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Neural Regeneration Research 2011年第29期6卷 2245-2250页

作者： Ming Yu Lei Qin Zhao Wang Xiaohong Lu Ying Zhu Wenhui Leng Xuan Wang Department of Neurology Affiliated Hospital of Jiangsu University Zhenjiang 212001 Jiangsu Province China Department of Preventive Medicine Nanjing University of Chinese Medicine Nanjing 210046 Jiangsu Province China Department of Biochemistry Basic Medical College of Jiamusi University Jiamusi 154007 Heilongjiang Province China Department of Neurology Affiliated First Hospital of Jiamusi University Jiamusi 154002 Heilongjiang Province China

The present study observed the effects of MCI-186 on the intracellular calcium ion concentration （[Ca2＋]i） and membrane fluidity of hippocampal neurons in Alzheimer＇s disease （AD） model rats to validate the neuroprotective effects of MCI-186. Compared with normal and sham-operated rats, the escape latency was obviously prolonged, spanning platform times were obviously reduced, [Ca2＋]i was increased, and microviscosity η value was increased in AD rats. MCI-186 at 0.5 mg/mL and 0.2 mg/mL obviously shortened escape latency, increased spanning platform times and decreased [Ca2＋]i and microviscosity η values in AD rats at 7 and 17 days after induction of the model. The differences in the above-mentioned indices between normal and MCI-186-treated rats were statistically significant. MCI-186 at 0.2 mg/mL yielded better curative effects than 0.5 mg/mL MCI-186. These findings suggest that MCI-186 improves learning and memory abilities in AD rats by decreasing [Ca2＋]i and increasing membrane fluidity of hippocampal neurons.

关键词： MCI-186 Alzheimer＇s disease learning memory calcium ion neurodegenerative diseases neural regeneration

Anti-amyloid beta single-chain Fv ameliorates behavioral impairment in Alzheimer's disease mice via adeno-associated virus delivery

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Neural Regeneration Research 2011年第2期6卷 96-100页

作者： Jiong Cai Yanwei Zhong Fang Li Shizhen Wang Department of Nuclear Medicine Peking Union Medical College Hospital Chinese Academy of Medical Sciences & Peking Union MedicalCollege Beijing 100730 China Viral Hepa-titis Research Laboratory Institute of Infectious Diseases the 302 Hospital of Chinese PLA Beijing 100039 China

Intracranial delivery of human Fc-deleted antibody specific to amyloid-β peptide （Aβ, anti-Aβ single-chain Fv, scFv） via adeno-associated virus （AAV） inhibits amyloid deposition in transgenic mice. However, the effects of AAV-mediated Fc-deleted antibody on animal behavior remain unclear. In this study, the anti-Aβ scFv antibody gone, isolated from phage display, was fused to the 5＇ end of the scFv antibody gone for antibody secretion by 2 rounds of polymerase chain reaction amplification. The fused antibody cDNA was cloned into a pSNAV2 plasmid under the control of the cytomegalovirus promoter. The sequence verified expression vector pSNAV2/scFv was transferred to BHK-21 ceils, and stable transfected BHK-21/scFv cells were established by G418 selection and infected with the recombinant herpes simplex virus rHSV/repcap for AAV production. Recombinant AAV was injected into the left quadriceps femoris of PDAPP transgenic mice. After 3 months, Morris water-maze results confirmed significantly improved cognitive function in a mouse model of Alzheimer＇s disease. Key Words： Alzheimer＇s disease; adeno-associated virus; amyloid-β peptide; single-chain antibody; neurodegenerative diseases; neural regeneration

关键词： Alzheimer＇s disease adeno-associated virus amyloid-13 peptide single-chain antibody neurodegenerative diseases neural regeneration

Correlation between iron deposition and Alzheimer's disease In vivo preliminary quantitative study with susceptibility-weighted imaging

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Neural Regeneration Research 2010年第10期5卷 725-728页

作者： Jun Zhang Jianhong Wang Ke Li Daoying Geng Meirong Chen Weijun Tang Zhenguo Zhao Yuehua Li Shiguo Ma Chenggong Yan Department of Radiology Huashan Hospital Fudan University Shanghai 200040 China Department of Neurology Huashan Hospital Fudan University Shanghai 200040 China Department of Radiology Pudong New Area People's Hospital Shanghai 201200 China Department of Radiology Pudong New Area Hospital of Traditional Chinese Medicine Shanghai 201200 China

BACKGROUND： Studies have demonstrated iron deposition in Alzheimer＇s disease （AD） patients. Therefore, quantitative measurements and tracing of iron deposition are important for early detection and treatment.OBJECTIVE： To quantitatively measure iron deposition in the brain and evaluate the relationship between iron deposition and AD using magnetic susceptibility-weighted imaging. DESIGN, TIME AND SETTING： A case-control study was performed at the Department of Radiology, Huashan Hospital of Fudan University from February to July 2008. PARTICIPANTS： A total of 20 AD patients, comprising 11 males and 9 females, with a mean age of 72.5 years （range, 51-80 years）, and 20 healthy volunteers, comprising 10 males and 10 females, with a mean age of 69.9 years （range, 55-78 years）, were selected. AD was diagnosed according to the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer Disease and Related Disorders Association criteria.METHODS： Sagittal T2-weighted images were acquired to locate precise positions of the anterior and posterior commissures. The susceptibility-weighted magnetic resonance images were parallel to the anterior-posterior commissural line through the use of a three-dimensional gradient-echo sequence. All participants underwent measurement of corrected phase （CP） value and Mini-Mental State Examination. Pearson correlation coefficients were used to assess the association between CP values and Mini-Mental State Examination results.MAIN OUTCOME MEASURES： CP values of regions of interest in the hippocampal regions were measured on CP images.RESULTS： CP values were significantly reduced in bilateral hippocampal regions of AD patients compared with normal controls （P〈0.01）, but there were no significant differences between left and right CP values （P〉0.05）. The hippocampal mean CP value positively correlated with the Mini-Mental State Examination score in AD patients and normal controls （r= 0.57, P〈0.01）. CONCLUSION： Susceptibility-weighted imaging can be used to measure CP v

关键词： magnetic resonance imaging hippocampus Alzheimer＇s disease neurodegenerative diseases neural regeneration

Can outbred mice be used as a mouse model of mild cognitive impairment?

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Neural Regeneration Research 2010年第21期5卷 1650-1656页

作者： Fang Wang Wenhua Xu Chao Wang Dewu Huang Guihai Chen Department of Neurology the First Affiliated Hospital of Anhui Medical University Hefei 230022 Anhui Province China Department of Neurology the People's Hospital of Huaibei City Huaibei 235000 Anhui Province China Laboratory of Animal Center Anhui Medical University Hefei 230032 Anhui Province China

Deficits in spatial learning and memory are some of the earliest symptoms in mild cognitive impairment （MCI）. However, there are few valid MCI animal models available to evaluate putative therapeutic strategies. The aim of this study was to obtain a natural animal model of MCI. Outbred Kunming （aged 5 and 12.5 months） and ICR （7 and 12 months） mice were utilized in the present study. Morris water maze and radial six-arm water maze （RAWM） were simultaneously used to evaluate impaired spatial learning and memory in middle-aged mice （approximately 12 months of age）. Compared with younger mice in the respective groups, the middle-aged mice suffered visible impairment of spatial memory in the Morris water maze and RAWM, and mild spatial learning deficiency occurred in the RAWM study alone. Thus outbred Kunming and ICR mice could be utilized as a natural animal model for MCI, in particular for memory impairment studies.

关键词： middle-aged mice animal models memory disorders Alzheimer＇s disease neurodegenerative diseases neural regeneration

Precise location of proton of beta-secretase for catalytic aspartates(Asp 32 and Asp 228)in Alzheimer’s patients

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Neural Regeneration Research 2010年第8期5卷 572-578页

作者： Shu Liu Huaqiao Wang Lihua Zhou Zhibin Yao Department of Anatomy and Brain Research Zhongshan School of Medicine Sun Yat-sen University Guangzhou 510080 GuangdongProvince China

BACKGROUND：β-secretase （β-site APP cleavage rate-limiting enzyme, BACE） has been proposed as a promising therapeutic target for Alzheimer＇s disease （AD）. BACE inhibition reduces production of β-amyloid peptide （Aβ） and promotes neural regeneration. Two catalytic aspartates （Asp 32 and Asp 228） exist in a monoprotonated state in the active BACE site, but the precise proton location remains unclear.OBJECTIVE：To explore the entire process of BACE enzymatic hydrolysis using quantum chemistry calculations, and to identify the precise proton location for Asp 32 and Asp 228 during the enzymatic process.DESIGN, TIME AND SETTING：According to protonation state of BACE, four tautomers were designed and quantum chemistry calculations were performed at the Department of Human Anatomy, Zhongshan School of Medicine, Sun Yat-sen University, China between October 2008 and March 2009.MATERIALS：Hardware：linux workstation （Department of Equipment, Sun Yat-sen University, China）; software：QSITE, Glide, Maestro （Schrodinger LLC, USA）, MOPAC 2007 （CAChe Research LLC, USA）, Triton 4.0 （National Centre for Biomolecular Research, Czech Republic） were used.METHODS：Using crystal structures of BACE to build a catalytic model （enzyme, catalytic water, and substrate peptide EVNLAAEF） on the computer and superimposition, four BACE tautomers （32i, 320, 228i, and 2280） in the monoprotonated state were developed with Schrodinger package. Hybrid quantum mechanical/molecular mechanic （QM/MM） calculations were performed at the B3LYP density functional theory level to identify the precise proton location for the dyad aspartic residues （Asp 32 and Asp 228）. Using the most possible tautomer as the reactant, the entire enzymatic hydrolysis of substrate EVNL/AAEF was simulated at the semiempirical level.MAIN OUTCOME MEASURES：The precise proton location of was measured by analyzing co-planarities of 4 BACE tautorners （32i, 32o, 228i, and 2280） in the monoprotonated state, because the dihedral formed by the carboxyl oxygen atoms of the dyad aspartic residue

关键词： Alzheimer＇s disease β-secretase QM/MM enzymatic hydrolysis quantum chemistry calculation digital medicine neurodegenerative diseases neural regeneration

Alpha-synuclein gene structure,evolution,and protein aggregation

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Neural Regeneration Research 2010年第18期5卷 1423-1428页

作者： Lili Xiong Peng Zhao Zhiyun Guo Jianhua Zhang Diqiang Li Canquan Mao School of Life Sciences and Bioengineering Southwest Jiaotong University Chengdu 610031 Sichuan Province China Department of Pathology University of Alabama at Birmingham Birmingham AL 35294-0017 UK Institute of Forest Ecology Environment and Protection the Chinese Academy of Forestry Beijing 100091 China

α-synuclein, a member of the synuclein family, is predominately expressed in brain tissues, where it is the major component of Lewy bodies, the major hallmark of Parkinson＇s disease. We analyzed the phylogenetics, gene structure, and effects of different forms of α-synuclein on in vitro protein aggregation. The synuclein phylogenetic tree showed that sequences could be classified into α, β, and y protein groups. The orthologous gene α-, β- and y-synuclein showed similar evolutionary distance to the paralogous gene α-, β- and y-synuclein. Bioinformatics analysis suggests that the amino-acid sequence of human a-synuclein can be divided into three regions： N-terminal amphipathic region （1-60）, central hydrophobic non-amyloid beta component segment （61-95）, and the C-terminal acidic part （96-140）. The mutant site of A30P is at the second exon of α-synuclein, whereas E46K is located at the third exon of α-synuclein. α-synuclein alternative splicing results in four isomers, and five exons, all of which participate in protein coding, comprising 140 amino acids to produce the major α-synuclein in vivo. The three α-synuclein isoforms are products of alternative splicing, α-synuclein 126, 112 and 98. We also review the genetic and cellular factors that affect the aggregation of α-synuclein and compounds that inhibit aggregation. A better understanding of α-synuclein sequences, structure, and function may allow better targeted therapy and diagnosis of α-synuclein in Parkinson＇s disease and other neurodegenerative diseases.

关键词： α-synuclein bioinformatics analysis aggregation in vitro Parkinson＇s disease neurodegenerative diseases review neural regeneration

Risk factors for Parkinson's disease and interaction analysis in Chinese patients

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Neural Regeneration Research 2010年第6期5卷 476-480页

作者： Xianhua Tan Shandong Sport University Shandong Sport Scientific Research Center Jinan 250002 Shandong Province China

BACKGROUND： The etiology of Parkinson＇s disease （PD） remains unclear. The majority of studies have focused on the correlation between various factors and PD, with very different conclusions. To date, there has been no study on the interaction between PD family history and other risk factors, and very few studies have reported on hedtability. OBJECTIVE： To explore the risk factors for PD, the interaction between family history and other risk factors, and the impact of genetic factors on PD. DESIGN, TIME AND SETTNG： A paired, retrospective, case-control study was performed at the Department of Neurology, Qilu Hospital of Shandong University from November 2006 to October 2008. PARTICIPANTS： The case group included 157 Chinese PD patients selected from the Department of Neurology, Qilu Hospital of Shandong University in China from 2006 to 2008. An additional 157 patients treated in the same department during the same period were selected as the control group, and they were paired with regard to gender, age, and nationality to the case group. METHODS： Various scored factors were investigated in all participants. The association between various factors and PD was analyzed using univariate and multivariate logistic regression analysis. Interaction analysis between family history and other risk factors was performed using a logistic regression model. Heritability analysis was performed with the Falconer method. MAIN OUTCOME MEASURES： Risk factors for PD, interaction between family history and other risk factors, and heritability. RESULTS： Logistic regression analysis showed that family history, mental work, insecticide exposure, alcohol, and depression positively correlated with PD （odds ratio = 6.75, 2.37, 2.42, 2.03, 5.20, P〈 0.05）, whereas smoking had a negative correlation with PD （odds ratio = 0.49, P 〈 0.001）. The proportions of the effect attributable to interaction of family history and insecticide exposure, alcohol, and depression were 55.2%, 34.0%, and 41.4%, respectively, with a relative excess risk due to int

关键词： Parkinson＇s disease case-control study risk factor interaction heritability neurodegenerative diseases neuroregeneration

Current progress of mitochondrial transplantation that promotes neuronal regeneration

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Translational Neurodegeneration 2019年第1期8卷 203-214页

作者： Chu-Yuan Chang Min-Zong Liang Linyi Chen Institute of Molecular Medicine National Tsing Hua University101Section 2Kuang-Fu RoadHsinchu 30013Taiwan China Department of Medical Science National Tsing Hua UniversityHsinchu 30013Taiwan China

Background:Mitochondria are the major source of intracellular adenosine triphosphate(ATP)and play an essential role in a plethora of physiological functions,including the regulation of metabolism and the maintenance of cellular homeostasis.Mutations of mitochondrial DNA,proteins and impaired mitochondrial function have been implicated in the neurodegenerative diseases,stroke and injury of the central nervous system(CNS).The dynamic feature of mitochondrial fusion,fission,trafficking and turnover have also been documented in these diseases.Perspectives:A major bottleneck of traditional approach to correct mitochondria-related disorders is the difficulty of drugs or gene targeting agents to arrive at specific sub-compartments of mitochondria.Moreover,the diverse nature of mitochondrial mutations among patients makes it impossible to develop one drug for one disease.To this end,mitochondrial transplantation presents a new paradigm of therapeutic intervention that benefits neuronal survival and regeneration for neurodegenerative diseases,stroke,and CNS injury.Supplement of healthy mitochondria to damaged neurons has been reported to promote neuronal viability,activity and neurite re-growth.In this review,we provide an overview of the recent advance and development on mitochondrial therapy.Conclusion:Key parameters for the success of mitochondrial transplantation depend on the source and quality of isolated mitochondria,delivery protocol,and cellular uptake of supplemented mitochondria.To expedite clinical application of the mitochondrial transplantation,current isolation protocol needs optimization to obtain high percentage of functional mitochondria,isolated mitochondria may be packaged by biomaterials for successful delivery to brain allowing for efficient neuronal uptake.

关键词： Mitochondrial dynamics Mitochondrial therapy neurodegenerative diseases Stroke Neuronal regeneration

Synaptic plasticity effects on FeCl_2-induced post-traumatic epilepsy onset in the rat

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Neural Regeneration Research 2010年第18期5卷 1373-1377页

作者： Yuanxiang Lin Feng Wang Ruxiang Xu Xiaodan Jiang Dezhi Kang Yiquan Ke Mouxuan Du Lishuang Xu Department of Neurosurgery First Affiliated Hospital Fujian Medical University Fuzhou 350005 Fujian Province China Department of Neurosurgery Zhujiang Hospital Southern Medical University Guangzhou 510282 Guangdong Province China

Studies have confirmed that iron induces epilepsy onset, and iron ion-induced epilepsy in anima models closely resembles the clinical situation. Models of post-traumatic epilepsy （PTE） were established by intracortical injection of FeCl2 using stereotactic techniques. Electron microscopy revealed neuronal degeneration, with shrinkage of the neuronal soma, hyperplasia of rough endoplasmic reticulum, ribosomal detachment from the endoplasmic reticulum, and vacuolar degeneration of glial cells in the right frontal lobe of FeCl2-induced PTE rats. With prolonged time injuries became more severe and neuronal apoptosis was observed. Synapses in the hippocampal neuropil significantly increased （primarily type I/excitatory synapses） at day 14 following injury. Type II synapses （inhibitory synapse） were observed in the rat hippocampus at day 30. Cortical neuronal degeneration, apoptosis, glial cell proliferation, and ultrastructural hippocampal changes, in particular changes in type of neuronal synapse, play an important role in PTE onset.

关键词： post-traumatic epilepsy animal model ferrous chloride synapse synaptic plasticity electron microscope electric wire neurodegenerative diseases neural regeneration

The role of gene variants in the pathogenesis of neurodegenerative disorders as revealed by next generation sequencing studies:a review

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Translational Neurodegeneration 2017年第1期6卷 245-255页

作者： Shirley Yin-Yu Pang Kay-Cheong Teo Jacob Shujui Hsu Richard Shek-Kwan Chang Miaoxin Li Pak-Chung Sham Shu-Leong Ho Division of Neurology Department of MedicineQueen Mary HospitalUniversity of Hong KongHong KongPeople’s Republic of China Centre for Genomic Sciences University of Hong KongHong KongPeople’s Republic of China Department of Medical Genetics Zhongshan School of MedicineSun Yat-sen UniversityGuangzhouPeople’s Republic of China Key Laboratory of Tropical Disease Control(SYSU) Ministry of EducationGuangzhouPeople’s Republic of China

The clinical diagnosis of neurodegenerative disorders based on phenotype is difficult in heterogeneous conditions with overlapping symptoms.It does not take into account the disease etiology or the highly variable clinical course even amongst patients diagnosed with the same disorder.The advent of next generation sequencing(NGS)has allowed for a system-wide,unbiased approach to identify all gene variants in the genome simultaneously.With the plethora of new genes being identified,genetic rather than phenotype-based classification of Mendelian diseases such as spinocerebellar ataxia(SCA),hereditary spastic paraplegia(HSP)and Charcot-Marie-Tooth disease(CMT)has become widely accepted.It has also become clear that gene variants play a role in common and predominantly sporadic neurodegenerative diseases such as Parkinson’s disease(PD)and amyotrophic lateral sclerosis(ALS).The observation of pleiotropy has emerged,with mutations in the same gene giving rise to diverse phenotypes,which further increases the complexity of phenotype-genotype correlation.Possible mechanisms of pleiotropy include different downstream effects of different mutations in the same gene,presence of modifier genes,and oligogenic inheritance.Future directions include development of bioinformatics tools and establishment of more extensive public genotype/phenotype databases to better distinguish deleterious gene variants from benign polymorphisms,translation of genetic findings into pathogenic mechanisms through in-vitro and in-vivo studies,and ultimately finding disease-modifying therapies for neurodegenerative disorders.

关键词： Next generation sequencing neurodegenerative diseases Genetics Pleiotropy