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Cerebrospinal fluid biomarkers of Alzheimer's disease

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Neuroscience Bulletin 2014年第2期30卷 233-242页

作者： Xiaojing Sui Jianjun Liu xifei yang Key Laboratory of Modern Toxicology of Shenzhen Shenzhen Center for Disease Control and Prevention

Alzheimer＇s disease （AD） is a fatal neurodegenerative disorder that takes about a decade to develop, making early diagnosis possible. Clinically, the diagnosis of AD is complicated, costly, and inaccurate, so it is urgent to find specific biomarkers. Due to its multifactorial nature, a panel of biomarkers for the multiple pathologies of AD, such as cerebral amyloidogenesis, neuronal dysfunction, synapse loss, oxidative stress, and inflammation, are most promising for accurate diagnosis. Highly sensitive and high-throughput proteomic techniques can be applied to develop a panel of novel biomarkers for AD. In this review, we discuss the metabolism and diagnostic performance of the well-established core candidate cerebrospinal fluid （CSF） biomarkers （β-amyloid, total tau, and hyperphosphorylated tau）. Meanwhile, novel promising CSF biomarkers, especially those identified by proteomics, updated in the last five years are also extensively discussed. Furthermore, we provide perspectives on how biomarker discovery for AD is evolving.

关键词： Alzheimer's disease biomarker cerebrospinal fluid β -amyloid tau proteomics

Discovery of the first potent proteolysis targeting chimera(PROTAC) degrader of indoleamine 2,3-dioxygenase 1

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Acta Pharmaceutica Sinica B 2020年第10期10卷 1943-1953页

作者： Mingxing Hu Weilin Zhou Yijie Wang Dongping Yao Tinghong Ye Yuqin Yao Bin Chen Gongping Liu xifei yang Wei Wang Yongmei Xie State Key Laboratory of Biotherapy and Cancer Center Department of Laboratory MedicineWest China HospitalSichuan University and Collaborative Innovation Center of BiotherapyChengdu 610041China Department of Pathophysiology School of Basic Medicine and the Collaborative Innovation Center for Brain ScienceKey Laboratory of Ministry of Education of China and Hubei Province for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Innovation Center of Neuroregeneration Nantong UniversityNantong 226019China Key Laboratory of Modern Toxicology of Shenzhen Shenzhen Centre for Disease Control and PreventionShenzhen 518055China

Cancer immunotherapy is revolutionizing oncology and has emerged as a promising strategy for the treatment of multiple *** 2,3-dioxygenase 1(IDO1),an immune checkpoint,plays an important role in tumor immune escape through the regulation of multiple immune cells and has been regarded as an attractive target for cancer *** Targeting Chimeras(PROTAC)technology has emerged as a new model for drug research and development for its advantageous ***,we reported the application of PROTAC technology in targeted degradation of IDO 1,leading to the discovery of the first IDO1 PROTAC degrader 2 c,which induced significant and persistent degradation of IDO1 with maximum degradation(Dmax)of 93%in HeLa ***-blot based mechanistic studies indicated that IDO 1 was degraded by 2 c through the ubiquitin proteasome system(UPS).Label-free real-time cell analysis(RTCA)indicated that 2 c moderately improved tumorkilling activity of chimeric antigen receptor-modified T(CAR-T)***,these data provide a new insight for the application of PROTAC technology in tumor immune-related proteins and a promising tool to study the function of IDO1.

关键词： IDO1 PROTAC Protein degradation Ubiquitin proteasome system Tumor immune escape

Recombinant human erythropoietin ameliorates cognitive dysfunction of APP/PS1 mice by attenuating neuron apoptosis via HSP90β

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Signal Transduction and Targeted Therapy 2022年第6期7卷 1878-1881页

作者： Hua-Li Wan Bing-Ge Zhang Chongyang Chen Qian Liu Ting Li Ye He Yongmei Xie xifei yang Jian-Zhi Wang Gong-Ping Liu Department of Pathophysiology School of Basic MedicineKey Laboratory of Ministry of Education of China and Hubei Province for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina State Key Laboratory of Biotherapy and Cancer Center West China HospitalSichuan University and Collaborative Innovation Center of BiotherapyChengdu 610041China Key Laboratory of Modern Toxicology of Shenzhen Shenzhen Medical Key Discipline of Health Toxicology(2020-2024)Shenzhen Center for Disease Control and PreventionShenzhen 518055China Co-innovation Center of Neurodegeneration Nantong UniversityNantongJ.S.China

Dear Editor,Recently,lower hemoglobin/anemia in the elderly is found to be associated with cognitive impairment and Alzheimer’s disease(AD),1 implying that erythropoietin(EPO)may be of benefit for *** a clinically safe-to-use drug,besides its hematopoietic function,recombinant human EPO(rhEPO)is reported to present multifaceted neuroprotective effects.2 Unfortunately,few clinical studies investigated the effect of rhEPO in AD patients.

关键词： protective anemia Alzheimer

Enriched gestation activates the IGF pathway to evoke embryo-adult benefits to prevent Alzheimer’s disease

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Translational Neurodegeneration 2019年第1期8卷 94-110页

作者： Enjie Liu Qiuzhi Zhou Ao-Ji Xie Mengzhu Li Shujuan Zhang Hezhou Huang Zhenyu Liuyang Yali Wang Bingjin Liu Xiaoguang Li Dongsheng Sun Yuping Wei Xiaochuan Wang Qun Wang Dan Ke xifei yang Ying yang Jian-Zhi Wang Department of Pathophysiology School of Basic Medicine and the Collaborative Innovation Center for Brain ScienceKey Laboratory of Ministry of Education of China for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Co-innovation Center of Neuroregeneration Nantong UniversityNantong 226000China Key Laboratory of Modern Toxicology of Shenzhen Shenzhen Centre for Disease Control and Prevention8 Longyuan RoadShenzhen 518055China Department of Pathology the First Affiliated Hospital of Zhengzhou UniversityZhengzhou 450052China

Background:Building brain reserves before dementia onset could represent a promising strategy to prevent Alzheimer’s disease(AD),while how to initiate early cognitive stimulation is *** that the immature brain is more sensitive to environmental stimuli and that brain dynamics decrease with ageing,we reasoned that it would be effective to initiate cognitive stimulation against AD as early as the fetal ***:After conception,maternal AD transgenic mice(3×Tg AD)were exposed to gestational environment enrichment(GEE)until the day of *** cognitive capacity of the offspring was assessed by the Morris water maze and contextual fear-conditioning tests when the offspring were raised in a standard environment to 7 months of *** blotting,immunohistochemistry,real-time PCR,immunoprecipitation,chromatin immunoprecipitation(ChIP)assay,electrophysiology,Golgi staining,activity assays and sandwich ELISA were employed to gain insight into the mechanisms underlying the beneficial effects of GEE on embryos and 7–10-month-old adult ***:We found that GEE markedly preserved synaptic plasticity and memory capacity with amelioration of hallmark pathologies in 7–10-m-old AD *** beneficial effects of GEE were accompanied by global histone hyperacetylation,including those at bdnf promoter-binding regions,with robust BDNF mRNA and protein expression in both embryo and progeny *** increased insulin-like growth factor 1(IGF1)and activated its receptor(IGF1R),which phosphorylates Ca^(2+)/calmodulin-dependent kinase IV(CaMKIV)at tyrosine sites and triggers its nuclear translocation,subsequently upregulating histone acetyltransferase(HAT)and BDNF *** upregulation of IGF1 mimicked the effects of GEE,while IGF1R or HAT inhibition during pregnancy abolished the GEE-induced CaMKIV-dependent histone hyperacetylation and BDNF ***:These findings suggest that activation of IGF1R/CaMKIV/HAT/BDNF signal

关键词： Alzheimer’s offspring Brain-derived neurotrophic factor Gestational environment enrichment Histone acetyltransferase Insulin-like growth factor 1 receptor

轴向张力作用下As_(2)S_(3)硫系光纤的光敏性及其在Bragg光栅刻写方面的应用

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中国激光 2023年第14期50卷 178-184页

作者：邹林儿尚磊杨熙飞沈云南昌大学物理与材料学院江西南昌330031

为进一步提高硫系光纤的光敏性,基于光纤法布里-珀罗标准具原理研究了As_(2)S_(3)硫系光纤在轴向张力作用下的光敏性,结果表明施加轴向张力能显著提高其光敏性。与未施加轴向压力相比,在第一快过程中,光致折射率负变化幅度减小,经历的... 详细信息

为进一步提高硫系光纤的光敏性,基于光纤法布里-珀罗标准具原理研究了As_(2)S_(3)硫系光纤在轴向张力作用下的光敏性,结果表明施加轴向张力能显著提高其光敏性。与未施加轴向压力相比,在第一快过程中,光致折射率负变化幅度减小,经历的时间可缩短至数十秒;在第二慢过程中,光致折射率变化Δn加快朝正方向恢复,在一定张力作用下光致折射率变化Δn出现正增长,Δn增长幅度可达到5.41×10^(-3)。基于这一显著光敏性刻写了As_(2)S_(3)硫系光纤Bragg光栅,在70~110 s的短曝光时间内,光栅透射深度平均值达到了9.46 dB,且光栅光谱质量良好。本研究为制备高反射率硫系光纤光栅提供了新思路和新途径。

关键词：光纤光学硫系玻璃光纤张力光敏性光纤光栅

基于AZ5214光致保护层的As2S3硫系脊型波导制备

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光子学报 2023年第10期52卷 220-227页

作者：尚磊邹林儿杨熙飞李乐沈云南昌大学物理与材料学院南昌330031

实验研究发现AZ5214光刻胶在一定曝光剂量下显影后会留存一定厚度的底膜,该底膜可以在干法刻蚀过程中避免As-S薄膜与碱性显影液直接接触,减轻薄膜表面损伤,起到保护作用。基于此,采用该底膜作为保护层制备As2S3脊型波导,研究结果表明,在... 详细信息

实验研究发现AZ5214光刻胶在一定曝光剂量下显影后会留存一定厚度的底膜,该底膜可以在干法刻蚀过程中避免As-S薄膜与碱性显影液直接接触,减轻薄膜表面损伤,起到保护作用。基于此,采用该底膜作为保护层制备As2S3脊型波导,研究结果表明,在AZ5214光刻胶匀胶厚度为2.1μm、紫外曝光剂量为200 mJ/cm2、显影时间为45 s的条件下会留存约为220 nm厚的光致保护层,该条件下保护层均匀性较好,且在刻蚀阶段可以完全去除。实验表明利用此保护层制备的As2S3脊型波导具有良好的形貌特征,波导脊宽约为3μm、脊高约为800 nm的As2S3脊型波导的传输损耗约为0.74 dB/cm@1 550 nm。

关键词：集成光学硫系玻璃脊型波导 AZ5214光刻胶光致保护层

地夫可特改善杜氏肌营养不良症小鼠运动能力及减轻肌肉炎症损伤

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实用医学杂志 2023年第13期39卷 1614-1619,1626页

作者：杨晓张欢张朝晖杨细飞南华大学衡阳医学院公共卫生学院湖南衡阳421001 深圳市疾病预防控制中心深圳市现代毒理学重点实验室深圳市卫生毒理学医学重点学科广东深圳518055

目的了解杜氏肌营养不良症(DMD)小鼠的运动能力和骨骼肌病理改变,探索地夫可特(Deflazacort)对DMD的治疗效果。方法选取10周龄转基因DMD小鼠,根据体重随机分为正常组、模型组、地夫可特组。每组7只,实验周期8周,小鼠每周称重1次。在小... 详细信息

目的了解杜氏肌营养不良症(DMD)小鼠的运动能力和骨骼肌病理改变,探索地夫可特(Deflazacort)对DMD的治疗效果。方法选取10周龄转基因DMD小鼠,根据体重随机分为正常组、模型组、地夫可特组。每组7只,实验周期8周,小鼠每周称重1次。在小鼠10周龄、14周龄和18周龄时,通过悬挂测试、爬杆测试、抓握力测试评估小鼠运动能力。18周龄时采取步态测试分析小鼠四肢步幅距离和步行速度变化。小鼠安乐死后,通过检测血清肌酸激酶、乳酸脱氢酶、肌肉病理组织学和形态学分析评估肌肉病变情况。结果与模型组小鼠相比,地夫可特组小鼠体质量无显著变化、悬挂时间延长(P<0.05)、爬杆耗时减少(P<0.01)、前肢抓力增大(P<0.05)、步幅距离和步行速度增加(P<0.01)、血清肌酸激酶值降低、骨骼肌炎性细胞浸润面积(P<0.01)和纤维化面积减少。结论地夫可特治疗具有改善DMD小鼠运动功能减退,步态缓滞失衡和骨骼肌炎症损伤的作用。

关键词：地夫可特杜氏肌营养不良症运动能力骨骼肌损伤炎症

Copper exposure aggravates motor phenotype via inhibiting mitophagy in SOD1G93A transgenic mice

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Copper exposure aggravates motor phenotype via inhibiting mi...

Lentivirus-mediated silencing of I2PP2A through RNA interference attenuates trichloroethylene-induced cytotoxicity in human hepatic L-02 cells

中国毒理学会第十次全国毒理学大会

作者： Huan Zhang Chuanyue Gao Deguang yang Lulin Nie Kaiwu He Chongyang Chen Shangming Li Guangqin Huang Li Zhou Jianjun Liu xifei yang

BACKGROUD Amyotrophic lateral sclerosis(ALS) is an age-dependent and incurable neurodegenerative disease. It is pathologically characterized by selective degeneration of motor neurons resulting in a catastrophic loss of motor function. Previous studies showed that excess copper(Cu) might have a role in ALS etiology. OBJECTIVE however, the underlying mechanism remains incompletely elucidated. Therefore, we aimed to investigate the neurotoxicity and underlying mechanism of Cu exposure in female ALS mice with SOD1G93A gene mutation. METHODS and RESULTS after three months of treatment with low-dose Cu exposure(0.13 PPM copper chloride drinking water), the ALS mice displayed increased movement disorder via multiple behavioral methods, including pole climbing, rotarod, hanging, grip, and gait analysis. Concurrently, Cu exposure worsened muscle fibrosis, aggravated spinal motor neuron loss and coincided with neuroinflammation. The proteomic analysis further showed that differentially expressed proteins among wild-type mice(WT), ALS mice, and Cutreated ALS mice were mainly involved in muscle contraction, ATP metabolic processes, immune responses, peroxisomes, mitochondrial electrons respiratory transport chain, GMP biological processes,and were co-related with disturbances in energy metabolism, which was reflected in mitochondrial dysfunction in ALS mice. Moreover, Cu treatment reduced the expression of mitochondrial function-related proteins, consistent with the results determined by proteomic analysis. CONCLUSION our findings showed that Cu exposure aggravates motor dysfunction and pathological changes in ALS mice via mitochondrial dysfunction.

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Lentivirus-mediated silencing of I2PP2A through RNA interfer...