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Transcranial magnetic stimulation to understand pathophysiology and as potential treatment for neurodegenerative diseases

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Translational Neurodegeneration 2015年第1期4卷 184-195页

作者： Zhen Ni Robert Chen Division of Neurology Krembil Neuroscience Centre and Toronto Western Research InstituteUniversity Health NetworkUniversity of TorontoTorontoONCanada MC-411 Toronto Western Hospital399 Bathurst StreetTorontoON M5T 2S8Canada

Common neurodegenerative diseases include Parkinson’s disease(PD),Alzheimer’s disease(AD),amyotrophic lateral sclerosis(ALS)and Huntington’s disease(HD).Transcranial magnetic stimulation(TMS)is a noninvasive and painless method to stimulate the human ***-and paired-pulse TMS paradigms are powerful ways to study the pathophysiological mechanisms of neurodegenerative *** evoked potential studied with single-pulse TMS is increased in PD,AD and ALS,but is decreased in *** in motor cortical excitability in neurodegenerative diseases may be related to functional deficits in cortical circuits or to compensatory *** or even absence of short interval intracortical inhibition induced by paired-pulse TMS is common in neurodegenerative diseases,suggesting that there are functional impairments of inhibitory cortical *** short latency afferent inhibition in AD,PD and HD may be related to the cortical cholinergic deficits in these *** plasticity tested by paired associative stimulation or theta burst stimulation is impaired in PD,AD and *** TMS(rTMS)refers to the application of trains of regularly repeating TMS ***-frequency facilitatory rTMS may improve motor symptoms in PD patients whereas low-frequency inhibitory stimulation is a potential treatment for levodopa induced *** delivered both to the left and right dorsolateral prefrontal cortex improves memory in AD *** motor cortical stimulation in low frequency may be useful for HD ***,the effects of treatment with multiple sessions of rTMS for neurodegenerative diseases need to be tested in large,sham-controlled studies in the future before they can be adopted for routine clinical practice.

关键词： Alzheimer’s disease Amyotrophic lateral sclerosis Huntington’s disease Parkinson’s disease Transcranial magnetic stimulation

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TROY interacts with RhoGDIa to mediate Nogo-induced inhibition of neurite outgrowth

TROY interacts with RhoGDIa to mediate Nogo-induced inhibiti...

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中国神经科学学会第十届全国学术会议

作者： Yan LU Xiu-jie LIU Jian-feng ZHOU Jia-zhen ZHOU Cheng HE Institute of neuroscience and MOE Key Laboratory of Molecular NeurobiologyNeuroscience Research Centre of Changzheng HospitalSecond Military Medical University

TROY can functionally substitute p75 to comprise Nogo receptor complex which transduces the inhibitory signal of myelin-associated inhibitory factors（MAIFs） on axon regeneration following central nervous system（CNS）*** inhibition of neurite extension rehes on TROY-dependent RhoA activation,but how TROY activates RhoA remains *** we firstly identified RhoGDIa as a binding partner of TROY using GST（glutathione S-transferase） pull-down combined with two-dimensional gel electrophoresis and mass spectra *** interaction was further confirmed by co-immunoprecipitation in vitro and in *** mutagenesis revealed that two regions of TROY intracellular domain（234-356 aa（amino acids） and 321-350 aa） were essential for the interaction with ***,TROY and RhoGDIa were co-expressed in postnatal dorsal root ganglion（DRG） neurons,cortex neurons and cerebellar granule neurons（CGNs）.Thirdly,TROY/RhoGDIa association was potentiated by Nogo-66 and was independent of p75/RhoGDIa ***,TROY/RhoGDIainteraction was still able to activate RhoA when p75 was *** activity was only slightly decreased in p75-deficient ***,RhoGDIa overexpression abohshed RhoA activation and following neurite outgrowth inhibition by Nogo-66 in both wild-type and p75-deficient *** results showed that the association with RhoGDIa of TROY contributed to TROY-dependent RhoA activation and neurite outgrowth inhibition after Nogo-66 stimulation.

关键词： TROY RhoGDIα neurite outgrowth RhoA Nogo-66

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Advance of large-area achromatic flat lenses

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Light(Science & Applications) 2023年第3期12卷 318-320页

作者： Yubin Fan Jin Yao Din Ping Tsai Department of Electrical Engineering City University of Hong KongKowloonHong Kong 999077China centre for Biosystems Neuroscienceand NanotechnologyCity University of Hong KongKowloonHong Kong 999077China The State Key Laboratory of Terahertz and Millimeter Waves City University of Hong KongKowloonHong Kong 999077China

A new framework of light coherence optimization is proposed to design non-ideal broadband achromatic lenses,enabling large-scale flat lenses'implementation and high *** strategy paves the way for practical planar opti... 详细信息

关键词： chromatic planar optimization

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Additive effect of cerebral atrophy on cognition in dementia-free elderly with cerebrovascular disease

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Stroke & Vascular Neurology 2019年第3期4卷 135-140页

作者： Xin Xu April Phua Simon L Collinson Saima Hilal Mohammad Kamran Ikram Tien Yin Wong Ching Yu Cheng Narayanaswamy Venketasubramanian Christopher Chen Department of Pharmacology National University Singapore Yong Loo Lin School of MedicineSingaporeSingapore Department of Psychological Medicine National University HospitalSingaporeSingapore Department of Psychology National University of SingaporeSingaporeSingapore Departments of Epidemiology and Neurology Erasmus Medical CentreRotterdamThe Netherlands Singapore National Eye Center Singapore Eye Research InstituteSingaporeSingapore Raffles neuroscience centre Raffles HospitalSingaporeSingapore Clinical Research centre Department of PharmacologyNational University Health SystemSingaporeSingapore

Objective To explore the additive effect of neurodegenerative diseases,measured by atrophy,on neurocognitive function in Asian dementia-free elderly with cerebrovascular disease(CeVD).Methods The present study employed a cross-sectional design and was conducted between 2010 and 2015 among community-dwelling elderly participants recruited into the *** participants were evaluated with an extensive neuropsychological battery and *** weighted CeVD burden scale comprising markers of both small-and large-vessel diseases was applied,with a score of≥2,indicating significant CeVD *** atrophy(CA)and medial temporal atrophy(MTA)were graded using the global cortical atrophy scale and Schelten's scale,*** and domain-specific(attention,executive function,language,visuomotor speed,visuoconstruction,visual memory,and verbal memory)neurocognitive performance was measured using a locally validated neuropsychological battery(Vascular Dementia Battery,VDB).Results A total of 819 dementia-free participants were included in the *** none-mild CeVD subjects,there was no significant difference in the global cognitive performance across atrophy groups(no atrophy,CA,and CA+MTA).However,in moderate-severe CeVD subjects,CA+MTA showed significantly worse global cognitive performance compared with those with CA alone(mean difference=?0.35,95%CI?0.60 to?0.11,p=0.002)and those without atrophy(mean difference=?0.46,95%CI?0.74 to?0.19,p<0.001,p<0.001).In domain-specific cognitive performance,subjects with CA+MTA performed worse than other groups in visual memory(p=0.005),executive function(p=0.001)and visuomotor speed(p<0.001)in moderate-severe CeVD but not in none-mild *** and relevance Atrophy and moderate-severe CeVD burden showed an additive effect on global and domain-specific cognitive *** study highlights the importance of investigating the mechanisms of clinico-pathological interactions between neurodegen

关键词： atrophy effect battery

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Endovascular thrombectomy for stroke: current best practice and future goals

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Stroke & Vascular Neurology 2016年第1期1卷 16-22页

作者： Bruce C V Campbell Geoffrey A Donnan Peter J Mitchell Stephen M Davis Department of Medicine and Neurology Melbourne Brain Centre at the Royal Melbourne HospitalUniversity of MelbourneParkvilleVictoriaAustralia The Florey Institute of neuroscience and Mental Health University of MelbourneParkvilleVictoriaAustralia Department of Radiology Royal Melbourne HospitalUniversity of MelbourneParkvilleVictoriaAustralia

Endovascular thrombectomy for large vessel ischaemic stroke substantially reduces disability,with recent positive randomised trials leading to guideline changes *** review discusses in detail the evidence provided by recent randomised trials and metaanalyses,the remaining areas of uncertainty and the future directions for *** data from existing trials have demonstrated the robust benefit of endovascular thrombectomy for internal carotid and proximal middle cerebral artery *** remains for more distal occlusions where the efficacy of alteplase is greater,less tissue is at risk and the safety of endovascular procedures is less *** artery occlusion was excluded from the trials,but with a dire natural history and proof of principle that rapid reperfusion is effective,it seems reasonable to continue treating these patients pending ongoing trial *** has been no evidence of heterogeneity in treatment effect in clinically defined subgroups by age,indeed,those aged>80 years have at least as great an overall reduction in disability and reduced *** there was no heterogeneity across the range of baseline stroke severities included in the *** that routine use of general anaesthesia reduces the benefit of endovascular thrombectomy is increasing and conscious sedation is generally preferred unless severe agitation or airway compromise is *** impact of time delays has become clearer with description of onset to imaging and imaging to reperfusion *** in the onset to imaging reduce the proportion of patients with salvageable brain ***,in the presence of favourable imaging,rapid treatment appears beneficial regardless of the onset to imaging time *** to reperfusion delays lead to decay in the clinical benefit achieved,particularly in those with less robust collateral *** brain imaging options to assess prognosis have various advantages and disadvan

关键词： routine epoch benefit

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Association of Polygenic Risk Score with Age at Onset and Cerebrospinal Fluid Biomarkers of Alzheimer’s Disease in a Chinese Cohort

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neuroscience Bulletin 2020年第7期36卷 696-704页

作者： Wei-Wei Li Zhen Wang Dong-Yu Fan Ying-Ying Shen Dong-Wan Chen Hui-Yun Li Ling Li Heng Yang Yu-Hui Liu Xian-Le Bu Wang-Sheng Jin Fan Zeng Zhi-Qiang Xu Jin-Tai Yu Li-Yong Chen Yan-Jiang Wang Department of Neurology and centre for Clinical neuroscience Duping HospitalThird Military Medical UniversityChongqing 400042China Department of Anaesthesiology Daping HospitalThird Military Medical UniversityChongqing 400042China Chongqing Key Laboratory of Aging and Diseases Chongqing 400042China centre for Excellence in Brain Science and Intelligence Technology Chinese Academy of SciencesShanghai 200031China Department of Neurology Huashan HospitalFudan UniversityShanghai 200040China

To evaluate whether the polygenic profile modifies the development of sporadic Alzheimer’s disease(sAD)and pathological biomarkers in cerebrospinal fluid(CSF),462 sAD patients and 463 age-matched cognitively normal(CN)controls were genotyped for 35 singlenucleotide polymorphisms(SNPs)that are significantly associated with ***,the alleles found to be associated with sAD were used to build polygenic risk score(PRS)models to represent the genetic *** operating characteristic(ROC)analyses and the Cox proportional hazards model were used to evaluate the predictive value of PRS for the sAD risk and age at *** measured the CSF levels of Aβ42,Aβ42/Aβ40,total tau(T-tau),and phosphorylated tau(P-tau)in a subgroup(60 sAD and 200 CN participants),and analyzed their relationships with the *** found that 14 SNPs,including SNPs in the APOE,BIN1,CD33,EPHA1,SORL1,and TOMM40 genes,were associated with sAD risk in our *** PRS models built with these SNPs showed potential for discriminating sAD patients from CN controls,and were able to predict the incidence rate of sAD and age at ***,the PRSs were correlated with the CSF levels of Aβ42,Aβ42/Aβ40,T-tau,and *** study suggests that PRS models hold promise for assessing the genetic risk and development of *** genetic risk profiles vary among populations,large-scale genome-wide sequencing studies are urgently needed to identify the genetic risk loci of sAD in Chinese populations to build accurate PRS models for clinical practice.

关键词： Alzheimer's disease Single nucleotide polymorphism Polygenic risk score Cerebrospinal fluid Biomarker Amyloid-beta Tau

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Exploring the contribution of the mitochondrial disulfide relay system to Parkinson’s disease:the PINK1/CHCHD4 interplay

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Neural Regeneration Research 2021年第11期16卷 2222-2224页

作者： Giuseppe Arena Nazanine Modjtahedi Rejko Kruger Translational neuroscience group Luxembourg Centre for Systems Biomedicine(LCSB)University of LuxembourgEsch-sur-AlzetteLuxembourg UniversitéParis-Saclay Gustave Roussy InstituteCNRSMetabolic and systemic aspects of oncogenesis for new therapeutic approachesVillejuifFrance Parkinson Research Clinic Centre Hospitalier du Luxembourg(CHL)Esch-sur-AlzetteLuxembourg Transversal Translational Medicine Luxembourg Institute of Health(LIH)Esch-sur-AlzetteLuxembourg

Parkinson’s disease(PD)is a common movement disorder of the elderly caused by the degeneration of dopaminergic neurons in the substantia nigra pars compacta of the *** environmental and genetic factors pointed out mitochondrial dysfunction as a major cause of neurodegeneration in *** studies using mitochondrial toxins revealed their ability to trigger dopaminergic cell death and irreversible parkinsonism in different animal models(Poewe et al.,2017).Typical features of mitochondrial dysfunction have been also observed in the human brain of idiopathic PD cases,showing alterations of respiratory chain complex I and IV activity,accumulation of mtDNA deletions and increased oxidative stress(Bender et al.,2006).Moreover,a number of genes found mutated in familial PD forms encode for proteins involved in the maintenance of mitochondrial homeostasis and quality *** these,the PINK1 gene encodes a mitochondrial serine/threonine kinase implicated in key neuroprotective functions,including mitophagy,regulation of mitochondrial transport,control of the mitochondria/endoplasmic reticulum crosstalk and calcium homeostasis(Brunelli et al.,2020).

关键词： PINK1 homeostasis protective

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Chromatic processing in mouse retinal ganglion cells

Chromatic processing in mouse retinal ganglion cells

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Tobias Breuninger Thomas Euler centre for Integrative neuroscience（CIN） /Institute for Ophthalmic Research University of Tbingen

＜正＞Objective Color processing has been intensively studied in ganglion cells of the primate retina,but in mouse correspondent knowledge is still *** expression in mouse photoreceptor has distinct features such as opsin gradient and co-expression,but it is quite unknown how these features contribute to color processing. The main purpose of our study is to explore this *** We used dichromatic light stimulation（in the photopic range）of the short（S）and the medium（M）wavelength-sensitive mouse cone photoreceptors by two LED light *** relative contribution of S-and M-opsin to ganglion cell input was estimated by modulating the intensity of the two chromatic stimulus components sinusoidally or in *** 2-photon imaging,we targeted GFP-positive ganglion cells in transgenic mice in whole-mounted retina for extracellular *** mouse line we used（GFP-O;Feng et ai,2000）features sparse labeling of various morphological types of retinal ganglion cells. The morphology of the targeted cell was classified using image stacks taken after the ***（1）Our data show that ON alpha ganglion cells（soma diameter＞20μm,dendritic field size＞200μm）received strong M-opsin but weak S-opsin input in dorsal retina,whereas in the ventral retina they received significantly stronger S-opsin input. This is consistent with the presence of a gradient in S-opsin co-expression in M-cones along dorsal-ventral axis in mouse retina.（2）Ratios of M-opsin and S-opsin input to a single alpha ganglion cell estimated by different sizes of stimuli vary in a systematic way,which could be explained by the cooperation of opsin gradient and center-surround *** ganglion cells close to the transition zone of opsin gradient show clear color opponency when tested with large stimuli.（3）Opsin gradient could be observed in the receptive field of a single retinal ganglion cell. Conclusion Large scale opsin inhomogeneity like opsin gradient could lead to differ

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Transplanting embryonic stem cells onto damaged human corneal endothelium

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World Journal of Stem Cells 2017年第8期9卷 127-132页

作者： Charles Hanson Arsaell Arnarsson Thorir Hardarson Ann Lindgard Mandana Daneshvarnaeini Catarina Ellerstrom Anita Bruun Ulf Stenevi Unit of Reproductive Medicine Sahlgrenska University Hospital neuroscience Laboratory University of Akureyri Fertility centre Scandinavia Carlanderska Hospital Department of Ophthalmology Gothenburg University Takara Bio Europe AB Arvid Wallgrens Backe 2041346 GothenburgSweden Department of Ophthalmology Lund University Hospital

AIM To investigate whether human embryonic stem cells(hESCs) could be made to attach, grow and differentiate on a human Descemet's membrane(DM).METHODS Spontaneously differentiated hESCs were transferred onto a human corneal button with the endothelial layer removed using ocular sticks. The cells were cultured on a DM for up to 15 d. The genetically engineered hESC line expressed green fluorescent protein, which facilitated identification during the culture experiments, tissue preparation, and analysis. To detect any differentiation into human corneal endothelial-like cells, we analysed the transplanted cells by immunohistochemistry using specific *** We found transplanted cells form a single layer of cells with a hexagonal shape in the periphery of the DM. The majority of the cells were negative for octamer-binding transcription factor 4 but positive for paired box 6 protein, sodium potassium adenosine triphosphatase(NaKATPase), and Zona Occludens protein 1. In four of the 18 trials, the transplanted cells were found to express CK3, which indicates that the stem cells differentiated into corneal epithelial cells in these cases. CONCLUSION It is possible to get cells originating from hESCs to become established on a human DM, where they grow and differentiate into corneal endothelial-like cells in vitro.

关键词： Embryonic stem cells Cornea Descemet’s membrane Endothelium Immunohistochemistry

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Ferroptosis promotes T-cell activation-induced neurodegeneration in multiple sclerosis

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Cellular & Molecular Immunology 2022年第8期19卷 913-943页

作者： Jinyuan Luoqian Wenyong Yang Xulong Ding Qing-zhang Tuo Zheng Xiang Zhaoyue Zheng Yu-jie Guo Li Li Pengbo Guan Scott Ayton Biao Dong Huiyuan Zhang Hongbo Hu Peng Lei Department of Neurology and Center for Immunology and Hematology State Key Laboratory of BiotherapyNational Clinical Research Center for GeriatricsWest China HospitalSichuan UniversityCollaborative Innovation Center for BiotherapyChengduSichuanChina Melbourne Dementia Research centre Florey Institute of Neuroscience and Mental HealthThe University of MelbourneParkvilleVICAustralia

While many drugs are effective at reducing the relapse frequency of multiple sclerosis (MS), there is an unmet need for treatments that slow neurodegeneration resulting from secondary disease progression. The mechanism of neurodegeneration in MS has not yet been established. Here, we discovered a potential pathogenetic role of ferroptosis, an iron-dependent regulated cell death mechanism, in MS. We found that critical ferroptosis proteins (acyl-CoA synthetase long-chain family member 4, ACSL4) were altered in an existing genomic database of MS patients, and biochemical features of ferroptosis, including lipid reactive oxygen species (ROS) accumulation and mitochondrial shrinkage, were observed in the experimental autoimmune encephalitis (EAE) mouse model. Targeting ferroptosis with ferroptosis inhibitors or reducing ACSL4 expression improved the behavioral phenotypes of EAE mice, reduced neuroinflammation, and prevented neuronal death. We found that ferroptosis was an early event in EAE, which may promote T-cell activation through T-cell receptor (TCR) signaling in vitro and in vivo. These data indicate that ferroptosis may be a potential target for treating MS.

关键词： Ferroptosis Multiple sclerosis EAE Neurodegeneration ACSL4

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