%O2), normoxia (21%O2) or mild hyperoxia (30%O2) for 28 days, sacrificed and brain tissue excised and analyzed. Although one might expect linear responses to %O2, only few of the examined variables exhibited this pattern, including neuroprotective phospho- protein kinase B and the erythropoietin receptor. The major reactive oxygen species (ROS) source in brain, NADPH oxidase subunit 4 increased in hypoxia but not in hyperoxia, whereas neither affected nuclear factor (erythroid-derived 2)-like 2, a transcription factor that regulates the expression of antioxidant proteins. As a result of the delicate equilibrium between ROS generation and antioxidant defense, neuron apoptosis and cerebral tissue hydroperoxides increased in both 10%O2 and 30%O2, as compared with 21%O2. Remarkably, the expression level of hypoxia-inducible factor (HIF)−2α (but not HIF-1α) was higher in both 10%O2 and 30%O2 with respect to 21%O2InnovationComparing the in vivo effects driven by mild hypoxia with those driven by mild hyperoxia helps addressing whether clinically relevant situations of O2 excess and scarcity are toxic for the organism.ConclusionProlonged mild hyperoxia leads to persistent cerebral damage, comparable to that inferred by prolonged mild hypoxia. The underlying mechanism appears related to a model whereby the imbalance between ROS generation and anti-ROS defense is similar, but occurs at higher levels in hypoxia than in hyperoxia.

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Section: Discussionmentioning

confidence: 99%

Brain adaptation to hypoxia and hyperoxia in mice

et al. 2017

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“…Supplementary O 2 appears to be a logical aid which may offset the negative side effects of hypobaric hypoxia on cognitive function, although a distinct lack of literature exists on this topic. Interestingly, altitude induced reductions in endogenous O 2 saturation have not been significantly correlated with cognitive decrement, suggesting inter and intra individual variation regarding the cognition hypoxia nexus (Gao et al, 2014 ). Further research is required to determine if these ergogenic aids improve cognitive function at high altitude.…”

Section: Hypoxia and Cognitive Functionmentioning

confidence: 99%

The Impact of Different Environmental Conditions on Cognitive Function: A Focused Review

et al. 2016

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Cognitive function defines performance in objective tasks that require conscious mental effort. Extreme environments, namely heat, hypoxia, and cold can all alter human cognitive function due to a variety of psychological and/or biological processes. The aims of this Focused Review were to discuss; (1) the current state of knowledge on the effects of heat, hypoxic and cold stress on cognitive function, (2) the potential mechanisms underpinning these alterations, and (3) plausible interventions that may maintain cognitive function upon exposure to each of these environmental stressors. The available evidence suggests that the effects of heat, hypoxia, and cold stress on cognitive function are both task and severity dependent. Complex tasks are particularly vulnerable to extreme heat stress, whereas both simple and complex task performance appear to be vulnerable at even at moderate altitudes. Cold stress also appears to negatively impact both simple and complex task performance, however, the research in this area is sparse in comparison to heat and hypoxia. In summary, this focused review provides updated knowledge regarding the effects of extreme environmental stressors on cognitive function and their biological underpinnings. Tyrosine supplementation may help individuals maintain cognitive function in very hot, hypoxic, and/or cold conditions. However, more research is needed to clarify these and other postulated interventions.

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“…A wide range of evidences have shown hypobaric hypoxia at high altitude results in a myriad of neurophysiological and neurocognitive dysfunction including vision, memory, language, mood, learning, and processing speed [ 3 – 5 ]. Further studies found that long term stay at high altitude caused psychological and cognitive impairment in adults [ 6 , 7 ] while not in adolescents [ 8 ]. Moreover, neuropsychological deficits may be persistent even after coming back to sea level from high altitude regions [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Cognitive Changes during Prolonged Stay at High Altitude and Its Correlation with C-Reactive Protein

Xiong

Dai

et al. 2016

PLoS ONE

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Hypersensitive C-reaction protein (hsCRP) may be a risk factor for cognitive impairment resulting from Alzheimer’s disease (AD), stroke, and vascular dementia. This study explored the correlation of peripheral blood hsCRP level with cognitive decline due to high altitude exposure. The study was conducted on 100 male military participants who had never been to high altitude. Cerebral oxygen saturation monitoring, event related potentials (P300, N200) detection, and neurocognitive assessment was performed and total hsCRP, interleukin-6 (IL-6), and homocysteine was estimated at 500m altitude, 3650m altitude, 3day, 1, and 3 month post arriving at the base camp (4400m), and 1 month after coming back to the 500m altitude. High altitude increased brain oxygen saturation, prolonged P300 and N200 latencies, injured cognitive functions, and raised plasma hsCRP levels. But they all recovered in varying degrees at 1 and 3 month post arriving at the base camp (4400m). P300 latencies and hsCRP levels were strongly correlated to cognitive performances. These results suggested that cognitive deterioration occurred during the acute period of exposure to high altitude and may recover probably owning to acclimatization after extended stay at high altitude. Plasma hsCRP is inversely correlated to neurological cognition and it may be a potential biomarker for the prediction of high altitude induced cognitive dysfunction.

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Psychological and cognitive impairment of long‐term migrators to high altitudes and the relationship to physiological and biochemical changes

Abstract: Long-term living at high altitudes causes significant impairment of psychological and cognitive function. Cerebral hypoxic extent, sleep quality and biochemical dysfunction are major influencing factors.

Cited by 39 publications

References 25 publications

Brain adaptation to hypoxia and hyperoxia in mice

Brain adaptation to hypoxia and hyperoxia in mice

The Impact of Different Environmental Conditions on Cognitive Function: A Focused Review

Cognitive Changes during Prolonged Stay at High Altitude and Its Correlation with C-Reactive Protein

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