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Progress on early diagnosing Alzheimer’s disease

Frontiers of Medicine 2024年第3期18卷 446-464页

作者： Yixin Chen Murad Al-Nusaif Song Li Xiang Tan huijia yang.huaibin cai Weidong Le Liaoning Provincial Key Laboratory for Research on the Pathogenic Mechanisms of Neurological Diseases The First Affiliated Hospital of Dalian Medical UniversityDalian116021China Transgenic Section Laboratory of NeurogeneticsNational Institute on AgingNational Institutes of HealthBethesdaMD20892USA Institute of Neurology Sichuan Provincial People’s HospitalUniversity of Electronic Science and Technology of ChinaChinese Academy of Sciences Sichuan Translational Medicine Research HospitalChengdu610072China

Alzheimer’s disease(AD)is a progressive neurodegenerative disorder that affects both cognition and non-cognition *** disease follows a continuum,starting with preclinical stages,progressing to mild cognitive and behavioral impairment,ultimately leading to *** detection of AD is crucial for better diagnosis and more effective ***,the current AD diagnostic tests of biomarkers using cerebrospinal fluid and/or brain imaging are invasive or expensive,and mostly are still not able to detect early disease ***,there is an urgent need to develop new diagnostic techniques with higher sensitivity and specificity during the preclinical stages of *** non-cognitive manifestations,including behavioral abnormalities,sleep disturbances,sensory dysfunctions,and physical changes,have been observed in the preclinical AD stage before occurrence of notable cognitive *** research advances have identified several biofluid biomarkers as early indicators of *** review focuses on these non-cognitive changes and newly discovered biomarkers in AD,specifically addressing the preclinical stages of the ***,it is of importance to explore the potential for developing a predictive system or network to forecast disease onset and progression at the early stage of AD.

关键词： Alzheimer’s disease early diagnosis non-cognitive symptoms biomarkers

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广东省贫困县土地利用多功能与脱贫成效耦合协调关系及障碍诊断

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农业资源与环境学报 2024年第4期41卷 976-988页

作者：蔡怀滨王枫华南农业大学公共管理学院广州510642 自然资源部华南热带亚热带自然资源监测重点实验室广州510700

为探究2014—2020年广东省贫困县土地利用多功能与脱贫成效耦合协调关系及其障碍因素,本研究基于土地利用多功能与脱贫成效耦合协调机理构建评价指标体系,运用熵权法、耦合协调度模型和障碍度模型测度二者的耦合协调关系及障碍因素。结... 详细信息

为探究2014—2020年广东省贫困县土地利用多功能与脱贫成效耦合协调关系及其障碍因素,本研究基于土地利用多功能与脱贫成效耦合协调机理构建评价指标体系,运用熵权法、耦合协调度模型和障碍度模型测度二者的耦合协调关系及障碍因素。结果表明:土地利用多功能与脱贫成效水平均呈增长态势且增幅水平基本相当;土地利用多功能综合评价指数均值由0.2397上升到0.2681,增长11.85%,空间上呈“核心-边缘”分布格局;脱贫成效综合评价指数均值由0.3567上升到0.3987,增长11.77%,空间上由均匀散布转向中部集聚增长;耦合协调度从0.5290上升到0.5598,增长5.82%,均以初级协调为主,空间上由整体均匀散布转向局部高等级提升;耦合协调类型以土地利用多功能滞后型为主,较为均匀散布全域;制约二者耦合协调的主要障碍因素(障碍度大于5%)相对稳定,集中于文化和社会类指标,但其障碍度呈现不同幅度上升或下降的演变态势。研究表明,广东省贫困县土地利用多功能与脱贫成效整体尚处于初级协调水平,未来促进二者耦合协调应强化对障碍因素的控制与管理,结合不同耦合协调类型分类施策,有序推进全域土地综合整治、有效衔接脱贫成果与乡村振兴、有力支撑同步协调联动机制。

关键词：土地利用多功能脱贫成效耦合协调度时空分异障碍因素贫困县广东省

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线粒体病分子诊断技术进展

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国际检验医学杂志 2024年第17期45卷 2049-2057页

作者：沈丽君王娅周怀彬陈连婷蔡雯方合志浙江省医学遗传学重点实验室/温州医科大学检验医学院(生命科学学院) 浙江温州325035

线粒体病是一类重要的遗传代谢病,其发病可覆盖全年龄段,尤其是儿童线粒体病致死致残率极高。随着生物化学及分子与细胞生物学技术的发展,线粒体病的实验室诊断经历了快速的发展,相关诊断路径和策略也从高度有创的实验室检测逐渐过渡到... 详细信息

线粒体病是一类重要的遗传代谢病,其发病可覆盖全年龄段,尤其是儿童线粒体病致死致残率极高。随着生物化学及分子与细胞生物学技术的发展,线粒体病的实验室诊断经历了快速的发展,相关诊断路径和策略也从高度有创的实验室检测逐渐过渡到以无创筛查为主。但是,线粒体病实验室诊断仍然存在单一检测策略的阳性诊断率不足、实验室漏检与待排查比例居高不下的困扰,因此新的线粒体病检测技术被开发并用于协助疾病的诊断。该文从基因、酶生物化学与代谢生物学3个层面对当前线粒体病实验室诊断的进展进行综述,旨在为特定场景下线粒体病实验室诊断策略选择提供参考,也为后续检测技术的研发提供一些建议。

关键词：线粒体病诊断标志物氧化磷酸化

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Opioid system in L-DOPA-induced dyskinesia

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Translational Neurodegeneration 2017年第1期6卷 1-5页

作者： Jing Pan huaibin cai Transgenics Section Laboratory of NeurogeneticsNational Institute on AgingNational Institutes of HealthBuilding 35Room 1A112MSC 370735 Convent DriveBethesdaMD 20892-3707USA

L-3,4-Dihydroxyphenylalanine(L-DOPA)-induced dyskinesia(LID)is a major clinical complication in the treatment of Parkinson’s disease(PD).This debilitating side effect likely reflects aberrant compensatory responses for a combination of dopaminergic neuron denervation and repeated L-DOPA *** endogenous opioid signal transduction pathways in basal ganglia have been well documented in *** receptors have been targeted to alleviate the ***,the exact role of this altered opioid activity is remains under active *** the present review,we discuss the current understanding of opioid signal transduction in the basal ganglia and how the malfunction of opioid signaling contributes to the pathophysiology of *** study of the opioid system in LID may lead to new therapeutic targets and improved treatment of PD patients.

关键词： opioid endogenous system

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AGE-induced neuronal cell death is enhanced in G2019S LRRK2 mutation with increased RAGE expression

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Translational Neurodegeneration 2018年第1期7卷 1-8页

作者： Hyun Jin Cho Chengsong Xie huaibin cai Department of Biochemistry and Biomedical Sciences Seoul National UniversityCollege of Medicine28 Yungun-dongJongro-guSeoul 110-799South Korea Transgenics Section Laboratory of NeurogeneticsNational Institute on AgingNational Institutes of HealthBuilding 35Room 1A112MSC 370735 Convent DriveBethesdaMD 20892–3707USA

Background:Leucine-rich repeat kinase 2(LRRK2)mutations represent the most common genetic cause of sporadic and familial Parkinson’s disease(PD).Especially,LRRK2 G2019S missense mutation has been identified as the most prevalent genetic cause in the late-onset *** glycation end products(AGEs)are produced in high amounts in diabetes and diverse aging-related disorders,such as cardiovascular disease,renal disease,and neurological *** trigger intracellular signaling pathway associated with oxidative stress and inflammation as well as cell ***,receptor of AGEs,is activated by interaction with AGEs and mediates AGE-induced *** AGE and RAGE are involved in the pathogenesis of mutant LRRK2 is ***:Using cell lines transfected with mutant LRRK2 as well as primary neuronal cultures derived from LRRK2 wild-type(WT)and G2019S transgenic mice,we compared the impact of AGE treatment on the survival of control and mutant cells by *** also examined the levels of RAGE proteins in the brains of transgenic mice and PD patients by western ***:We show that LRRK2 G2019S mutant-expressing neurons were more sensitive to AGE-induced cell death compared to ***,we found that the levels of RAGE proteins were upregulated in LRRK2 G2019S mutant ***:These data suggest that enhanced AGE-RAGE interaction contributes to LRRK2 G2019S mutation-mediated progressive neuronal loss in PD.

关键词： Parkinson’s disease LRRK2 G2019S AGE RAGE Neuronal death

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Aldehyde Dehydrogenase 1 making molecular inroads into the differential vulnerability of nigrostriatal dopaminergic neuron subtypes in Parkinson’s disease

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Translational Neurodegeneration 2014年第1期3卷 212-218页

作者： huaibin cai Guoxiang Liu Lixin Sun Jinhui Ding Transgenics Section Laboratory of NeurogeneticsNational Institute on AgingNational Institutes of HealthBethesdaMD 20892USA Computational Biology Core Laboratory of NeurogeneticsNational Institute on AgingNational Institutes of HealthBethesdaMD 20892USA

A preferential dysfunction/loss of dopaminergic(DA)neurons in the substantia nigra pars compacta(SNpc)accounts for the main motor symptoms of Parkinson’s disease(PD),the most common degenerative movement ***,the neuronal loss is not stochastic,but rather displays regionally selectivity,indicating the existence of different DA subpopulations in the *** identify the underlying molecular determinants is thereby instrumental in understanding the pathophysiological mechanisms of PD-related neuron dysfunction/loss and offering new therapeutic ***,we have demonstrated that aldehyde dehydrogenase 1(ALDH1A1)is one such molecular determinant that defines and protects an SNpc DA neuron subpopulation preferentially affected in *** this review,we provide further analysis and discussion on the roles of ALDH1A1 in the function and survival of SNpc DA neurons in both rodent and human *** also explore the feasibility of ALDH1A1 as a potential biomarker and therapeutic target for PD.

关键词： Parkinson’s disease Substantia nigra pars compacta Dopaminergic neuron Aldehyde dehydrogenase 1,α-synuclein Neurodegeneration Aging

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No apparent transmission of transgenic α–synuclein into nigrostriatal dopaminergic neurons in multiple mouse models

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Translational Neurodegeneration 2015年第1期4卷 196-204页

作者： Namratha Sastry Wang Zheng Guoxiang Liu Helen Wang Xi Chen Michael cai Parth Contractor Carmelo Sgobio Lixin Sun Chengsong Xie huaibin cai Transgenics Section Laboratory of NeurogeneticsNational Institute on AgingNational Institutes of HealthBuilding 35Room 1A112MSC 370735 Convent DriveBethesdaMD 20892-3707USA Unit on Synapse Development Plasticity Clinical Brain Disorder BranchNational Institute of Mental HealthNational Institutes of HealthBethesdaMD 20892USA Present addresses:Feinberg School of Medicine Northwestern UniversityChicagoIL 60611USA Present addresses:Swarthmore College SwarthmorePA 19081USA Present addresses:Centennial High School Elicott CityMD 21042USA Present addresses:George Washington University WashingtonDC 20052USA

Background:α–synuclein(α–syn)is the main component of intracytoplasmic inclusions deposited in the brains of patients with Parkinson’s disease(PD)and certain other neurodegenerative *** studies have explored the ability ofα–syn to propagate between or across neighboring neurons and supposedly“infect”them with a prion–like ***,much of this research has used stereotaxic injections of heterologousα–syn fibrils to induce the spreading of inclusions in the rodent ***α–syn is able to transmit from the host cells to their neighboring cells in vivo is ***:Using immunestaining,we examined the potential propagation ofα–syn into nigrostriatal dopaminergic(DA)neurons in three lines of transgenic mice that overexpress human wild–typeα–syn(hα–syn)in different neuron ***:After testing for three different routes by which hα–syn propagation might occur,we were unable to find any evidence that hα–syn behaved like a prion and could be transmitted overtime into the DA neurons initially lack of hα–syn ***:In transgenic mice hα–syn does not have the ability to propagate at pathologically significant levels between or across *** must be noted that these observations do not disprove the studies that show its prion–like qualities,but rather that propagation is not detectable in transgenic models that do not use any injections of heterologous proteins or viral vectors to induce a spreading state.

关键词： Parkinson’s disease α-synuclein Propagation Dopaminergic neurons Transgenic mice

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ER Transport and Stress in Parkinson’s disease and ALS

ER Transport and Stress in Parkinson’s disease and ALS

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中国神经科学学会第十二届全国学术会议

作者： huaibin cai NIH-NIA

Impairments of ER transport and associated ER stress have been implicated in the pathogenesis of degenerative neurological disorders, including Parkinson’s disease（PD） and amyotrophic lateral sclerosis（ALS）. Leucine-rich repeat kinase 2（LRRK2） has been linked to PD and other disorders. However, its normal physiological functions and pathogenic properties remain elusive. Here we show that LRRK2 regulates the anterograde ER-Golgi transport through anchoring Sec16 A at the endoplasmic reticulum exit sites（ERES）. LRRK2 interacted and co-localized with Sec16 A, a key protein in the formation of ERES. Lrrk2 depletion caused a dispersion of Sec16 A from ERES and impaired ER export. In neurons, LRRK2 and Sec16 A showed extensive co-localization at the dendritic ERES（d ERES） that locally regulate the transport of proteins to the dendritic spines. A loss of Lrrk2 affected the association of Sec16 A with d ERES and impaired the activity-dependent targeting of glutamate receptors onto the cell/synapse surface. Furthermore, the PD-related LRRK2 R1441 C missense mutation in the GTPase domain interfered with the interaction of LRRK2 with Sec16 A and also affected ER-Golgi transport, while LRRK2 kinase activity was not required for these functions. Therefore, our findings reveal a new physiological function of LRRK2 in ER-Golgi transport, suggesting ERES dysfunction may contribute to the pathogenesis of PD. The substitution of Proline with Serine at residue 56（P56 S） of vesicle-associated membrane proteinassociated protein B（VAPB） has been linked to an atypical autosomal dominant form of familial ALS（ALS8）. To investigate the pathogenic mechanism of P56 S VAPB in ALS, we generated transgenic（Tg） mice that heterologously express human wild-type（WT） and P56 S VAPB under the control of a pan-neuronal promoter Thy1.2. While WT VAPB Tg mice did not exhibit any overt motor behavioral phenotypes, P56 S VAPB Tg mice developed progressive hyperactivities and other motor abnormalities. VAPB

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A calcineurin and NFAT-dependent pathway is involved in asynuclein-induced degeneration of midbrain dopaminergic neurons

A calcineurin and NFAT-dependent pathway is involved in asyn...

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中国生物化学与分子生物学会第十一次会员代表大会暨201...

作者：骆静 huaibin cai 北京师范大学

Parkinson’s disease(PD),the most common degenerative movement disorder,is causedby a preferential loss of midbrain dopaminergic(mDA)*** a-synuclein(a-syn)missense and multiplication mutations have been linked to ***,the underlyingintracellular signalling transduction pathways of a-syn-mediated mDA neurodegenerationremain ***,we show that transgenic expression of PD-related human a-syn A53Tmissense mutation promoted calcineurin(CN)activity and the subsequent nuclear translocationof nuclear factor of activated T-cells(NFAT)in mDA neurons.a-syn enhanced thephosphatase activity of CN in both cell-free assays and cell lines transfected with either humanwild-type or A53T ***,over-expression of a-syn A53T mutation significantlyincreased the CN-dependent nuclear import of NFATc3 in the mDA neurons oftransgenic *** importantly,a pharmacological inhibition of CN by cyclosporine A(CsA)ameliorated the a-syn-induced loss of mDA *** findings demonstrate theactive involvement of the CNand NFAT-mediated signalling pathway in the a-synmediateddegeneration of mDA neurons in PD.

关键词： Parkinson Disease calcineurin alpha-synuclein NFAT midbrain A53T transgenic mice

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高原训练对游泳运动员凝血纤溶系统的影响

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中国体育科技 2022年第8期58卷 22-26页

作者：林微微陈慧佳蔡力韩照岐浙江体育职业技术学院浙江杭州311231

目的:通过TF、TFPI-1、TF/TFPI-1以及t-PA、PAI-1、t-PA/PAI-1的变化情况,分析高原训练对游泳运动员血液凝血纤溶功能的影响。方法:10名游泳运动员在昆明体育训练基地进行高原训练,高原训练前5天及高原训练第3、10、17、24、31天清晨空... 详细信息

目的:通过TF、TFPI-1、TF/TFPI-1以及t-PA、PAI-1、t-PA/PAI-1的变化情况,分析高原训练对游泳运动员血液凝血纤溶功能的影响。方法:10名游泳运动员在昆明体育训练基地进行高原训练,高原训练前5天及高原训练第3、10、17、24、31天清晨空腹抽取静脉血,采用酶联免疫法检测HIF-1、TF、TFPI-1、t-PA、PAI-1的含量变化。结果:HIF-1:高原训练第10天的HIF-1显著高于高原训练前5天及第3天水平;第31天的HIF-1显著低于第10天水平。TF、TFPI-1:高原训练第10天的TF、TFPI-1显著高于高原训练前5天水平;第17天的TF显著低于第10天水平;第17天的TF/TFPI-1显著或非常显著低于高原训练前5天、第3天及第10天水平;第31天的TF/TFPI-1非常显著低于高原训练前5天水平。t-PA:高原训练第10天的t-PA显著高于前5天水平;第17天的t-PA显著或非常显著高于高原训练前5天及第3天水平;第24、31天的t-PA显著高于高原训练前5天水平,同时,显著低于第17天水平。PAI-1:高原训练第17天的PAI-1显著或非常显著高于高原训练前5天、第3天及第10天水平;第24、31天的PAI-1显著低于第17天水平。t-PA/PAI-1:高原训练期间的t-PA/PAI-1均显著或非常显著高于高原训练前5天水平。结论:在高原训练中,游泳运动员血液凝血功能先升后降,但纤溶功能维持较高水平,从而避免促凝可能引起的血栓形成。

关键词：游泳高原训练低氧诱导因子-1 凝血纤溶

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