IntroductionTranscranial direct current stimulation (tDCS) has been proposed as a potential tool for enhancing the benefits of cognitive training, but its added value for working memory in healthy adults remains unclear. This systematic review and robust variance estimation meta-analysis examined whether active tDCS combined with cognitive training improves post-training working memory performance compared with sham tDCS combined with the same training, and whether the effect varies by outcome type, assessment time point, and training characteristics.MethodsPubMed, Scopus, and Web of Science were searched from database inception to January 2026. Eligible studies were randomized controlled trials involving healthy adults, comparing active tDCS plus structured cognitive training with sham tDCS plus otherwise identical training, and reporting at least one post-training working memory outcome. Multiple correlated effect sizes within studies were synthesized using robust variance estimation. Outcomes were classified as trained-task outcomes or untrained working-memory outcomes, and both immediate post-test and follow-up assessments were included.ResultsA total of 23 studies contributing 135 effect sizes were included. Active tDCS combined with cognitive training produced a small but statistically significant improvement in post-training working memory performance, Hedges’ g = 0.191, 95% CI [0.062, 0.320], p = 0.006. Effects were significant for trained-task outcomes, whereas effects on untrained working-memory outcomes were smaller and not statistically significant; however, the direct difference between the two outcome categories was not significant. Immediate post-test effects were significant, whereas follow-up effects remained positive and similar in magnitude but lay at the conventional alpha threshold, with no significant difference between time points. Stimulation timing, age group, and training type did not significantly moderate the effect. Sensitivity analyses confirmed the stability of the overall estimate, and no clear evidence of small-study effects was detected.DiscussionThese findings suggest that tDCS may provide a small adjunctive benefit when combined with cognitive training in healthy adults, with the most consistent benefits observed for trained-task performance and more limited evidence for transfer to untrained working-memory outcomes.

PURPOSE:This meta-analysis aims to comprehensively evaluate the impact of high-altitude hypoxia on multidimensional cognitive functions, considering moderating variables such as altitude, exposure time, cognitive domain, and experimental design. METHODS:A three-level meta-analysis was conducted on 59 studies (1966-2024) comprising 739 effect sizes. Studies were screened and coded according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Cognitive tasks were categorized into seven domains: executive control, working memory, long-term memory, perceptual ability, psychomotor skill, attention, and others. Hedges' g was used as the effect size measure, and multilevel modeling was applied to account for dependent effect sizes. FINDINGS:High-altitude hypoxia significantly impaired overall cognitive function (g = -0.424, p < 0.001). Long-term memory and perceptual functions were most affected, followed by executive control, attention, and psychomotor skills; working memory was least impacted. Cognitive impairment was significant at altitudes above 2500 m. Acute (< 3 days) and chronic (> 30 days) exposure significantly affected cognition, while intermediate exposures (3-30 days) did not. Subgroup analyses revealed varying sensitivity across cognitive domains to altitude and exposure duration. CONCLUSION:High-altitude hypoxia adversely affects cognitive function, with severity varying by cognitive domain, altitude, and exposure duration. These findings highlight the need for tailored interventions and further research into acclimatization and de-acclimatization processes.

Acute hypobaric hypoxic exposure, defined as rapid ascent to high altitude with brief sojourn, triggers profound physiological adaptations while increasing risks of acute mountain sickness (e.g., gastrointestinal distress, pulmonary/cerebral edema). Beyond these somatic manifestations, cognitive deficits frequently emerge under hypoxic stress, yet the neural substrates mediating these impairments remain poorly mapped. To systematically characterize hypoxia-induced brain activation patterns, we conducted whole-brain mapping of neuronal activity changes in mice exposed to acute hypobaric hypoxia versus normoxic controls using c-Fos immunofluorescence, a robust marker of neuronal activation. Our functional analysis focused on key brain regions governing: cardiorespiratory homeostasis, attention, memory, emotional processing, motivation and reward. Quantitative c-Fos mapping revealed increased neural activity in several brainstem nuclei and repressed neural activity in higher-order forebrain after exposure to 24 h-6000 m hypobaric hypoxia. These datas establish the first brain-wide map of hypoxia-responsive neural networks, providing mechanistic insights into physiological adaptation and cognitive vulnerability after acute hypobaric hypoxic exposure.

Acute mountain sickness (AMS) is a major health issue for lowlanders when they ascend rapidly to altitudes above 2500 m. Thyroid hormones are essential for adaptive responses to the hypoxic environment of high altitude. However, there is limited evidence regarding the association between thyroid function and the prevalence of AMS. This study included 70 healthy euthyroid Chinese lowlanders who ascended from Beijing (44 m above sea level) to Lhasa (3650 m above sea level) by aircraft (flight time, approximately 5 h). The dataset was divided into a training set (80%) and a validation set (20%) for the development and validation of a prediction model. Thyroid hormones, demographic data and blood biochemical data were measured in the week before the ascent. The subjects in the training set were divided into an AMS group and a non‐AMS group based on the 2018 Lake Louise Acute Mountain Sickness Scale score. Thyroid hormones and thyroid hormone sensitivity indices were compared between the groups. Multivariable logistic regression analysis revealed that a higher baseline total triiodothyronine (TT3) level (odds ratio (OR) 2.474, 95% confidence interval (CI) 1.083–5.653) and a higher free triiodothyronine/free thyroxine (FT3/FT4) ratio (OR 3.427; 95% CI 1.266–9.280) were independent risk factors for development of AMS. The receiver‐operating characteristic and calibration curves showed that the model had good predictive ability and consistency in both the training and validation sets. In China, euthyroid lowlanders with a higher TT3 level or FT3/FT4 ratio are more susceptible to AMS after exposure to high altitudes.

Tick-borne encephalitis virus (TBEV), a zoonotic pathogen, can cause severe neurological complications and fatal outcomes in humans. Early diagnosis of TBEV infection is crucial for clinical practice. Although serological assays are frequently employed for detection, the lack of antibodies in the early stages of infection and the cross-reactivity of antibodies limit their efficacy. Conventional molecular diagnostic methods such as RT-qPCR can achieve early and accurate identification but require specialized instrumentation and professionals, hindering their application in resource-limited areas. Our study developed a rapid and visual TBEV molecular detection method by combining RT-recombinase-aided amplification, the CRISPR/Cas13a system, and lateral flow dipsticks. The diagnostic sensitivity of this method is 50 CFU/ml, with no cross-reactivity with a variety of viruses. The detection can be carried out within 1 h at a temperature between 37 and 42 °C, and the results can be visually determined without the need for complex instruments and professionals. Subsequently, this assay was used to analyze clinical samples from 15 patients suspected of TBEV infection and 10 healthy volunteers, and its sensitivity and specificity reached 100 %, which was consistent with the results of RT-qPCR. These results indicate that this new method can be a promising point-of-care test for the diagnosis of tick-borne encephalitis.

Postpartum depression (PPD) is a significant contributor to maternal morbidity and mortality. The Sigma-1 (σ-1) receptor has received increasing attention in recent years because of its ability to link different signaling systems and exert its function in the brain through chaperone actions, especially in neuropsychiatric disorders. YL-0919, a novel σ-1 receptor agonist developed by our institute, has shown antidepressive and anxiolytic effects in a variety of animal models, but effects on PPD have not been revealed. In the present study, excitatory/inhibitory signaling in the hippocampus was reflected by GABA and glutamate and their associated excitatory-inhibitory receptor proteins, the HPA axis hormones in the hippocampus were assessed by ELISA. Finally, immunofluorescence for markers of newborn neuron were undertaken in the dentate gyri, along with dendritic spine staining and dendritic arborization tracing. YL-0919 rapidly improves anxiety and depressive-like behavior in PPD-like mice within one week, along with normalizing the excitation/inhibition signaling as well as the HPA axis activity. YL-0919 rescued the decrease in hippocampal dendritic complexity and spine density induced by estrogen withdrawal. The study results suggest that YL-0919 elicits a therapeutic effect on PPD-like mice; therefore, the σ-1 receptor may be a novel promising target for PPD treatment in the future.

The present study assessed the behavior of morphine-addicted rats using behavioral video coding technology, to evaluate effective methods for identifying morphine addiction. Rats were divided into a control group (n=15) and a morphine addiction group (n=15). The morphine addiction model was established with a 14-day increasing dose scheme, confirmed using a conditional place preference (CPP) experiment. After successful modeling, the rats' behavior was recorded for 12 h, then coded and analyzed using Observer XT behavior analysis software. Compared with the control group, morphine-addicted rats showed increased heat pain tolerance time (P=0.039) and spent more time in the white box during the CPP experiment (P<0.001). Video coding analysis revealed significant behavioral changes in morphine-addicted rats compared to controls. In addition to being lighter, morphine-addicted rats showed decreased water intake, reduced licking of forelimbs and hind limbs, and altered sleeping posture (sleeping curled up) during the day (all P<0.05). In conclusion, chronic morphine administration in rats leads to distinctive behavioral changes, including decreased licking frequency, reduced water intake and altered sleep posture. Video coding analysis, as a safe and non-invasive method, may provide a convenient and efficient approach for studying morphine addiction in rats.

This study explores the role and mechanism of Annexin-A1 Tripeptide (ANXA1sp) in mitigating neuronal damage and promoting functional recovery in a mouse model of traumatic brain injury (TBI). Our goal is to identify ANXA1sp as a potential therapeutic drug candidate for TBI treatment. Adult male C57BL/6J mice were subjected to controlled cortical impact (CCI) to simulate TBI, supplemented by an in vitro model of glutamate-induced TBI in HT22 cells. We assessed neurological deficits using the Modified Neurological Severity Score (mNSS), tested sensorimotor functions with beam balance and rotarod tests, and evaluated cognitive performance via the Morris water maze. Neuronal damage was quantified using Nissl and TUNEL staining, while microglial activation and inflammatory responses were measured through immunostaining, quantitative PCR (qPCR), Western blotting, and ELISA. Additionally, we evaluated cell viability in response to glutamate toxicity using the Cell Counting Kit-8 (CCK-8) assay and lactate dehydrogenase (LDH) release. Intraperitoneal administration of ANXA1sp significantly enhanced neurological outcomes, markedly reducing sensorimotor and cognitive impairments caused by TBI. This treatment resulted in a significant reduction in lesion volume and decreased neuronal cell death in the ipsilateral cortex. Moreover, ANXA1sp effectively diminished microglial activation around the brain lesion and decreased the levels of pro-inflammatory markers such as IL-6, IL-1β, TNF-α, and TGF-β in the cortex, indicating a significant reduction in neuroinflammation post-TBI. ANXA1sp also offered protection against neuronal cell death induced by glutamate toxicity, primarily by inhibiting the nuclear translocation of ANXA1, highlighting its potential as a neuroprotective strategy in TBI management. Administration of ANXA1sp significantly reduced neuroinflammation and neuronal cell death, primarily by blocking the nuclear translocation of ANXA1. This treatment substantially reduced brain damage and improved neurological functional recovery after TBI. Consequently, ANXA1sp stands out as a promising neuroprotective agent for TBI therapy.

Hypoxic environments like those present at high altitudes may negatively affect brain function. Varying levels of hypoxia, whether acute or chronic, are previously shown to impair cognitive function in humans. Assessment and prevention of such cognitive impairment require detection of cognitive changes and impairment using specific cognitive function assessment tools. This paper summarizes the findings of previous research, outlines the methods for cognitive function assessment used at a high altitude, elaborates the need to develop standardized and systematic cognitive function assessment tools for high-altitude hypoxia environments.

BackgroundSwift and accurate detection of Vibrio parahaemolyticus, which is a prominent causative pathogen associated with seafood contamination, is required to effectively combat foodborne disease and wound infections. The toxR gene is relatively conserved within V. parahaemolyticus and is primarily involved in the expression and regulation of virulence genes with a notable degree of specificity. The aim of this study was to develop a rapid, simple, and constant temperature detection method for V. parahaemolyticus in clinical and nonspecialized laboratory settings.MethodsIn this study, specific primers and CRISPR RNA were used to target the toxR gene to construct a reaction system that combines recombinase polymerase amplification (RPA) with CRISPR‒Cas13a. The whole-genome DNA of the sample was extracted by self-prepared sodium dodecyl sulphate (SDS) nucleic acid rapid extraction reagent, and visual interpretation of the detection results was performed by lateral flow dipsticks (LFDs).ResultsThe specificity of the RPA-CRISPR/Cas13a-LFD method was validated using V. parahaemolyticus strain ATCC-17802 and six other non-parahaemolytic Vibrio species. The results demonstrated a specificity of 100%. Additionally, the genomic DNA of V. parahaemolyticus was serially diluted and analysed, with a minimum detectable limit of 1 copy/µL for this method, which was greater than that of the TaqMan-qPCR method (102 copies/µL). The established methods were successfully applied to detect wild-type V. parahaemolyticus, yielding results consistent with those of TaqMan-qPCR and MALDI-TOF MS mass spectrometry identification. Finally, the established RPA-CRISPR/Cas13a-LFD method was applied to whole blood specimens from mice infected with V. parahaemolyticus, and the detection rate of V. parahaemolyticus by this method was consistent with that of the conventional PCR method.ConclusionsIn this study, we describe an RPA-CRISPR/Cas13a detection method that specifically targets the toxR gene and offers advantages such as simplicity, rapidity, high specificity, and visual interpretation. This method serves as a valuable tool for the prompt detection of V. parahaemolyticus in nonspecialized laboratory settings.

HAdV infections are readily transmittable and, in some instances, highly contagious. Early and rapid diagnosis is essential for disease control.

Hypoxia as a microenvironment or niche stimulates proliferation of neural stem cells (NSCs). However, the underlying mechanisms remain elusive. Autophagy is a protective mechanism by which recycled cellular components and energy are rapidly supplied to the cell under stress. Whether autophagy mediates the proliferation of NSCs under hypoxia and how hypoxia induces autophagy remain unclear. Here, we report that hypoxia facilitates embryonic NSC proliferation through HIF-1/mTORC1 signaling pathway-mediated autophagy. Initially, we found that hypoxia greatly induced autophagy in NSCs, while inhibition of autophagy severely impeded the proliferation of NSCs in hypoxia conditions. Next, we demonstrated that the hypoxia core regulator HIF-1 was necessary and sufficient for autophagy induction in NSCs. Considering that mTORC1 is a key switch that suppresses autophagy, we subsequently analyzed the effect of HIF-1 on mTORC1 activity. Our results showed that the mTORC1 activity was negatively regulated by HIF-1. Finally, we provided evidence that HIF-1 regulated mTORC1 activity via its downstream target gene BNIP3. The increased expression of BNIP3 under hypoxia enhanced autophagy activity and proliferation of NSCs, which was mediated by repressing the activity of mTORC1. We further illustrated that BNIP3 can interact with Rheb, a canonical activator of mTORC1. Thus, we suppose that the interaction of BNIP3 with Rheb reduces the regulation of Rheb toward mTORC1 activity, which relieves the suppression of mTORC1 on autophagy, thereby promoting the rapid proliferation of NSCs. Altogether, this study identified a new HIF-1/BNIP3-Rheb/mTORC1 signaling axis, which regulates the NSC proliferation under hypoxia through induction of autophagy.

The most intriguing characteristic of the sigma-1 receptor is its ability to regulate multiple functional proteins directly via protein-protein interactions, giving the sigma-1 receptor the powerful ability to regulate several survival and metabolic functions in cells, fine tune neuronal excitability, and regulate the transmission of information within brain circuits. This characteristic makes sigma-1 receptors attractive candidates for the development of new drugs. Hypidone hydrochloride (YL-0919), a novel structured antidepressant candidate developed in our laboratory, possess a selective sigma-1 receptor agonist profile, as evidenced by molecular docking, radioligand receptor binding assays, and receptor functional experiments. In vivo studies have revealed that YL-0919 elicits a fast-onset antidepressant activity (within one week) that can be attenuated with pretreatment of the selective sigma-1 receptor antagonist, BD-1047. Taken together, the findings of the current study suggest that YL-0919 activates the sigma-1 receptor to partially mediate the rapid onset antidepressant effects of YL-0919. Thus, YL-0919 is a promising candidate as a fast-onset antidepressant that targets the sigma-1 receptor.

Intermittent hypoxia training (IHT) is a promising approach that has been used to induce acclimatization to hypoxia and subsequently lower the risk of developing acute mountain sickness (AMS). However, the effects of IHT on cognitive and cerebrovascular function after acute hypoxia exposure have not been characterized. In the present study, we first confirmed that the simplified IHT paradigm was effective at relieving AMS at 4300 m. Second, we found that IHT improved participants’ cognitive and neural alterations when they were exposed to hypoxia. Specifically, impaired working memory performance, decreased conflict control function, impaired cognitive control, and aggravated mental fatigue induced by acute hypoxia exposure were significantly alleviated in the IHT group. Furthermore, a reversal of brain swelling induced by acute hypoxia exposure was visualized in the IHT group using magnetic resonance imaging. An increase in cerebral blood flow (CBF) was observed in multiple brain regions of the IHT group after hypoxia exposure as compared with the control group. Based on these findings, the simplified IHT paradigm might facilitate hypoxia acclimatization, alleviate AMS symptoms, and increase CBF in multiple brain regions, thus ameliorating brain swelling and cognitive dysfunction.

Background Ischemic cerebral infarction is the most common type of stroke with high rates of mortality, disability, and recurrence. However, the known diagnostic biomarkers and therapeutic targets for ischemic stroke (IS) are limited. In the current study, we aimed to identify novel inflammation-related biomarkers for IS using machine learning analysis and to explore their relationship with the levels of immune-related cells in whole blood samples. Methods Gene expression profiles of healthy controls and patients with IS were download from the Gene Expression Omnibus. Analysis of differentially expressed genes (DEGs) was performed in healthy controls and patients with IS. Single-sample gene set enrichment analysis was performed to calculate inflammation scores, and weighted gene co-expression network analysis was used to analyze genes in significant modules associated with inflammation scores. Key DEGs in significant modules were then analyzed using LASSO regression analysis for constructing a diagnostic model. The effectiveness and specificity of the diagnostic model was verified in healthy controls and patients with IS and with cerebral hemorrhage (CH) using qRT-PCR. The relationship between diagnostic score and the levels of immune-related cells in whole blood were analyzed using Pearson correlations. Results A total of 831 DEGs were identified. Both chronic and acute inflammation scores were higher in patients with IS, while 54 DEGs were also clustered in the gene modules associated with chronic and acute inflammation scores. Among them, a total of 9 genes were selected to construct a diagnostic model. Interestingly, RT-qPCR showed that the diagnostic model had better diagnostic value for IS but not for CH. The levels of lymphocytes were lower in blood of patients with IS, while the levels of monocytes and neutrophils were increased. The diagnostic score of the model was negatively associated with the levels of lymphocytes and positively associated with levels of monocytes and neutrophils. Conclusions Taken together, the diagnostic model constructed using the inflammation-related genes TNFSF10, ID1, PAQR8, OSR2, PDK4, PEX11B, TNIP1, FFAR2, and JUN exhibited high and specific diagnostic value for IS and reflected the condition of lymphocytes, monocytes, and neutrophils in the blood. The diagnostic model may contribute to the diagnosis of IS.

Mitophagy is an important metabolic mechanism that modulates mitochondrial quality and quantity by selectively removing damaged or unwanted mitochondria. BNIP3 (BCL2/adenovirus e1B 19 kDa protein interacting protein 3), a mitochondrial outer membrane protein, is a mitophagy receptor that mediates mitophagy under various stresses, particularly hypoxia, since BNIP3 is a hypoxia-responsive protein. However, the underlying mechanisms that regulate BNIP3 and thus mediate mitophagy under hypoxic conditions remain elusive. Here, we demonstrate that in hypoxia JNK1/2 (c-Jun N-terminal kinase 1/2) phosphorylates BNIP3 at Ser 60/Thr 66, which hampers proteasomal degradation of BNIP3 and drives mitophagy by facilitating the direct binding of BNIP3 to LC3 (microtubule-associated protein 1 light chain 3), while PP1/2A (protein phosphatase 1/2A) represses mitophagy by dephosphorylating BNIP3 and triggering its proteasomal degradation. These findings reveal the intrinsic mechanisms cells use to regulate mitophagy via the JNK1/2-BNIP3 pathway in response to hypoxia. Thus, the JNK1/2-BNIP3 signaling pathway strongly links mitophagy to hypoxia and may be a promising therapeutic target for hypoxia-related diseases.

Zhang, Guangbo, Yanzhao Zhou, Zhengtao Cao, Xiang Cheng, Xiangpei Yue, Tong Zhao, Ming Zhao, Yongqi Zhao, Ming Fan, and Lingling Zhu. Preliminary intermittent hypoxia training alleviates the damage of sustained normobaric hypoxia on human hematological indexes and cerebral white matter. High Alt Med Biol. 23:273-283, 2022. Background: We aimed to examine the effects of preliminary intermittent hypoxia training (IHT) on human hematological indexes and cerebral white matter (WM) after exposure to a simulated altitude of 4,300 m. Methods: We recruited 20 young healthy volunteers. Participants were then randomized to either the IHT group (n = 10) or the control group (n = 10). We measured the physiological function of the control group at sea level and after exposure to a simulated altitude of 4,300 m, respectively. The IHT group performed the above tests at three time points: before and after hypoxia training, and after exposure to a simulated altitude of 4,300 m, respectively. Results: We found that mean SpO2 during day 10 of hypoxia training showed a significant increase compared with mean SpO2 on day 1 (88.3% ± 1.5% vs. 90.0% ± 1.6%, p < 0.05), and erythrocyte P50 of post-training was significantly increased compared with pretraining (37.8 ± 2.9 mmHg vs. 45.9 ± 6.4 mmHg, p < 0.05). Mean SpO2 measures after acute exposure to high altitude exhibited a significant difference, with the IHT group showing significantly greater SpO2 than the control group (73.8% ± 3.7% vs. 77.4% ± 3.2%, p < 0.05), and the Lake Louise Score was also lower than the control group (2.55 ± 2.1 vs. 6.67 ± 2.5, p < 0.05). After daily IHT, brain-derived neurotrophic factor plasma levels of participants in the IHT group did not change but significantly increased in response to high-altitude hypoxia (103.5% ± 70.4% vs. 29.7% ± 73.2%, p < 0.05). Interleukin-10 (IL-10) plasma level did not change before and after IHT in the IHT group, whereas the IL-10 plasma level of the control group after high-altitude exposure was significantly higher. Furthermore, we found that fractional anisotropy values in the left corticospinal tract and splenium of the corpus callosum in the IHT group were significantly higher than those in the control group after high-altitude hypoxia. Conclusions: These results demonstrate that IHT alleviates the damage of sustained normobaric hypoxia on human hematological indexes and cerebral WM.

Depression is the most common type of neuropsychiatric illness and has increasingly become a major cause of disability. Unfortunately, the recent global pandemic of COVID-19 has dramatically increased the incidence of depression and has significantly increased the burden of mental health care worldwide. Since full remission of the clinical symptoms of depression has not been achieved with current treatments, there is a constant need to discover new compounds that meet the major clinical needs. Recently, the roles of sigma receptors, especially the sigma-1 receptor subtype, have attracted increasing attention as potential new targets and target-specific drugs due to their translocation property that produces a broad spectrum of biological functions. Even clinical first-line antidepressants with or without affinity for sigma-1 receptors have different pharmacological profiles. Thus, the regulatory role of sigma-1 receptors might be useful in treating these central nervous system (CNS) diseases. In addition, long-term mental stress disrupts the homeostasis in the CNS. In this review, we discuss the topical literature concerning sigma-1 receptor antidepressant mechanism of action in the regulation of intracellular proteostasis, calcium homeostasis and especially the dynamic Excitatory/Inhibitory (E/I) balance in the brain. Furthermore, based on these discoveries, we discuss sigma-1 receptor ligands with respect to their promise as targets for fast-onset action drugs in treating depression.

Background Alzheimer’s disease (AD) is a progressive, degenerative, and terminal disease without cure. There is an urgent need for a new strategy to treat AD. The aim of this study was to investigate the effects of intermittent hypoxic treatment (IHT) on cognitive functions in a mouse model of AD and unravel the mechanism of action of IHT. Methods Six-month-old APPswe/PS1dE9 (APP/PS1) male mice were exposed to hypoxic environment (14.3% O 2 ) 4 h/day for 14 days or 28 days. Cognitive functions were measured by Morris water maze test after either 14 days or 42 days of interval. Thereafter the distribution of amyloid plaque and microglial activation were determined by mouse brain immunohistochemistry, while the amyloid beta (Aβ) and inflammatory cytokines were measured by ELISA and Western Blot. Microarray was used for studying gene expressions in the hippocampus. Results IHT for 14 days or 28 days significantly improved the spatial memory ability of the 6-month-old APP/PS1 mice. The memory improvement by 14 days IHT lasted to 14 days, but not to 42 days. The level of Aβ plaques and neurofilament accumulations was reduced markedly after the IHT exposure. IHT reduced the pro-inflammatory cytokines IL-1β, IL-6 levels, and β-secretase cleavage of APP processing which implies reduced Aβ production. Microarray analysis revealed a large number of genes in the hippocampus were significantly altered which are known to be metabolism-regulated genes. Conclusions This study provides evidence of the beneficial effect of IHT on the progression of AD by alleviating memory impairment, reducing Aβ accumulation and inflammation in the brain. IHT can be developed as a novel measure to relieve the progression of AD by targeting multiple pathways in the AD pathogenesis.

目的 探讨急性高原低氧对脑电(Electroencephalogram,EEG)功率的影响.方法 采用低压低氧舱模拟海拔4300 m低氧环境,采集并分析EEG信号.结果(1)各频段功率受氧气环境影响显著,低氧环境下功率增强,尤其是alpha、delta、theta频段功率显著增强.(2)急性低氧后,常氧下额区活动呈左偏侧化的个体,偏侧化指标有所降低;常氧下额区活动呈右侧化的个体,偏侧化指标则略为上升.结论 模拟低氧环境影响了个体的额区偏侧化指标,导致个体情绪调节灵活性变差.