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amyloid beta deposition related retinal pigment epithelium cell impairment and subretinal microglia activation in aged APPswePS1 transgenic mice

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International Journal of Ophthalmology(English edition) 2018年第5期11卷 747-755页

作者： Zhi-Zhang Dong Juan Li Yi-Feng Gan Xue-Rong Sun Yun-Xia Leng Jian Ge The 2^(nd) Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University Wenzhou 325200 Zhejiang Province China Xi'an No.4 Hospital Xi'an 710000 Shaanxi Province China Institute of Aging Research Guangdong Medical CollegeDongguan 523000 Guangdong Province China Guangzhou First Municipal People's Hospital Guangzhou 510060 Guangdong Province China State Key Laboratory of Ophthalmology Zhongshan Ophthalmic Center Sun Yat-sen University Guangzhou 510060 Guangdong Province China

AIM：To identify the pathological role of amyloid beta（Aβ） deposition in retinal degeneration,and explore Aβ deposition on the retinal pigment epithelium cells（RPE） layer and the associated structural and functional changes in Alzheimer＇s disease transgenic mice.METHODS：RPE changes in the eyes of APPswe/PS1 transgenic and none transgenic（NTG） mice over 20 months old were examined.Histological changes were investigated via hematoxylin and eosin（H＆E） staining and transmission electron microscopy（TEM） examination,whereas the expression of amyloid precursor protein（APP）,Aβ,Zonula occludens-1（ZO-1） and Ionized calcium binding adaptor molecule-1（IBA-1） were investigated using immunohistochemistry and immunofluorescence techniques.All of the obtained results were quantitatively and statistically analyzed.RESULTS：In aged transgenic mice,an APP-positive immunoreaction and Aβ deposition were detected on the RPE layer but were undetectable in NTG mice.The RPE demonstrated some vacuole changes,shortened basal infoldings and basal deposition in histopathological examination and TEM tests,wherein irregular shapes were indicated by ZO-1 disorganization through fluorescence.Furthermore,IBA-1 positive cells were observed to have accumulated and infiltrated into the RPE layer and localized beneath the RPE/Bruch＇s membrane（Br M） complex,which was accompanied by an increase in BrM thickness in aged transgenic mice in comparison to NTG mice.The IBA-1 positive cells were found to be co-stained with Aβ deposition on the RPE flat mounts.CONCLUSION：The observed Aβ deposition in the RPE layer may cause RPE dysfunction,which is associated with microglia cells infiltration into the retina of aged transgenic mice,suggesting that Aβ deposition probably plays a significant role in RPE-related degenerative disease.

关键词： amyloid beta retinal pigment epithelium cells retina age related macular degeneration Alzheimer＇s disease

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The relationship between amyloid-beta and brain capillary endothelial cells in Alzheimer's disease

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Neural Regeneration Research 2022年第11期17卷 2355-2363页

作者： Yan-Li Zhang Juan Wang Zhi-Na Zhang Qiang Su Jun-Hong Guo Department of Neurology First Hospital of Shanxi Medical UniversityTaiyuanShanxi ProvinceChina Department of Neurology Sixth Hospital of Shanxi Medical University(General Hospital of Tisco)TaiyuanShanxi ProvinceChina School of Public Health Shanxi Medical UniversityTaiyuanShanxi ProvinceChina

Neurovascular dysfunction,as an integral part of Alzheimer's disease,may have an important influence on the onset and progression of chronic neurodegenerative processes.The bloodbrain barrier(BBB)pathway is one of the main pathways that mediates the clearance of amyloidbeta(Aβ)in the brain parenchyma.A large number of studies have shown that receptors and ATPbinding cassette transporte rs expressed on endothelial cells play an important role in Aβtransport across the BBB,but the specific mechanism is not clear.In this review,we summarize the possible mechanisms of Aβproduction and clearance,and in particular the relationship between Aβand brain capillary endothelial cells.Aβis produced by abnormal cleavage of the amyloid precursor protein via amyloidogenic processing under pathological conditions.Dys regulation of Aβclearance is considered to be the main reason for the massive accumulation of Aβin the brain parenchyma.Several pathways mediating Aβclearance from the brain into the periphery have been identified,including the BBB pathway,the blood-cerebros pinal fluid barrier and arachnoid granule pathway,and the lymphoidrelated pathway.Brain ca pilla ry endothelial cells are the key components of Aβclearance mediated by BBB.Receptors(such as LRP1,RAGE,and FcRn)and ATP-binding cassette transporters(such as P-gp,ABCA1,and ABCC1)expressed on endothelial cells play a critical role in Aβtranscytosis across the BBB.The toxic effects of Aβcan induce dysregulation of receptor and transpo rter expression on endothelial cells.Excessive Aβexerts potent detrimental cerebrovascular effects by promoting oxidative stress,inducing chronic inflammation,and impairing endothelial structure and functions.All of these are main causes for the reduction in Aβclearance across the BBB and the accumulation of Aβin the brain parenchyma.Therefo re,studies on the intera ctions between Aβand brain capillary endothelial cells,including their receptors and transporters,studies on inhibition of the toxic effects of Aβon endothelial cells,and stud

关键词： Alzheimer's disease amyloid beta Aβclearance blood-brain barrier cerebral amyloid angiopathy dementia endothelial cells oxidative stress review therapeutics transcytosis

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Suppression of a core metabolic enzyme dihydrolipoamide dehydrogenase (dld ) protects against amyloid beta toxicity in C.elegans model of Alzheimer’s disease

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Genes & Diseases 2021年第6期8卷 849-866页

作者： Waqar Ahmad Paul R.Ebert School of Biological Sciences The University of QueenslandBrisbaneQLD 4072Australia

A decrease in energy metabolism is associated with Alzheimer’s disease(AD),but it is not known whether the observed decrease exacerbates or protects against the disease.The importance of energy metabolism in AD is reinforced by the observation that variants of dihydrolipoamide dehydrogenase(DLD),is genetically linked to late-onset AD.To determine whether DLD is a suitable therapeutic target,we suppressed the dld-1 gene in Caenorhabditis elegans that express human Ab peptide in either muscles or neurons.Suppression of the dld-1 gene resulted in significant restoration of vitality and function that had been degraded by Ab pathology.This included protection of neurons and muscles cells.The observed decrease in proteotoxicity was associated with a decrease in the formation of toxic oligomers rather than a decrease in the abundance of the Ab peptide.The mitochondrial uncoupler,carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone(FCCP),which like dld-1 gene expression inhibits ATP synthesis,had no significant effect on Ab toxicity.Proteomics data analysis revealed that beneficial effects after dld-1 suppression could be due to change in energy metabolism and activation of the pathways associated with proteasomal degradation,improved cell signaling and longevity.Thus,some features unique to dld-1 gene suppression are responsible for the therapeutic benefit.By direct genetic intervention,we have shown that acute inhibition of dld-1 gene function may be therapeutically beneficial.This result supports the hypothesis that lowering energy metabolism protects against Ab pathogenicity and that DLD warrants further investigation as a therapeutic target.

关键词： Alzheimer’s disease amyloid beta C.elegans Dihydrolipoamide dehydrogenase(dld) Energy metabolism Neurodegeneration Proteomics

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Protective effects of Dendrobium nobile Lindl. alkaloids on amyloid beta(25–35)-induced neuronal injury

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Neural Regeneration Research 2017年第7期12卷 1131-1136页

作者： Wei Zhang Qin Wu Yan-liu Lu Qi-hai Gong Feng Zhang Jing-shan Shi Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry ofEducation Zunyi Medical University Zunyi Guizhou Province China

Dendrobium nobile Lindl.alkaloids（DNLA）,the active ingredients of a traditional Chinese medicine Dendrobium,have been shown to have anti-oxidative effects,anti-inflammatory action,and protective effect on neurons against oxygen-glucose deprivation.However,it is not clear whether DNLA reduces amyloid-beta（Aβ）-induced neuronal injury.In this study,cortical neurons were treated with DNLA at different concentrations（0.025,0.25,and 2.5 mg/L）for 24 hours,followed by administration of Aβ（25-35）（10μM）.Aβ（25-35） treatments increased cell injury as determined by the leakage of lactate dehydrogenase,which was accompanied by chromatin condensation and mitochondrial tumefaction.The damage caused by Aβ（25-35） on these cellular properties was markedly attenuated when cells were pretreated with DNLA.Treatment with Aβ（25-35）down-regulated the expressions of postsynaptic density-95 mRNA and decreased the protein expression of synaptophysin and postsynaptic density-95,all changes were significantly reduced by pretreatment of cells with DNLA.These findings suggest that DNLA reduces the cytotoxicity induced by Aβ（25-35） in rat primary cultured neurons.The protective mechanism that DNLA confers on the synaptic integrity of cultured neurons might be mediated,at least in part,through the upregulation of neurogenesis related proteins synaptophysin and postsynaptic density-95.

关键词： nerve regeneration Dendrobium nobile Lindl. alkaloids amyloid beta neurons synapse synaptophysin postsynaptic density-95 cognitive impairment neuroprotection neural regeneration

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amyloid beta通过激活NLRP3炎症小体在湿性年龄相关性黄斑变性发病中的分子机制研究

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川北医学院学报 2020年第4期35卷 551-554,567页

作者：齐赟高珊史强程育宏西安交通大学第一附属医院眼科陕西西安710061

目的:探讨amyloid beta(Aβ)通过激活核苷酸结合寡聚化结构域样受体3(NLRP3)炎症小体在湿性年龄相关性黄斑变性发病中的分子机制。方法:30只C57BL/6J小鼠按数表法随机分为对照组、实验1组与实验2组,每组各10只。实验1组与实验2组进行A... 详细信息

目的:探讨amyloid beta(Aβ)通过激活核苷酸结合寡聚化结构域样受体3(NLRP3)炎症小体在湿性年龄相关性黄斑变性发病中的分子机制。方法:30只C57BL/6J小鼠按数表法随机分为对照组、实验1组与实验2组,每组各10只。实验1组与实验2组进行Aβ玻璃体腔注射,注入剂量为1μL(1μmmol/L)Aβ与10μL(1μmmol/L)Aβ,对照组玻璃体腔内注射等量生理盐水。检测小鼠视网膜功能与NLRP3炎症小体表达变化情况。结果:所有小鼠在注射后7 d与14 d的视网膜各层结构清晰、细胞排列整齐,未出现炎症细胞浸润与明显的组织结构紊乱。玻璃体注射后7 d与14 d,实验1组与实验2组的视网膜a波振幅、b波振幅均低于对照组,且实验2组低于实验1组(P<0.05)。实验1组与实验2组玻璃体中的IL-6、TNF-α值与NLRP3、Caspase-1蛋白相对表达水平高于对照组,且实验2组高于实验1组(P<0.05)。玻璃体注射后7 d与14 d,实验1组与实验2组眼球中的SOD活性低于对照组,且实验2组低于实验1组(P<0.05)。结论:Aβ可通过激活NLRP3炎症小体的表达,抑制SOD活性,诱发炎症因子的释放,从而在湿性年龄相关性黄斑变性发病中发挥重要作用。

关键词： amyloid beta 核苷酸结合寡聚化结构域样受体3 炎症小体湿性年龄相关性黄斑变性

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amyloid beta在湿性年龄相关性黄斑变性患者中的表达及意义

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现代生物医学进展 2020年第18期20卷 3486-3489页

作者：程育宏吉梦王华齐赟史强西安交通大学第一附属医院眼科陕西西安710061 安康市中医医院眼科陕西安康725000

目的:探讨amyloid beta(Aβ)在湿性年龄相关性黄斑变性患者中的表达及意义。方法:2017年9月到2019年5月选择在本院诊治的湿性年龄相关性黄斑变性患者72例(72眼),检测血清Aβ含量,调查患者的一般资料、临床特征并进行相关性分析。结果:... 详细信息

目的:探讨amyloid beta(Aβ)在湿性年龄相关性黄斑变性患者中的表达及意义。方法:2017年9月到2019年5月选择在本院诊治的湿性年龄相关性黄斑变性患者72例(72眼),检测血清Aβ含量,调查患者的一般资料、临床特征并进行相关性分析。结果:在72例患者中,平均血清Aβ含量为203.29±14.29 ng/mL,其中Aβ含量≥180 ng/mL 40例。Aβ阳性组的脉络膜厚度显著高于Aβ阴性组(P0.05)。直线相关性分析显示血清Aβ含量与脉络膜厚度、患眼动脉舒张末期血流速度和收缩期峰值血流速度都有显著相关性(P<0.05),其中Aβ含量与脉络膜厚度呈正相关(r=0.566,P=0.003),Aβ含量与患眼动脉舒张末期血流速度和收缩期峰值血流速度呈负相关(r=-0.673,P=0.000;r=-0.455,P=0.010)。结论:Aβ在湿性年龄相关性黄斑变性患者中多呈现高表达状况,血清Aβ含量与脉络膜厚度、患眼动脉舒张末期血流速度和收缩期峰值血流速度相关,从而影响患者病情的进展。

关键词： amyloid beta 湿性年龄相关性黄斑变性脉络膜厚度血流速度

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Cerebrospinal fluid amyloid beta and tau proteins in atypical Parkinsonism: a review

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Neuroimmunology and Neuroinflammation 2020年第2期7卷 120-131页

作者： Vasilios C.Constantinides George P.Paraskevas Fotini Boufidou Mara Bourbouli Panagiotis G.Paraskevas Leonidas Stefanis Elisabeth Kapaki 1st Department of Neurology National and Kapodistrian University of AthensAthensP.C.11528Greece Department of Neurology University of CreteHeraklion 70013Greece Department of Nursing Technological Educational Institute of CreteHeraklion 71500Greece

Progressive supranuclear palsy,corticobasal degeneration,multiple system atrophy and dementia with Lewy bodies are the most common causes of atypical Parkinsonism and enter the differential diagnosis of Parkinson's disease.multiple system atrophy,dementia with Lewy bodies and Parkinson's disease are synucleinopathies,whereas progressive supranuclear palsy and corticobasal degeneration are tauopathies.Multiple cerebrospinal fluid markers have been applied on cohorts of patients with Parkinsonism,with the aim to develop biomarkers for these disorders.Total tau(τΤ),phosphorylated tau at threonine 181(τP-181)and amyloid-beta with 42 amino acids(Aβ42)are considered classical biomarkers for Alzheimer's disease.The aim of the present study is to review the literature regarding these classical cerebrospinal fluid biomarkers in cohorts with Parkinsonism,as well as present data on novel approaches regarding analysis of these proteins.

关键词： Biomarkers cerebrospinal fluid progressive supranuclear palsy corticobasal degeneration multiple system atrophy dementia with Lewy bodies tau protein phosphorylated tau protein amyloid beta

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Alzheimer’s disease risk after COVID-19:a view from the perspective of the infectious hypothesis of neurodegeneration

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Neural Regeneration Research 2023年第7期18卷 1404-1410页

作者： Eugenia Olivera Albany Sáez Lila Carniglia Carla Caruso Mercedes Lasaga Daniela Durand Instituto de Investigaciones Biomédicas INBIOMED UBA-CONICET Facultad de MedicinaUniversidad de Buenos AiresArgentina

In light of the rising evidence of the association between viral and bacterial infections and neurodegeneration,we aimed at revisiting the infectious hypothesis of Alzheimer’s disease and analyzing the possible implications of COVID-19 neurological sequelae in long-term neurodegeneration.We wondered how SARS-CoV-2 could be related to the amyloid-βcascade and how it could lead to the pathological hallmarks of the disease.We also predict a paradigm change in clinical medicine,which now has a great opportunity to conduct prospective surveillance of cognitive sequelae and progression to dementia in people who suffered severe infections together with other risk factors for Alzheimer’s disease.

关键词： Alzheimer amyloid beta antimicrobial cognitive decline COVID-19 infectious hypothesis long-term sequelae neurodegeneration neuroinflammation neurological symptoms neurotropism SARS-CoV-2

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Altered O-GlcNAcylation and mitochondrial dysfunction,a molecular link between brain glucose dysregulation and sporadic Alzheimer's disease

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Neural Regeneration Research 2023年第4期18卷 779-783页

作者： Chia-Wei Huang Nicholas C.Rust Hsueh-Fu Wu Gerald W.Hart Complex Carbohydrate Research Center University of GeorgiaAthensGAUSA Department of Biochemistry and Molecular Biology University of GeorgiaAthensGAUSA Center for Molecular Medicine University of GeorgiaAthensGAUSA

Alzheimer’s disease is a neurodegenerative disease that affected over 6.5 million people in the United States in 2021,with this number expected to double in the next 40 years without any sort of treatment.Due to its heterogeneity and complexity,the etiology of Alzheimer’s disease,especially sporadic Alzheimer’s disease,remains largely unclear.Compelling evidence suggests that brain glucose hypometabolism,preceding Alzheimer’s disease hallmarks,is involved in the pathogenesis of Alzheimer’s disease.Herein,we discuss the potential causes of reduced glucose uptake and the mechanisms underlying glucose hypometabolism and Alzheimer’s disease pathology.Specifically,decreased O-Glc NAcylation levels by glucose deficiency alter mitochondrial functions and together contribute to Alzheimer’s disease pathogenesis.One major problem with Alzheimer’s disease research is that the disease progresses for several years before the onset of any symptoms,suggesting the critical need for appropriate models to study the molecular changes in the early phase of Alzheimer’s disease progression.Therefore,this review also discusses current available sporadic Alzheimer’s disease models induced by metabolic abnormalities and provides novel directions for establishing a human neuronal sporadic Alzheimer’s disease model that better represents human sporadic Alzheimer’s disease as a metabolic disease.

关键词： Alzheimer’s disease amyloid beta brain glucose deficiency glucose uptake hypometabolism mitochondrial dysfunction neurodegenerative disease neurons O-GlcNAc Tau

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Effects of ischemia on degradation of amyloid beta

Effects of ischemia on degradation of amyloid beta

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中国神经科学学会第四次会员代表大会暨第七届全国学术会议

作者： Mi LI,Yi LIU,Xin-Ying LIU,Li-Na WANG,Miao SUN,De-Hua CHUI Neuroscience Research Institute and Department of Neurobiology Key Laboratory for Neuroscience,Ministry of Education Key Laboratory for Neuroscience,Ministry of Public Health,Peking University,Beijing 100083,.China

＜正＞Objective To investigate the changes of amyloid precursor protein（APP） processing under ischemic condition and the effects of ischemia on the expression of beta amyloid degradation enzyme neprilysin.Furthermore,to explain the new mechanisms why ischemia exacerbate the pathogenesis of Alzheimer’s disease.Methods Cells were treated with ischemia through transferring them to a ischemic humidity chamber（1%O2）.Intracellular APP metabolites were analyzed by immunoblotting.And the mRNA and protein levels of neprilysin were detected via RT-PCR and immunoblotting respectively.Results（1） Intracellular APP metabolites were increased under ischemic condition.（2） Ischemia decreased the mRNA and protein levels of neprilysin.Conclusion The increase of APP metabolites under ischemic condition is due to the reduction of neprilysin expression.

关键词： ischemia amyloid beta degradation

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