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中国睡眠研究会第九届学术年会

作者： Shu Qing Wu Rui Chen Department of Respiratory Medicine Northern Jiangsu People's HospitalClinical Medical School Yangzhou University Department of Respiratory Medicine Second Affiliated Hospital of Soochow University

Purpose Obstructive sleep apnea hypopnea syndrome（OSAHS） is associated with neurocognitive impairment.We examined the role of the systemic inflammatory response,measured by highsensitivity C-reactive protein（hsCRP） as- say,and the effect of CPAP treatment on hsCRP and cognitive impairment in patients with OSAHS.Methods Eligible subjects（n = 178） were categorized into two groups:absent or mild OSAHS,and moderate to severe OSAHS.First,the Montreal cognitive Assessment（MoCA） and serum hsCRP concentration were measured.Then,the moderate to severe OSAHS group was further divided into a conservative treatment subgroup（n = 68） and a CPAP sub- group（n = 68）.After 6 months of treatment,MoCA scores and hsCRP concentrations were re-measured in the moderate to severe group.Results Compared with the absent or mild OSAHS group,hsCRP concentration was higher（1.00 ±1.28 mg/L versus 2.71 ± 1.8,p ＜ 0.001） and MoCA scores were significantly lower（27.4 ± 1.4 versus26.3 + 2.0,p ＜ 0.001） in the moderate to severe group.After adjustment for age,education,body mass index,and neck circumference,hsCRP and MoCA scores correlated with parameters of overnight hypoxia.hsCRP and the proportion of time spent with blood oxygen saturation ＜ 90%（T90） predicted MoCA score.hsCRP and MoCA score improved,and the subdomains of the MoCA were partially improved,in the CPAP treatment subgroup.In conservatively managed patients,hsCRP concentration in- creased,and there was no improvement in neurocognitive dysfunction,with the memory subdomain significantly worse.Conclusions hsCRP may play a role in neurocognitive dys- function in OSAHS.Long-term CPAP treatment could nor- malize the serum hsCRP concentration and partially reverse cognitive dysfunction in OSAHS.

关键词： Obstructive sleep apnea hypopnea syndrome Systemic inflammation cognitive impairment Continuous positive airway pressure Polysomnography

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Mechanisms Underlying Brain Aging Under Normal and Pathological Conditions

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Neuroscience Bulletin 2023年第2期39卷 303-314页

作者： Menglong Jin Shi-Qing Cai Institute of Neuroscience and State Key Laboratory of Neuroscience CAS Center for Excellence in Brain Science and Intelligence TechnologyChinese Academy of SciencesShanghai 200031China University of Chinese Academy of Sciences Beijing 100049China

Aging is a major risk factor for many human diseases,including cognitive impairment,which affects a large population of the elderly.In the past few decades,our understanding of the molecular and cellular mechanisms underlying the changes associated with aging and age-related diseases has expanded greatly,shedding light on the potential role of these changes in cognitive impairment.In this article,we review recent advances in understanding of the mechanisms underlying brain aging under normal and pathological conditions,compare their similarities and differences,discuss the causative and adaptive mechanisms of brain aging,and finally attempt to find some rules to guide us on how to promote healthy aging and prevent age-related diseases.

关键词： Healthy aging Pathological aging cognitive impairment

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Agomelatine:a potential novel approach for the treatment of memory disorder in neurodegenerative disease

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Neural Regeneration Research 2023年第4期18卷 727-733页

作者： Qiang Su Tian Li Guo-Wei Liu Yan-Li Zhang Jun-Hong Guo Zhao-Jun Wang Mei-Na Wu Jin-Shun Qi Key Laboratory of Cellular Physiology Ministry of EducationShanxi Medical UniversityTaiyuanShanxi ProvinceChina Department of Physiology Shanxi Medical UniversityTaiyuanShanxi ProvinceChina Department of Neurology First Hospital of Shanxi Medical UniversityTaiyuanShanxi ProvinceChina Department of Laboratory Medicine Fenyang College of Shanxi Medical UniversityFenyangShanxi ProvinceChina Department of Neurology Sixth Hospital of Shanxi Medical University(General Hospital of Tisco)TaiyuanShanxi ProvinceChina

Agomelatine is a selective agonist of melatonin receptor 1A/melatonin receptor 1B(MT/MT)and antagonist of 5-hydroxytryptamine 2C receptors.It is used clinically to treat major depressive episodes in adults.The pro-chronobiological activity of agomelatine reconstructs sleep-wake rhythms and normalizes circadian disturbances via its agonistic effect of melatonin receptor 1A/melatonin receptor 1B,which work simultaneously to counteract depression and anxiety disorder.Moreover,by antagonizing neocortical postsynaptic 5-hydroxytryptamine 2C receptors,agomelatine enhances the release of dopamine and noradrenaline in the prefrontal cortex,increases the activity of dopamine and noradrenaline,and thereby reduces depression and anxiety disorder.The combination of these two effects means that agomelatine exhibits a unique pharmacological role in the treatment of depression,anxiety,and disturbance of the circadian rhythm.Emotion and sleep are closely related to memory and cognitive function.Memory disorder is defined as any forms of memory abnormality,which is typically evident in a broad range of neurodegenerative diseases,including Alzheimer’s disease.Memory impairment and cognitive impairment are common symptoms of neurodegenerative and psychiatric diseases.Therefore,whether agomelatine can improve memory and cognitive behaviors if used for alleviating depression and circadian-rhythm sleep disorders has become a research“hotspot”.This review presents the latest findings on the effects of agomelatine in the treatment of psychologic and circadian-rhythm sleep disorders in clinical trials and animal experiments.Our review evaluates recent studies on treatment of memory impairment and cognitive impairment in neurodegenerative and psychiatric diseases.

关键词： agomelatine antidepressant anxiety apathy circadian-rhythm sleep disorder cognitive impairment depression melatonergic memory disorder mood disorder neurodegenerative disease

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Ketogenic diet alleviates cognitive dysfunction and neuroinflammation in APP/PS1 mice via the Nrf2/HO-1 and NF-κB signaling pathways

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Neural Regeneration Research 2023年第12期18卷 2767-2772页

作者： Jingwen Jiang Hong Pan Fanxia Shen Yuyan Tan Shengdi Chen Department of Neurology and Institute of Neurology Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghaiChina Lab of Translational Research of Neurodegenerative Diseases Institute of ImmunochemistryShanghaiTech UniversityShanghaiChina

Alzheimer's disease is a progressive neurological disorder characterized by cognitive decline and chronic inflammation within the brain.The ketogenic diet,a widely recognized therapeutic intervention for refractory epilepsy,has recently been proposed as a potential treatment for a variety of neurological diseases,including Alzheimer's disease.However,the efficacy of ketogenic diet in treating Alzheimer's disease and the underlying mechanism remains unclear.The current investigation aimed to explore the effect of ketogenic diet on cognitive function and the underlying biological mechanisms in a mouse model of Alzheimer's disease.Male amyloid precursor protein/presenilin 1(APP/PS1)mice were randomly assigned to either a ketogenic diet or control diet group,and received their respective diets for a duration of 3 months.The findings show that ketogenic diet administration enhanced cognitive function,attenuated amyloid plaque formation and proinflammatory cytokine levels in APP/PS1 mice,and augmented the nuclear factor-erythroid 2-p45 derived factor 2/heme oxygenase-1 signaling pathway while suppressing the nuclear factor-kappa B pathway.Collectively,these data suggest that ketogenic diet may have a therapeutic potential in treating Alzheimer's disease by ameliorating the neurotoxicity associated with Aβ-induced inflammation.This study highlights the urgent need for further research into the use of ketogenic diet as a potential therapy for Alzheimer's disease.

关键词： Alzheimer's disease APP/PS1 mice cognitive impairment ketogenic diet neuroinflammation nuclear factor-kappa B pathway nuclear factor-erythroid 2-p45 derived factor 2/heme oxygenase-1 therapeutic benefits

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Ribosylation induces cognitive impairment and neural cell death

Ribosylation induces cognitive impairment and neural cell de...

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中国生物化学与分子生物学会第十二届全国会员代表大会暨2...

作者： Yan WEI Rongqiao HE State Key laboratory of Brain and cognitive Science Institute of BiophysicsChinese Academy of Sciences

D-ribose in cells and human serum participates in the glycation of proteins resulting in advanced glycation end products(AGEs) that affect cell metabolism and induce cell death.AGEs have been shown to be implicated in the senile plaques and neurofibrillary tangles in the brain of Alzheimer’s patients.Abnormally high levels of ribose,along with glucose were found in the urine of patients with type 2 diabetic mellitus.Here,the effects of D-ribose and ribosylation on protein,cell and animal were investigated by biochemical,cellular and animal experiments.Glycation with D-ribose induced protein to misfold rapidly and form globular amyloid-like aggregations which play an important role in cytotoxicity to neural cells.D-ribose also decreased cell viability and induced more AGE accumulation in cells.Intraperitoneal injection,oral administration and tail intravenous injection of D-ribose caused impairment of spatial learning and memory ability in animals,along with A deposition,tau hyperphosphorylation and glia activation,which were the key pathological features in Alzheimer’s disease.There may be some mechanistic link between ribosylation and cognitive impairment.Targeting ribosylation could be a promising therapeutic strategy to prevent Alzheimer’s disease and diabetic encephalopathies.

关键词： ribosylation Alzheimer’s disease tau hyperphosphorylation cognitive impairment

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Quantitative proteomic and phosphoproteomic analyses of the hippocampus reveal the involvement of NMDAR1 signaling in repetitive mild traumatic brain injury

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Neural Regeneration Research 2023年第12期18卷 2711-2719页

作者： Zhicheng Tian Zixuan Cao Erwan Yang Juan Li Dan Liao Fei Wang Taozhi Wang Zhuoyuan Zhang Haofuzi Zhang Xiaofan Jiang Xin Li Peng Luo Department of Neurosurgery Xijing HospitalFourth Military Medical UniversityXi’anShaanxi ProvinceChina The Sixth Regiment School of Basic MedicineFourth Military Medical UniversityXi’anShaanxi ProvinceChina Department of Neurobiology School of Basic MedicineFourth Military Medical UniversityXi’anShaanxi ProvinceChina Medical Experiment Center Shaanxi University of Chinese MedicineXianyangShaanxi ProvinceChina Department of Anesthesiology The Second Hospital of Jilin UniversityJilin UniversityChangchunJilin ProvinceChina School of Life Science Northwest UniversityXi’anShaanxi ProvinceChina Department of Anesthesiology Xijing HospitalFourth Military Medical UniversityXi’anShaanxi ProvinceChina

The cumulative damage caused by repetitive mild traumatic brain injury can cause long-term neurodegeneration leading to cognitive impairment.This cognitive impairment is thought to result specifically from damage to the hippocampus.In this study,we detected cognitive impairment in mice 6 weeks after repetitive mild traumatic brain injury using the novel object recognition test and the Morris water maze test.Immunofluorescence staining showed that p-tau expression was increased in the hippocampus after repetitive mild traumatic brain injury.Golgi staining showed a significant decrease in the total density of neuronal dendritic spines in the hippocampus,as well as in the density of mature dendritic spines.To investigate the specific molecular mechanisms underlying cognitive impairment due to hippocampal damage,we performed proteomic and phosphoproteomic analyses of the hippocampus with and without repetitive mild traumatic brain injury.The differentially expressed proteins were mainly enriched in inflammation,immunity,and coagulation,suggesting that non-neuronal cells are involved in the pathological changes that occur in the hippocampus in the chronic stage after repetitive mild traumatic brain injury.In contrast,differentially expressed phosphorylated proteins were mainly enriched in pathways related to neuronal function and structure,which is more consistent with neurodegeneration.We identified N-methyl-D-aspartate receptor 1 as a hub molecule involved in the response to repetitive mild traumatic brain injury,and western blotting showed that,while N-methyl-D-aspartate receptor 1 expression was not altered in the hippocampus after repetitive mild traumatic brain injury,its phosphorylation level was significantly increased,which is consistent with the omics results.Administration of GRP78608,an N-methyl-D-aspartate receptor 1 antagonist,to the hippocampus markedly improved repetitive mild traumatic brain injury-induced cognitive impairment.In conclusion,our findings suggest that N-methyl-D-aspartate receptor 1 sig

关键词： cognitive impairment Grin1 hippocampus learning memory N-methyl-D-aspartate N-methyl-D-aspartate receptor 1 phosphoproteomic proteomic repetitive mild traumatic brain injury(rmTBI) secondary injury

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Transduction pathway in the cognitive impairment of epileptic rats

Transduction pathway in the cognitive impairment of epilepti...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Sun ZHANG~(1 *) Wei-Ping WANG~2 1 Department of Neurology Bethune International Peace Hospital Shijiazhuang 050082 2 Department of Neurology Hebei Medical University 2nd hospital Shijiazhuang 050080

＜正＞Epilepsy is one of the most common diseases in nervous system.Besides the seizure attacks,about 30%-40% epileptic patients are suffering from symptoms of cognitive impairment.PI3K/Akt pathway is one of the most crucial intracellular signal transduction pathways associated with cell apoptosis,survival,proliferation,framework,and is necessary for the expression of long-term potentiation（LTP） in the dentate gyrus and CA1 region of the hippocampus.Objective To observe the changes of Akt,p-Akt（Ser473）,GSK-3β,p-GSK-3β（Ser9）,p-Tau protein in the hippocampus of epileptic rats kindled by PTZ.Methods The changes of p-Akt（Ser473）,p-GSK-3β（Ser9）,p-Tau were tested wkh immunohistochemical PV methods and the absorbency of immunohistochemical products were also detected.Total protein was extracted and the expression levels of Akt,p-Akt（Ser473）,GSK-3β,p-GSK-3β（Ser9） protein were detected by Western blot.Conclusions The protein level of p-Tau protein in the hippocampus of epileptic rats kindled by PTZ were increased postepileptic,that were coincident with the decline of learning and mnemonic capacity of epileptic model,indicating p-Tau protein in the hippocampus is a possible participant in the postepileptic cognitive dysfunction.

关键词： epilepsy cognitive impairment PI3K Akt GSK-3β

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Roles of RyRs activated calcium disorder in lead induced cognitive impairment in rats

Roles of RyRs activated calcium disorder in lead induced cog...

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2016中国毒理学会神经毒理专业委员会学术年会

作者： Fankun Zhou Guihua Du Junwang Gu Shuyun Zhang Wei Zhang Jie Xie Haizhen Liu Yanyan Gao Guangming Yin Dandan Bo Yuanyuan Zhang Chang Feng Guangqin Fan Department of Occupational Health and Toxicology School of Public HealthNanchang University

＜正＞Objective:The calcium ion,as a second messenger,plays a fundamental role in orchestrating dynamic changes in the function and structure of nerve cell circuits in the brain.Our previous and other studies found th... 详细信息

关键词： lead calcium disorder RyRs cognitive impairment

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Gut microbiome,cognitive function and brain structure:a multi-omics integration analysis

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Translational Neurodegeneration 2022年第1期11卷 178-191页

作者： Xinxiu Liang Yuanqing Fu Wen-ting Cao Zhihong Wang Ke Zhang Zengliang Jiang Xiaofang Jia Chun-ying Liu Hong-rou Lin Haili Zhong Zelei Miao Wanglong Gou Menglei Shuai Yujing Huang Shengdi Chen Bing Zhang Yu-ming Chen Ju-Sheng Zheng College of Life Sciences Zhejiang UniversityHangzhou 310058China School of Life Sciences Westlake University18 Shilongshan RdCloud TownHangzhou 310024China Guangdong Provincial Key Laboratory of Food Nutrition and HealthDepartment of Medical Statistics and EpidemiologySchool of Public HealthSun Yat-Sen UniversityGuangzhou 510080China Chinese Center for Disease Control and Prevention National Institute for Nutrition and HealthBeijing 100050China School of Public Health Hainan Medical UniversityHaikou 571199China Westlake Intelligent Biomarker Discovery Lab Westlake Laboratory of Life Sciences and BiomedicineHangzhou 310024China Department of Neurology and Institute of Neurology Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghai 200025China Key Laboratory of Trace Element Nutrition National Health CommissionBeijing 100050China Institute of Basic Medical Sciences Westlake Institute for Advanced StudyHangzhou 310024China.

Background:Microbiome-gut-brain axis may be involved in the progression of age-related cognitive impairment and relevant brain structure changes,but evidence from large human cohorts is lacking.This study was aimed to investigate the associations of gut microbiome with cognitive impairment and brain structure based on multi-omics from three independent populations.Methods:We included 1430 participants from the Guangzhou Nutrition and Health Study(GNHS)with both gut microbiome and cognitive assessment data available as a discovery cohort,of whom 272 individuals provided fecal samples twice before cognitive assessment.We selected 208 individuals with baseline microbiome data for brain magnetic resonance imaging during the follow-up visit.Fecal 16S rRNA and shotgun metagenomic sequencing,tar-geted serum metabolomics,and cytokine measurements were performed in the GNHS.The validation analyses were conducted in an Alzheimer’s disease case-control study(replication study 1,n=90)and another community-based cohort(replication study 2,n=1300)with cross-sectional dataset.Results:We found protective associations of specific gut microbial genera(Odoribacter,Butyricimonas,and Bac-teroides)with cognitive impairment in both the discovery cohort and the replication study 1.Result of Bacteroides was further validated in the replication study 2.Odoribacter was positively associated with hippocampal volume(β,0.16;95%CI 0.06-0.26,P=0.002),which might be mediated by acetic acids.Increased intra-individual alterations in gut microbial composition were found in participants with cognitive impairment.We also identified several serum metabolites and inflammation-associated metagenomic species and pathways linked to impaired cognition.Conclusions:Our findings reveal that specific gut microbial features are closely associated with cognitive impair-ment and decreased hippocampal volume,which may play an important role in dementia development.

关键词： Gut microbiome cognitive impairment Brain structure Metagenomics Microbiome-gut-brain axis Cohort

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Mesenchymal stromal cell biotherapy for Parkinson’s disease premotor symptoms

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Chinese Neurosurgical Journal 2023年第4期9卷 300-314页

作者： Jinmei Sun Wei Zhang Zheng Zachory Wei Xiaopeng Song Liu Jian Feng Jiang Shuanglin Wang Haibo Li Yongbo Zhang Houzhen Tuo The CtrLyin Group Clinical Diagnosis and Treatment Center for Parkinson’s Disease Beijing Friendship HospitalBeijingChina Laboratories of Biological Therapeutic Medical Technology Department of NeurologyBeijing Friendship Hospital Center for Neurological DisordersCapital Medical UniversityBeijingChina National Clinical Research Center for Digestive Diseases Beijing Friendship HospitalNeuroscience InstituteBeijingChina Department of Anesthesiology Emory University School of MedicineAtlantaGAUSA Beijing Tropical Medicine Research Institute BeijingChina McLean Imaging Center McLean HospitalHarvard Medical SchoolBelmontMAUSA Neuroscience Research Institute Peking UniversityBeijingChina Casstar Zhongguancun No.1 Global Key&Core Technology(AI)Innovation CenterBeijingChina Department of Critical Care Medicine Airport Hospital of Tianjin Medical University General HospitalTianjinChina Department of Cardiovascular Thoracic Surgery Tianjin Medical University General HospitalTianjinChina Department of Biochemistry and Cell Biology Geisel School of MedicineDartmouth CollegeHanoverNHUSA 不详

Parkinson’s disease(PD)is a neurodegenerative disorder with motor deficits due to nigrostriatal dopamine depletion and with the non-motor/premotor symptoms(NMS)such as anxiety,cognitive dysfunction,depression,hyposmia,and sleep disorders.NMS is presented in at least one-fifth of the patients with PD.With the histological information being investigated,stem cells are shown to provide neurotrophic supports and cellular replacement in the damaging brain areas under PD conditions.Pathological change of progressive PD includes degeneration and loss of dopaminergic neurons in the substantia nigra of the midbrain.The current stem cell beneficial effect addresses dopamine boost for the striatal neurons and gliovascular mechanisms as competing for validated PD drug targets.In addition,there are clinical interventions for improving the patient’s NMS and targeting their autonomic dysfunction,dementia,mood disorders,or sleep problems.In our and many others’research using brain injury models,multipotent mesenchymal stromal cells demonstrate an additional and unique ability to alleviate depressive-like behaviors,independent of an accelerated motor recovery.Intranasal delivery of the stem cells is discussed for it is extensively tested in rodent animal models of neurological and psychiatric disorders.In this review,we attempt to discuss the repairing potentials of transplanted cells into parkinsonism pathological regions of motor deficits and focus on preventive and treatment effects.From new approaches in the PD biological therapy,it is believed that it can as well benefit patients against PD-NMS.

关键词： Cell therapy cognitive impairment Depression Neuronal survival and differentiation Parkinson's disease

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