Association of neutrophil to lymphocyte ratio and D-dimer with functional outcome in patients with cerebral venous sinus thrombosis.

BACKGROUND: Investigations on the risk factors for the prognosis of cerebral venous sinus thrombosis (CVST) are limited. This study aimed to explore whether specific inflammatory factors and coagulation indictors are associated with functional outcome in patients treated for CVST. METHODS: This retrospective study included 137 patients admitted to our hospital between January 2010 and October 2021. The functional outcome was assessed with the modified Rankin Scale (mRS) score at discharge. Patients were divided into two groups, 102 patients with favorable outcomes (mRS 0-1) and 35 patients with poor outcomes (mRS 2-6). The clinical indexes were compared between two groups. Multivariable logistic regression was performed to identify the independent influencing factors for poor outcomes of CVST patients. The prognostic indicators were analyzed using the receiver operating characteristic (ROC) curve. RESULTS: Compared with the favorable outcome group, the incidence of impaired consciousness and brain lesion, the levels of D-dimer, RDW, neutrophil count, neutrophil to lymphocyte ratio (NLR) and red blood cell distribution width to platelet ratio (%) on admission were significantly higher in the poor outcome group, while the level of lymphocyte count was significantly lower. After multivariable logistic regression analysis, baseline D-dimer level (odds ratio (OR), 1.180; 95% confidence interval (CI), 1.019-1.366, P = 0.027) and NLR (OR, 1.903; 95%CI, 1.232-2.938, P = 0.004) were significantly associated with unfavorable outcome at discharge. The ROC curve analysis showed that the areas under the curve of D-dimer, NLR and their combined detection for predicting worse outcome were 0.719, 0.707 and 0.786, respectively. CONCLUSIONS: Elevated D-dimer level and NLR on admission were associated with an increased risk of poor functional outcome in patients with CVST.

Higher inflammation and cerebral white matter injury associated with cognitive deficit in asthmatic patients with depression.

OBJECTIVE: Depression is a common co-morbidity in asthma, worsening asthma control and impairing quality of life. Previous studies have reported a higher risk of cognitive deficit in depression, yet little research has focused on the level of cognition in asthmatic patients with depression. Evidence shows that inflammation may play an important role in both asthma and depression. Cerebral white matter injury, possibly induced by inflammation, has been associated with depression. This study assesses cognitive function in patients with asthma and a depression comorbidity, compared to patients with asthma only or depression only. METHODS: Four groups were studied: Asthma comorbid Depression group (A + D, n = 26), Depression group (D, n = 25), Asthma group (A, n = 33) and Normal controls (N, n = 28). Cognitive function was evaluated using Montreal Cognitive Assessment (MoCA). Inflammatory cytokines were measured, including interleukin-1ß (IL-1ß), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), high-mobility group box 1(HMGB1) and Netrin-1. Cerebral white matter injury was assessed by serum myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG), and their correlations with cognitive performance were calculated. RESULTS: A + D group showed the highest incidence of cognitive deficit, with the cognitive domain particularly affected. Compared to N group, serum levels of IL-6, HMGB1, Netrin-1, MBP and MOG were significantly elevated in A + D group. MOG level negatively correlated with the MoCA score. CONCLUSION: Patients with comorbidities presented with more severe cognitive deficits and higher levels of inflammatory cytokines. Cerebral white matter injury may account for the cognitive deficit in patients and MOG could be a potential biomarker for this process.

Neural network correlates of high-altitude adaptive genetic variants in Tibetans: A pilot, exploratory study.

Although substantial progress has been made in the identification of genetic substrates underlying physiology, neuropsychology, and brain organization, the genotype-phenotype associations remain largely unknown in the context of high-altitude (HA) adaptation. Here, we related HA adaptive genetic variants in three gene loci (EGLN1, EPAS1, and PPARA) to interindividual variance in a set of physiological characteristics, neuropsychological tests, and topological attributes of large-scale structural and functional brain networks in 135 indigenous Tibetan highlanders. Analyses of individual HA adaptive single-nucleotide polymorphisms (SNPs) revealed that specific SNPs selectively modulated physiological characteristics (erythrocyte level, ratio between forced expiratory volume in the first second to forced vital capacity, arterial oxygen saturation, and heart rate) and structural network centrality (the left anterior orbital gyrus) with no effects on neuropsychology or functional brain networks. Further analyses of genetic adaptive scores, which summarized the overall degree of genetic adaptation to HA, revealed significant correlations only with structural brain networks with respect to local interconnectivity of the whole networks, intermodule communication between the right frontal and parietal module and the left occipital module, nodal centrality in several frontal regions, and connectivity strength of a subnetwork predominantly involving in intramodule edges in the right temporal and occipital module. Moreover, the associations were dependent on gene loci, weight types, or topological scales. Together, these findings shed new light on genotype-phenotype interactions under HA hypoxia and have important implications for developing new strategies to optimize organism and tissue responses to chronic hypoxia induced by extreme environments or diseases.

Association between alpha-synuclein (SNCA) rs11931074 variability and susceptibility to Parkinson's disease: an updated meta-analysis of 41,811 patients.

BACKGROUND AND OBJECTIVES: Parkinson's disease (PD) is one of the most common forms of neurodegenerative disorders, and its etiology remains unclear. Single nucleotide polymorphisms (SNPs) of alpha-synuclein (SNCA) have been found to be significantly associated with PD risk. In particular, the variant rs11931074 was found in one meta-analysis to appear to play a role in the occurrence of PD. This finding has been questioned in subsequent studies, however. The aim of this study was to determine the relationship between PD risk and rs11931074 polymorphism. METHODS: We performed a systematic online search, including PubMed, Web of Science, EMBASE, Cochrane Library, and CNKI (China National Knowledge Infrastructure), aiming to identify case-control studies looking at the role of rs11931074 in PD. We performed calculations of pooled odds ratio (OR) and 95% confidence interval (95% CI) to assess the associations, and subgroup meta-analyses to verify differences between various ethnicities of different study populations. RESULTS: A total of 13 studies involving 13,403 cases and 28,408 controls met the inclusion criteria after assessment by two reviewers. Overall, there exists significant associations between SNCA rs11931074 polymorphism and the risk of PD under five genetic models (allele contrast model: T vs. G, OR = 1.28, 95% CI = 1.12-1.45, P = 0.0001; homozygote model: TG vs. GG, OR = 1.55, 95% CI = 1.17-2.05, P = 0.002; heterozygote model (TT vs. GG, OR = 1.23, 95% CI = 1.05-1.42, P = 0.009; dominant model: TG+TT vs. GG: OR = 1.25, 95% CI = 1.05-1.50, P = 0.01 and recessive model: TT vs. TG+GG: OR = 1.40, 95% CI = 1.18-1.68, P = 0.0002). When ethnicities were stratified, significant associations were found in the allelic, homozygote, and recessive models for Asians, and in the allelic model for Caucasians. CONCLUSION: SNCA rs11931074 polymorphism is found to be associated with PD risk and this risk appears to be influenced by genetic status and ethnicity.

Neuro-regeneration or Repair: Cell Therapy of Neurological Disorders as A Way Forward.

The human central nervous system (CNS) has a limited capacity for regeneration and repair, as many other organs do. Partly as a result, neurological diseases are the leading cause of medical burden globally. Most neurological disorders cannot be cured, and primary treatments focus on managing their symptoms and slowing down their progression. Cell therapy for neurological disorders offers several therapeutic potentials and provides hope for many patients. Here we provide a general overview of cell therapy in neurological disorders such as Parkinson's disease (PD), Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Wilson's disease (WD), stroke and traumatic brain injury (TBI), involving many forms of stem cells, including embryonic stem cells and induced pluripotent stem cells. We also address the current concerns and perspectives for the future. Most studies for cell therapy in neurological diseases are in the pre-clinical stage, and there is still a great need for further research to translate neural replacement and regenerative therapies into clinical settings.

A developmental critical period for ocular dominance plasticity of binocular neurons in mouse superior colliculus.

Detecting visual features in the environment is crucial for animals' survival. The superior colliculus (SC) is implicated in motion detection and processing, whereas how the SC integrates visual inputs from the two eyes remains unclear. Using in vivo electrophysiology, we show that mouse SC contains many binocular neurons that display robust ocular dominance (OD) plasticity in a critical period during early development, which is similar to, but not dependent on, the primary visual cortex. NR2A- and NR2B-containing N-methyl-D-aspartate (NMDA) receptors play an essential role in the regulation of SC plasticity. Blocking NMDA receptors can largely prevent the impairment of predatory hunting caused by monocular deprivation, indicating that maintaining the binocularity of SC neurons is required for efficient hunting behavior. Together, our studies reveal the existence and function of OD plasticity in SC, which broadens our understanding of the development of subcortical visual circuitry relating to motion detection and predatory hunting.

N6-methyladenosine (m6A) modification and its clinical relevance in cognitive dysfunctions.

BACKGROUND: N6 adenosine methylation (m6A) is the most abundant internal RNA modification in eukaryotic cells. Dysregulation of m6A has been associated with the perturbations of cell proliferation and cell death in different diseases. However, the roles of m6A in the neurodegenerative process and cognitive dysfunction are unclear. METHODS: We systematically investigated the molecular alterations of m6A regulators and their clinical relevance with cognitive dysfunctions using published datasets of Alzheimer's Disease (AD), vascular dementia, and mild cognitive impairment (MCI). FINDINGS: The expressions of m6A regulators vary in different tissues and closely correlate with neurodegenerative pathways. We identified co-expressive m6A regulators SNRPG and SNRPD2 as potential biomarkers to predict transformation from MCI to AD. Moreover, we explored correlations between Apolipoprotein E4 and m6A methylations. INTERPRETATION: Collectively, these findings suggest that m6A methylations as potential biomarkers and therapeutic targets for cognitive dysfunction. FUNDING: This work was supported by the National Natural Science Foundation of China (81871040) and the Shanghai Health System Talent Training Program (2018BR29).

Anxiety and Depression Diagnosis Method Based on Brain Networks and Convolutional Neural Networks.

At present, only professional doctors can use the professional scales to diagnose depression and anxiety in clinical practice. In recent years, the problems of detecting the presence of anxiety or depression using Electroencephalography (EEG) has received attention as a way to implement assistant diagnosis, and some researchers explored that there are differences in the degree of prefrontal lateralization and functional connectivity of brain networks between patients with anxiety and depression and normal people. In this paper, we proposed a new approach that combines functional connectivity of brain networks and convolutional neural networks (CNN) for EEG-based anxiety and depression recognition. EEG data are collected from subjects consisting ten healthy controls and ten patients with anxiety or depression. In this way, we achieved 67.67% classification accuracy. It points out the way to further explore the application of functional connectivity of brain networks and deep learning technology in EEG about patients with anxiety and depression.

Anti-mouse CX3CR1 Antibody Alleviates Cognitive Impairment, Neuronal Loss and Myelin Deficits in an Animal Model of Brain Ischemia.

White matter lesions are common when global cerebral ischemia (GCI) occurs in the elderly, and cause damage to neurological and psychological functions. Remyelination often fails because of the limited recruitment of oligodendrocyte progenitor cells (OPCs) to the demyelinated site or the inefficient differentiation of OPCs to mature oligodendrocytes (OLs). The activation of microglia, the most important immune cells in the central nervous system, and subsequent inflammation have been implicated in myelination repair disorder. Little is known about the role of the Fractalkine/CX3CR1 signaling pathway, the key regulator of microglia activation, on myelin in microglia. In this study, a GCI animal model was generated through bilateral common carotid artery occlusion to induce ischemic inflammation and white matter damage; then, we downregulated CX3CR1 by intracerebroventricular administration of neutralizing antibody anti-FKR. Downregulation of CX3CR1 significantly reversed the depression-like behavior and cognitive impairment in GCI mice. Activation of microglia was inhibited, and the peripheral inflammatory responses were also ameliorated as revealed by decreased serum levels of IL-1ß, IL-6 and TNF-α. CX3CR1 block substantially reversed demyelination in striatum, cortex and hippocampus and promoted differentiation and maturation of OPCs into mature OLs in the hippocampus. No effect was found on myelin in the corpus callosum. Besides, hippocampal neurons were protected by anti-FKR treatment after GCI. Collectively, our data demonstrated that downregulating of the Fractalkine/CX3CR1 signaling pathway had an anti-depressant and cognition-improvement effect by inhibiting microglia activation, promoting OPCs maturation and remyelination.

Clinical and Imaging Features of Spinal Dural Arteriovenous Fistula: Clinical Experience of 15 Years for a Major Tertiary Hospital.

BACKGROUND: Spinal dural arteriovenous fistula (SDAVF) is a rare spinal vascular malformation which can cause permanent neurologic dysfunction. The purpose of this study was to investigate the relationship between the clinical and imaging characteristics of SDAF and its prognosis. METHODS: All patients diagnosed with SDAVF and hospitalized in our hospital from February 2004 to September 2018 were retrospectively recruited. The clinical and imaging data of these patients were collected, and then a subgroup analysis was performed to find the association between clinical and imaging characteristics of SDAF and its prognosis. RESULTS: A total of 79 patients were included in the analysis. The median age of the patients was 59 years, with men having a predominant morbidity (84.4%). The mean duration of symptoms was 7 months, and most patients had more than 2 symptoms before hospitalization (n = 43, 44.4%). The fistula mainly occurred in the lower thoracic spine (n = 40, 50.6%), followed by the lumbar spine (n = 18, 22.8%) and upper thoracic spine (n = 16, 20.3%). Of 58 patients with magnetic resonance images available, 45 (77.6%) were identified with high T2-weighted image (T2WI) signal in the spinal cord, and 51 (87.9%) with T2WI flow voids on the spinal surface. Multivariate logistic regression analysis found that preoperative Aminoff-Logue Scale (ALS) scores were associated with postoperative function improvement after adjustment for sex, age, and duration of symptoms (P = 0.013; odds ratio, 1.375; 95% confidence interval, 1.07-1.77). CONCLUSIONS: Preoperative ALS scores are associated with improved prognosis in patients with SDAVF. Both surgical ligation and endovascular embolization can improve functional outcomes and delay disease progression.

Strong Association of Serum GSK-3ß/BDNF Ratio with Mild Cognitive Impairment in Elderly Type 2 Diabetic Patients.

BACKGROUND: Glycogen Synthase Kinase (GSK)-3ß and Brain-derived Neurotrophic Factor (BDNF) play vital roles in both Mild Cognitive Impairment (MCI) and Type 2 Diabetes Mellitus (T2DM). The underlying mechanisms may involve inflammation and oxidative stress. OBJECTIVES: To investigate the association of the GSK-3ß/BDNF ratio with MCI in elderly patients with T2DM and whether GSK-3ß/BDNF ratio can serve as a new diagnostic biomarker for MCI in comorbid with T2DM (MD). METHODS: A total of 326 old Chinese T2DM patients were included and stratified according to cognition and GSK-3ß/BDNF ratio quartiles. MCI was diagnosed according to the National Institute on Aging Alzheimer's Association workgroups criteria. In addition to routine hematuria and biochemical examinations, Montreal Cognitive Assessment (MoCA) scale was also used to evaluate the cognitive function, and ELISA method was used to measure GSK-3ß activity and the serum levels of BDNF, interleukin 1ß (IL-1ß), high mobility group box-1 (HMGB1) protein, Malonaldehyde (MDA) and 8-isoprostaglandinF2α (8-iso-PGF2α). RESULTS: We found that GSK-3ß activity was negatively correlated with BDNF (r=-0.270, P=0.008), and patients with higher GSK-3ß/BDNF ratio had lower MoCA scores (P=0.001). When compared with T2DM patients without MCI (nMD), MD patients had higher GSK-3ß activity and GSK-3ß/BDNF ratio, but lower BDNF levels. As for inflammation and oxidative stress, IL-1ß was inversely correlated with GSK-3ß activity, while 8-isoPGF2α was positively correlated with GSK-3ß activity and GSK-3ß/BDNF ratio. The odds ratio for MCI increased gradually when GSK-3ß/BDNF ratio quartile rose from the lowest to the highest (6.90, 95% CI 3.22-14.78). MoCA score was conversely related to GSK-3ß/BDNF ratio, age and fast blood glucose (FBG), with GSK-3ß/BDNF ratio having the most significant influence on cognition (ß=-0.199, P<0.001). CONCLUSION: Our data provide evidence for a strong link between GSK-3ß/BDNF ratio and MCI. GSK- 3ß/BDNF ratio may serve as a better diagnostic biomarker for MD than either GSK-3ß or BDNF alone and increased GSK-3ß/BDNF ratio indicates a worse cognitive function.

NLR Is Associated With Geriatric Depression in Chinese Women: A Community-Based Cross-Sectional Study in Eastern China.

In recent years, the prevalence of depression has been increasing, causing a serious global burden of disease. Previous studies have proved that low-grade inflammation is involved in the process of depression. To explore the role of inflammation in the pathogenesis of senile depression, neutrophil to lymphocyte ratio (NLR) was used in this study, as a biological marker for non-specific inflammation. The present study was conducted among elderly adults from a randomly selected Community in Yangpu District, Shanghai from November 1 to December 30, 2017. 665 participants were included in the present study, including 276 males (median age was 68 years old) and 389 females (median age was 67 years old). NLR was calculated based on results of hematology examination. Depressive symptoms were assessed using the simplified version of Geriatric Depression Scale (GDS), the participant with total score greater than five points was considered to be depressed. The association between NLR and depression was evaluated separately for men and women. The prevalence of depression was 35.1% for men and 34.4% for women. No associations were found between NLR and depression among males. Nevertheless, compared with normal women, NLR was significantly increased in women with depressive symptoms (P = 0.020). Logistic regression analysis showed that NLR was independently associated with geriatric depression in women. The odds ratios (ORs) of depression was 2.152 (1.095, 4.227; P = 0.026) for the fourth compared with the first quartile of NLR. In conclusion, this study showed increased NLR was significantly associated with geriatric depression in women, but not men.

Minocycline Ameliorates Depressive-Like Behavior and Demyelination Induced by Transient Global Cerebral Ischemia by Inhibiting Microglial Activation.

Global cerebral ischemia (GCI) commonly occurs in the elderly. Subcortical white matter lesions and oligodendrocyte (OLG) loss caused by cerebral ischemia have been implicated in the development of post-ischemic depression and cognitive impairment. OLGs are necessary for axonal myelination; the disrupted differentiation of OLG progenitor cells (OPCs) is associated with impaired remyelination. Evidence has indicated that increased levels of inflammatory cytokines released from activated microglia induce depression-like behaviors by affecting neurotransmitter pathways, but the mechanisms remain elusive. We explored the potential mechanisms that link microglia activation with GCI-induced depression and cognitive dysfunction by studying effects of minocycline on white matter damage, cytokine levels, and the monoaminergic neurotransmitters. An acute GCI animal model was generated through bilateral common carotid artery occlusion to induce ischemic inflammation and subcortical white matter damage. Minocycline, an inhibitor of microglia activation, was intraperitoneally administrated immediately after surgery and continued daily for additional six days. Minocycline shortened the immobile duration in tail suspension test and forced swimming test, while no improvement was found in Morris water maze test. The plasma levels of IL-1ß, IL-6, TNF-α, HMGB1, and netrin-1 were significantly reduced with the treatment of minocycline. Minocycline treatment substantially reversed demyelination in corpus callosum and hippocampus, alleviated hippocampal microglia activation, and promoted OPCs maturation, while no effect was found on hippocampal neurodegeneration. Besides, the content of dopamine (DA) in the hippocampus was upregulated by minocycline treatment after GCI. Collectively, our data demonstrated that minocycline exerts an anti-depressant effect by inhibiting microglia activation, promoting OPCs maturation and remyelination. Increased DA in hippocampus may also play a role in ameliorating depressive behavior with minocycline treatment.

Alteration of Spontaneous Brain Activity After Hypoxia-Reoxygenation: A Resting-State fMRI Study.

Zhang, Jiaxing, Ji Chen, Cunxiu Fan, Jinqiang Li, Jianzhong Lin, Tianhe Yang, and Ming Fan. Alteration of spontaneous brain activity after hypoxia-reoxygenation: A resting-state fMRI study. High Alt Med Biol. 18:20-26, 2017.-The present study was designed to investigate the effect of hypoxia-reoxygenation on the spontaneous neuronal activity in brain. Sixteen sea-level (SL) soldiers (20.5 ± 0.7 years), who garrisoned the frontiers in high altitude (HA) (2300-4400 m) for two years and subsequently descended to sea level for one to seven days, were recruited. Control group consisted of 16 matched SL natives. The amplitude of low-frequency fluctuations (ALFF) of regional brain functional magnetic resonance imaging signal in resting state and functional connectivity (FC) between brain regions was analyzed. HA subjects showed significant increases of ALFF at several sites within the bilateral occipital cortices and significant decreases of ALFF in the right anterior insula and extending to the caudate, putamen, inferior frontal orbital cortex, temporal pole, and superior temporal gyrus; lower ALFF values in the right insula were positively correlated with low respiratory measurements. The right insula in HA subjects had increases of FC with the right superior temporal gyrus, postcentral gyrus, rolandic operculum, supramarginal gyrus, and inferior frontal triangular area. We thus demonstrated that hypoxia-reoxygenation had influence on the spontaneous neuronal activity in brain. The decrease of insular neuronal activity may be related to the reduction of ventilatory drive, while the increase of FC with insula may indicate a central compensation.

Increased Intraregional Synchronized Neural Activity in Adult Brain After Prolonged Adaptation to High-Altitude Hypoxia: A Resting-State fMRI Study.

The human brain is intrinsically plastic such that its functional architecture can be reorganized in response to environmental pressures and physiological changes. However, it remains unclear whether a compensatory modification of spontaneous neural activity occurs in adult brain during prolonged high-altitude (HA) adaptation. In this study, we obtained resting-state functional magnetic resonance (MR) images in 16 adults who have immigrated to Qinghai-Tibet Plateau (2300-4400 m) for 2 years and in 16 age-matched sea level (SL) controls. A validated regional homogeneity (Reho) method was employed to investigate the local synchronization of resting-state functional magnetic resonance imaging (fMRI) signals. Seed connectivity analysis was carried out subsequently. Cognitive and physiological assessments were made and correlated with the image metrics. Compared with SL controls, global mean Reho was significantly increased in HA immigrants as well as a regional increase in the right inferolateral sensorimotor cortex. Furthermore, mean z-Reho value extracted within the inferolateral sensorimotor area showed trend-level significant inverse correlation with memory search reaction time in HA immigrants. These observations, for the first time, provide evidence of adult brain resilience of spontaneous neural activity after long-term HA exposure without inherited and developmental effects. Resting-state fMRI could yield valuable information for central mechanisms underlying respiratory and cognitive compensations in adults during prolonged environmentally hypoxic adaptation, paving the way for future HA-adaptive training.

Alteration of spontaneous brain activity in COPD patients.

BACKGROUND AND OBJECTIVE: Airflow limitation in chronic obstructive pulmonary disease (COPD) results in a decrease in oxygen transport to the brain. The aim of the present study was to explore the alteration of spontaneous brain activity induced by hypoxia in patients with COPD. PATIENTS AND METHODS: Twenty-five stable patients with COPD and 25 matching healthy volunteers were investigated. Amplitude of low-frequency fluctuation (ALFF) of blood oxygenation level-dependent signal at resting state in the brain was analyzed using functional magnetic resonance imaging. RESULTS: Whole-brain analysis using functional magnetic resonance imaging revealed significant decreases in ALFF in the bilateral posterior cingulate gyri and right lingual gyrus and an increase in ALFF in the left postcentral gyrus of patients with COPD. After controlling for SaO2, patients with COPD only showed an increase in ALFF in the left postcentral gyrus. Region of interest analysis showed a decrease in ALFF in the left precentral gyrus and an increase in ALFF in the left caudate nucleus of patients with COPD. In all subjects, ALFF in the bilateral posterior cingulate gyri and right lingual gyrus showed positive correlations with visual reproduction. CONCLUSION: We demonstrated abnormal spontaneous brain activity of patients with COPD, which may have a pathophysiologic meaning.

Reversible Brain Abnormalities in People Without Signs of Mountain Sickness During High-Altitude Exposure.

A large proportion of lowlanders ascending to high-altitude (HA) show no signs of mountain sickness. Whether their brains have indeed suffered from HA environment and the persistent sequelae after return to lowland remain unknown. Thirty-one sea-level college students, who had a 30-day teaching on Qinghai-Tibet plateau underwent MRI scans before, during, and two months after HA exposure. Brain volume, cortical structures, and white matter microstructure were measured. Besides, serum neuron-specific enolase (NSE), C-reactive protein, and interleukin-6 and neuropsychiatric behaviors were tested. After 30-day HA exposure, the gray and white matter volumes and cortical surface areas significantly increased, with cortical thicknesses and curvatures changed in a wide spread regions; Anisotropy decreased with diffusivities increased in multiple sites of white matter tracts. Two months after HA exposure, cortical measurements returned to basal level. However, increased anisotropy with decreased diffusivities was observed. Behaviors and serum inflammatory factor did not significant changed during three time-point tests. NSE significantly decreased during HA but increased after HA exposure. Results suggest brain swelling occurred in people without neurological signs at HA, but no negative sequelae in cortical structures and neuropsychiatric functions were left after the return to lowlands. Reoxygenation changed white matter microstructure.