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Comparative study of histopathology changes between the PS1/APP double transgenic mouse model and Aβ_(1-40)-injected rat model of Alzheimer disease 被引量:7
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作者 Da-Bing LI Jun TANG +3 位作者 Xiao-Tang FAN Min SONG Hai-Wei XU Yun BAI 《Neuroscience Bulletin》 SCIE CAS CSCD 2006年第1期52-57,共6页
Objective To identify the genetype of the PS1/APP double transgenie mouse model, then to analyse the histopathological changes in the brain and compare the differences between the transgenie mice models and Aβ1-40-in... Objective To identify the genetype of the PS1/APP double transgenie mouse model, then to analyse the histopathological changes in the brain and compare the differences between the transgenie mice models and Aβ1-40-injeeted rats models of Alzheimer disease. Methods The modified congo red staining, Nissl's staining and immunohistology staining was used to observe the Aβ deposits, activation of astrocyte respectively. Results ①The PS1/APP transgenic mouse extensively displayed Aβ deposits in the cortex and hippocampal structures, and GFAP positive cells were aggregated in mass and surrounded the congo red-positive plaque. ②The Aβ1-40-intrahippocmnpal-injeeted rat model showed the Aβ plaque deposits in the dentate gyrus of the hippocampus, with the astrocyte surrounded. The neurons loss was significant in the injection point and pin hole of injection with Nissl's staining methods. GFAP-positive cells increased significantly compared with the uninjected lateral of the hippocampus. Conclusion Although Aβ1-40-injected rat models could simulate some characteristic pathological features of human Alzheimer diseases, Aβ deposits and neurons loss in partial hippocampal, it would not simulate the progressive degenenration in the brain of AD. The double transgenie PS1/APP mice could simulate the specific pathogenesis and progressive changes of AD, mainly is Aβ deposits and the spongiocyte response , while no neurons loss were observed in this model. 展开更多
关键词 alzheimer disease transgenic mouse RAT Β-AMYLOID
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Transgenic Mouse (Tg2576) Is an Ideal Model for the Biological Characterization of [<sup>18</sup>F]-FDDNP for Identifying Alzheimer’s Disease
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作者 Kang-Wei Chang Shih-Ying Lee Chia-Chieh Chen 《Journal of Biosciences and Medicines》 2015年第12期1-6,共6页
[18F]-FDDNP was synthesized and characterized as a positron-emitting probe to identify Alzheimer’s disease (AD) in transgenic mouse models (Tg2576 and dE9) expressing the AD pathology. We observed in in vitro, in viv... [18F]-FDDNP was synthesized and characterized as a positron-emitting probe to identify Alzheimer’s disease (AD) in transgenic mouse models (Tg2576 and dE9) expressing the AD pathology. We observed in in vitro, in vivo, and ex vivo studies that [18F]-FDDNP accumulated specifically in the Ab-overexpressing brain regions and that this accumulation was significantly reduced by co-incubation with non-radioactive FDDNP. In ex vivo and in vivo studies of brain sections, the retention of radioactivity was more specific in Tg2576 mice than in dE9 mice. Using in vitro, ex vivo, in vivo, and ELISA analyses, we characterized the utility of [18F]-FDDNP in mapping b-amyloid in the Tg2576 mouse brain, to assess its potential application in imaging strategies. 展开更多
关键词 [18F]-FDDNP alzheimer’s disease transgenic Mice Β-AMYLOID PLAQUEs
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Liuwei Dihuang Decoction improves cognitive impairments via regulating immune system in APP/PS1 transgenic mouse, a mouse model of Alzheimer disease
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作者 Xi LEI Jian-hui WANG +5 位作者 Xiao-rui CHENG Xiao-rui ZHANG Gang LIU Jun-ping CHENG Wen-xia ZHOU Yong-xiang ZHANG 《中国药理学与毒理学杂志》 CAS CSCD 北大核心 2018年第4期291-291,共1页
OBJECTIVE To investigate the effect and mechanisms of Liuwei Dihuang Decoction(LW) on cognition in PrP-hAβPPswe/PS1ΔE9(APP/PS1) transgenic mice.METHODS LW was adminis.trated with oral for 3 months.The locomotor acti... OBJECTIVE To investigate the effect and mechanisms of Liuwei Dihuang Decoction(LW) on cognition in PrP-hAβPPswe/PS1ΔE9(APP/PS1) transgenic mice.METHODS LW was adminis.trated with oral for 3 months.The locomotor activity test was performed to investigate the spontaneous motor activity of mice.The Morris water maze test and shuttle box test were performed to investigate the spatial learning and memory and active avoidance response respectively.The Αβ deposits and neuron loss in the hippocampus was detected by immunofluorescence staining and nissl staining respectively.The flow cytometry was employed to investigate the lymphocyte subsets of the mice.The 3 H-thymidine incorporation was performed to investigate the splenocytes proliferation.RESULTS The treatment of LW ameliorated the impairments of spatial learning and memory and active and passive avoidance in APP/PS1 mice.The administration of LW alleviated neuron loss in the brain,suppressed amyloid-β(Αβ) deposits in the hippocampus of APP/PS1 mice.The treatment of LW significantly increased ConAand LPS-induced proliferation of splenocytes,increased CD3+ T cells and CD19+ B cells in the spleen lymphocytes and reduced Gr1+ cells in APP/PS1 mice.CONCLUSION This data indicated the adminis.tration of LW ameliorated behavioral and pathological deterioration via regulating immune function. 展开更多
关键词 六味地黄汤 中医 治疗方法 临床分析
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Mesenchymal stem cell-derived exosomes promote neurogenesis and cognitive function recovery in a mouse model of Alzheimer’s disease 被引量:27
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作者 Edwin E. Reza-Zaldivar Mercedes A. Hernández-Sapiéns +6 位作者 Yanet K. Gutiérrez-Mercado Sergio Sandoval-ávila Ulises Gomez-Pinedo Ana L. Márquez-Aguirre Estefanía Vázquez-Méndez Eduardo Padilla-Camberos Alejandro A. Canales-Aguirre 《Neural Regeneration Research》 SCIE CAS CSCD 2019年第9期1626-1634,共9页
Studies have shown that mesenchymal stem cell-derived exosomes can enhance neural plasticity and improve cognitive impairment.The purpose of this study was to investigate the effects of mesenchymal stem cell-derived e... Studies have shown that mesenchymal stem cell-derived exosomes can enhance neural plasticity and improve cognitive impairment.The purpose of this study was to investigate the effects of mesenchymal stem cell-derived exosomes on neurogenesis and cognitive capacity in a mouse model of Alzheimer’s disease.Alzheimer’s disease mouse models were established by injection of beta amyloid 1?42 aggregates into dentate gyrus bilaterally.Morris water maze and novel object recognition tests were performed to evaluate mouse cognitive deficits at 14 and 28 days after administration.Afterwards,neurogenesis in the subventricular zone was determined by immunofluorescence using doublecortin and PSA-NCAM antibodies.Results showed that mesenchymal stem cells-derived exosomes stimulated neurogenesis in the subventricular zone and alleviated beta amyloid 1?42-induced cognitive impairment,and these effects are similar to those shown in the mesenchymal stem cells.These findings provide evidence to validate the possibility of developing cell-free therapeutic strategies for Alzheimer’s disease.All procedures and experiments were approved by Institutional Animal Care and Use Committee(CICUAL)(approval No.CICUAL 2016-011)on April 25,2016. 展开更多
关键词 alzheimer’s disease neurodegenerative disease COGNITIVE impairment memory alzheimer’s disease mouse model mesenchymal stem cell EXOsOMEs NEUROGENEsIs COGNITIVE improvement cell-free therapy neural regeneration
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Compound Danshen tablets downregulate amyloid protein precursor mRNA expression in a transgenic cell model of Alzheimer's disease Effects and a comparison with donepezil 被引量:8
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作者 Ren'an Qin Desheng Zhou +4 位作者 Jiajun Wang Hua Hu Yang Yang Xiaoxuan Yao Xiaopeng Sun 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第9期659-663,共5页
After gene mutation, the pcDNA3.1/APP595/596 plasmid was transfected into HEK293 cells to establish a cell model of Alzheimer's disease. The cell model was treated with donepezil or compound Danshen tablets after cul... After gene mutation, the pcDNA3.1/APP595/596 plasmid was transfected into HEK293 cells to establish a cell model of Alzheimer's disease. The cell model was treated with donepezil or compound Danshen tablets after culture for 72 hours. Reverse transcription-PCR showed that the mRNA expression of amyloid protein precursor decreased in all groups following culture for 24 hours, and that there was no significant difference in the amount of decrease between donepezil and compound Danshen tablets. Our results suggest that compound Danshen tablets can reduce expression of the mRNA for amyloid protein precursor in a transgenic cell model of Alzheimer's disease, with similar effects to donepezil. 展开更多
关键词 amyloid protein precursor alzheimer’s disease transgenic cell model compound Danshen tablets Chinese medicine neural regeneration
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Can mouse models mimic sporadic Alzheimer’s disease? 被引量:4
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作者 Bettina M.Foidl Christian Humpel 《Neural Regeneration Research》 SCIE CAS CSCD 2020年第3期401-406,共6页
Alzheimer’s disease(AD)is a progressive neurodegenerative disorder and the most common form of dementia worldwide.As age is the main risk factor,>97%of all AD cases are of sporadic origin,potentiated by various ri... Alzheimer’s disease(AD)is a progressive neurodegenerative disorder and the most common form of dementia worldwide.As age is the main risk factor,>97%of all AD cases are of sporadic origin,potentiated by various risk factors associated with life style and starting at an age>60 years.Only<3%of AD cases are of genetic origin caused by mutations in the amyloid precursor protein or Presenilins 1 or 2,and symptoms already start at an age<30 years.In order to study progression of AD,as well as therapeutic strategies,mouse models are state-of-the-art.So far many transgenic mouse models have been developed and used,with mutations in the APP or presenilin or combinations(3×Tg,5×Tg).However,such transgenic mouse models more likely mimic the genetic form of AD and no information can be given how sporadic forms develop.Several risk genes,such as Apolipoprotein E4 and TREM-2 enhance the risk of sporadic AD,but also many risk factors associated with life style(e.g.,diabetes,hypercholesterolemia,stress)may play a role.In this review we discuss the current situation regarding AD mouse models,and the problems to develop a sporadic mouse model of AD. 展开更多
关键词 alzheimer’s disease BETA-AMYLOID cerebral AMYLOID ANGIOPATHY cognitive impairment sPORADIC and genetic mouse models tau vascular risk factors
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Aquaporin 4 deficiency eliminates the beneficial effects of voluntary exercise in a mouse model of Alzheimer’s disease 被引量:7
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作者 Yun Liu Pan-Pan Hu +6 位作者 Shuang Zhai Wei-Xi Feng Rui Zhang Qian Li Charles Marshall Ming Xiao Ting Wu 《Neural Regeneration Research》 SCIE CAS CSCD 2022年第9期2079-2088,共10页
Regular exercise has been shown to reduce the risk of Alzheimer’s disease(AD).Our previous study showed that the protein aquaporin 4(AQP4),which is specifically expressed on the paravascular processes of astrocytes,i... Regular exercise has been shown to reduce the risk of Alzheimer’s disease(AD).Our previous study showed that the protein aquaporin 4(AQP4),which is specifically expressed on the paravascular processes of astrocytes,is necessary for glymphatic clearance of extracellular amyloid beta(Aβ)from the brain,which can delay the progression of Alzheimer’s disease.However,it is not known whether AQP4-regulated glymphatic clearance of extracellular Aβis involved in beneficial effects of exercise in AD patients.Our results showed that after 2 months of voluntary wheel exercise,APP/PS1 mice that were 3 months old at the start of the intervention exhibited a decrease in Aβburden,glial activation,perivascular AQP4 mislocalization,impaired glymphatic transport,synapse protein loss,and learning and memory defects compared with mice not subjected to the exercise intervention.In contrast,APP/PS1 mice that were 7 months old at the start of the intervention exhibited impaired AQP4 polarity and reduced glymphatic clearance of extracellular Aβ,and the above-mentioned impairments were not alleviated after the 2-month exercise intervention.Compared with age-matched APP/PS1 mice,AQP4 knockout APP/PS1 mice had more serious defects in glymphatic function,Aβplaque deposition,and cognitive impairment,which could not be alleviated after the exercise intervention.These findings suggest that AQP4-dependent glymphatic transport is the neurobiological basis for the beneficial effects of voluntary exercises that protect against the onset of AD. 展开更多
关键词 alzheimer’s disease AMYLOID-BETA AsTROCYTEs AQUAPORIN-4 glymphatic system learning and memory synaptic protein transgenic mice voluntary exercise
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Animal models of Alzheimer's disease:Current strategies and new directions
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作者 Qing Wang Bai-Ting Zhu Peng Lei 《Zoological Research》 SCIE CSCD 2024年第6期1385-1407,共23页
Animal models constructed using pathogenic factors have significantly advanced drug development for Alzheimer's disease(AD).These predominantly transgenic models,mainly in mice,replicate pathological phenotypes th... Animal models constructed using pathogenic factors have significantly advanced drug development for Alzheimer's disease(AD).These predominantly transgenic models,mainly in mice,replicate pathological phenotypes through gene mutations associated with familial AD cases,thus serving as vital tools for assessing drug efficacy and for performing mechanistic studies.However,the speciesspecific differences and complex,heterogeneous nature of AD etiology pose considerable challenges for the translatability of these animal models,limiting their utility in drug development.This review offers a comprehensive analysis of widely employed rodent(mice and rats)and non-rodent models(Danio rerio(zebrafish),Drosophila melanogaster,and Caenorhabditis elegans),detailing their phenotypic features and specific research applications.This review also examines the limitations inherent in these models and introduces various strategies for expanding AD modeling across diverse species,emphasizing recent advancement in non-human primates(NHPs)as valuable models.Furthermore,potential insights from the integration of innovative technologies in AD research are discussed,while providing valuable perspectives on the future development of AD animal models. 展开更多
关键词 alzheimer’s disease Animal models TAU Non-human primates
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Influence of flavone extract from cultivated saussurea on learning and memory in a mouse model of Alzheimer's disease A comparison with estradiol benzoate 被引量:1
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作者 Weiqiang Chen Shuiming Gong +3 位作者 Yan Li Ming Li Zemin Yang Lirong Zhanf 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第30期2332-2336,共5页
The present study established a mouse model of Alzheimer's disease, and investigated the effects of treatment with flavone extract from artificially cultivated saussurea. A positive control group was treated with est... The present study established a mouse model of Alzheimer's disease, and investigated the effects of treatment with flavone extract from artificially cultivated saussurea. A positive control group was treated with estradiol benzoate, and learning and memory ability were examined in the 8-arm radial maze. The learning and recognition ability of mice with Alzheimer's disease treated with flavone extract was significantly improved and the number of hippocampal neurons was significantly increased in the flavone-treated and positive control groups compared with the model group. The results indicate that flavone extract from artificially cultivated saussurea can improve learning and memory deficits in mice with Alzheimer's disease, exerting effects similar to those of estradiol benzoate. 展开更多
关键词 flavone extract from saussurea alzheimers disease mouse EsTROGEN neurodegenerative disease neural regeneration
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Inhibiting 5-hydroxytryptamine receptor 3 alleviates pathological changes of a mouse model of Alzheimer's disease 被引量:1
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作者 Li-Fen Liu Yu-Tong Liu +5 位作者 Dan-Dan Wu Jie Cheng Na-Na Li Ya-Ni Zheng Liang Huang Qiong-Lan Yuan 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第9期2019-2028,共10页
Extracellular amyloid beta(Aβ) plaques are main pathological feature of Alzheimer’s disease.However,the specific type of neuro ns that produce Aβ peptides in the initial stage of Alzheimer’s disease are unknown.In... Extracellular amyloid beta(Aβ) plaques are main pathological feature of Alzheimer’s disease.However,the specific type of neuro ns that produce Aβ peptides in the initial stage of Alzheimer’s disease are unknown.In this study,we found that 5-hydroxytryptamin receptor 3A subunit(HTR3A) was highly expressed in the brain tissue of transgenic amyloid precursor protein and presenilin-1 mice(an Alzheimer’s disease model) and patients with Alzheimer’s disease.To investigate whether HTR3A-positive interneurons are associated with the production of Aβ plaques,we performed double immunostaining and found that HTR3A-positive interneurons were clustered around Aβ plaques in the mouse model.Some amyloid precursor protein-positive or β-site amyloid precursor protein cleaving enzyme-1-positive neurites near Aβ plaques were co-localized with HTR3A interneurons.These results suggest that HTR3A-positive interneurons may partially contribute to the generation of Aβ peptides.We treated 5.0-5.5-month-old model mice with tro pisetron,a HTR3 antagonist,for 8 consecutive weeks.We found that the cognitive deficit of mice was partially reversed,Aβ plaques and neuroinflammation we re remarkably reduced,the expression of HTR3 was remarkably decreased and the calcineurin/nuclear factor of activated T-cell 4 signaling pathway was inhibited in treated model mice.These findings suggest that HTR3A interneurons partly contribute to generation of Aβ peptide at the initial stage of Alzheimer’s disease and inhibiting HTR3 partly reve rses the pathological changes of Alzheimer’s disease. 展开更多
关键词 5-hydroxytryptamin receptor 3 alzheimer’s disease amyloid beta plaques CALCINEURIN cognitive deficits HTR3 interneurons iCa2%PLUs% nuclear factor of activated T-cells transgenic amyloid precursor protein and presenilin-1 mice TROPIsETRON
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Developing a better mouse model of Alzheimer disease with clinically relevant phenotypes in tau pathology
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作者 SUN An-yang 《中国药理学与毒理学杂志》 CAS CSCD 北大核心 2018年第9期687-688,共2页
OBJECTIVE Transgenic mouse model has been widely used in pathogenesis study and preclinical drug evaluation in Alzheimer disease(AD).However,key differences are found between current animal models and clinical AD pati... OBJECTIVE Transgenic mouse model has been widely used in pathogenesis study and preclinical drug evaluation in Alzheimer disease(AD).However,key differences are found between current animal models and clinical AD patients regarding phenotypes.Lack of complete models that recapitulate broad spectrum of human AD neuropathology restricts efficacy of research projects and leads to frequent failure in AD drug development at clinical trial stages.This study aims to develop better mouse models of AD through modifying key phenotype insufficiency.METHODS By crossing different single and double transgenic mice with different mutations of APP/PS1 or tau and under prion,Thy1 or PDGF-β promoter,as well as selected knockout mice,I produced a dozen of bigenic models for neuropathology screening.Further neurochemical,behavioral and pharmacological validations were conducted in the optimized mouse model.RESULTS Neuropathology phenotyping found remarkable differences in tau pathology and neurodegeneration among individual APP/PS1/tau transgenic models.I had identified a triple mouse model named FADT that showed(1) huge mature tau pathology in hippocampus and cortex;(2) abundant tau truncation,as seen in human AD brain;(3)progressive neurodegeneration;(4)selective brain atrophy in hippocampus and entorhinal cortex;(5) reproducible and late onset spatial memory defects,etc.Importantly,remarkable tau pathology in this FADT model is mainly driven by beta-amyloid pathology,which differs from high expression of tau in rTg4510 model.CONCLUSION I had developed a new triple transgenic mouse model that recapitulates broad spectrum of human AD neuropathology features.This study will not only establish a solid model basis for AD pathophysiology investigation and drug development,but also reveal important clues on the interaction of beta-amyloid and tau pathologies in the brain. 展开更多
关键词 alzheimer disease transgenic mice PHENOTYPEs model optimization TAU PATHOLOGY
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Neuroprotective profiles of anti-aging gene Klotho in Alzheimer disease mouse model
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作者 DU Jun-rong ZHAO Yue +1 位作者 ZENG Chen-ye YANG Ting-ting 《中国药理学与毒理学杂志》 CAS 北大核心 2019年第6期431-431,共1页
OBJECTIVE Alzheimer disease(AD) is the most common type of senile dementia. The anti-aging gene Klotho is reported to decline in the brain of patients and animals with AD. However, the role of Klotho in the progressio... OBJECTIVE Alzheimer disease(AD) is the most common type of senile dementia. The anti-aging gene Klotho is reported to decline in the brain of patients and animals with AD. However, the role of Klotho in the progression of AD remains elusive. The present study explored the effects and underlying mechanism of Klotho in amyloid precursor protein/presenilin 1(APP/PS1) transgenic mice. METHODS The upregulation of cerebral Klotho expression was mediated by intracerebroventricular administration of a lentiviral vector that encoded Klotho(LV-KL) in APP/PS1 transgenicmice.RESULTS LV-KL significantly increased Klotho overexpression and effectively ameliorated cognitive deficits and AD-like pathology in aged AD mice. LV-KL might induce autophagy activation and protein kinase B/mammalian target of rapamycin inhibition in both AD mice and cultured BV2 murine microglia. Meanwhile, LV-KL altered the expression of low density lipoprotein receptor-related protein 1(LRP-1), receptor for advanced glycation end products, P-glycoprotein and ABCA1 both at the brain microvascular and choroid plexus as well as the contents of plasma s LRP-1 in aged AD mice.CONCLUSION The current results indicate that Klotho plays a crucial role in the clearance of cerebral amyloid β protein and the progression of AD in mice. These findings highlight the preventive and therapeutic potential of Klotho for the treatment of AD. 展开更多
关键词 KLOTHO alzheimer disease APP/Ps1 transgenic mouse
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Transgenic dry eye mouse models: powerful tools to study dry eye disease
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作者 Dan-Yi Qin Li-Xiang Wang Ying-Ping Deng 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2022年第4期635-645,共11页
Dry eye disease(DED) is one of the most common chronic multifactorial ocular surface diseases with high prevalence and complex pathogenesis. DED results in several ocular discomforts, vision fluctuation, and even pote... Dry eye disease(DED) is one of the most common chronic multifactorial ocular surface diseases with high prevalence and complex pathogenesis. DED results in several ocular discomforts, vision fluctuation, and even potential damage of the ocular surface, bringing heavy burdens both on individuals and the society. The pathology of DED consists of tear film hyperosmolarity and immune responses on the ocular surface. Mice are widely used for developing models that simulate human DED features for investigating its pathogenesis and treatment. DED can be classified into aqueous-deficiency dry eye(ADDE) and evaporative dry eye(EDE). ADDE can be further divided into Sj?gren syndrome dry eye(SSDE) and non-Sj?gren syndrome dry eye(NSSDE). SSDE mouse models include natural strains, typified by non-obese diabetic(NOD) mice, and genetically engineered ones, like Aire-/-and Id3 knockout mice. Intrinsic EDE mainly refers to meibomian gland dysfunction(MGD). Eda-/-Tabby, Sod1-/-, Elovl1-/-are the most common transgenic MGD mouse models. Transgenic mouse models provide useful tools for studying the pathogenesis of DED and evaluating its novel therapies. This review compares the major transgenic dry eye mouse models and discusses their applications in DED research. 展开更多
关键词 dry eye disease transgenic mouse models ocular surface PATHOLOGY
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Rotating magnetic field inhibits Aβ protein aggregation and alleviates cognitive impairment in Alzheimer’s disease mice
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作者 Ruo-Wen Guo Wen-Jing Xie +5 位作者 Biao Yu Chao Song Xin-Miao Ji Xin-Yu Wang Mei Zhang Xin Zhang 《Zoological Research》 SCIE CSCD 2024年第4期924-936,共13页
Amyloid beta(Aβ)monomers aggregate to form fibrils and amyloid plaques,which are critical mechanisms in the pathogenesis of Alzheimer’s disease(AD).Given the important role of Aβ1-42 aggregation in plaque formation... Amyloid beta(Aβ)monomers aggregate to form fibrils and amyloid plaques,which are critical mechanisms in the pathogenesis of Alzheimer’s disease(AD).Given the important role of Aβ1-42 aggregation in plaque formation,leading to brain lesions and cognitive impairment,numerous studies have aimed to reduce Aβaggregation and slow AD progression.The diphenylalanine(FF)sequence is critical for amyloid aggregation,and magnetic fields can affect peptide alignment due to the diamagnetic anisotropy of aromatic rings.In this study,we examined the effects of a moderate-intensity rotating magnetic field(RMF)on Aβaggregation and AD pathogenesis.Results indicated that the RMF directly inhibited Aβamyloid fibril formation and reduced Aβ-induced cytotoxicity in neural cells in vitro.Using the AD mouse model APP/PS1,RMF restored motor abilities to healthy control levels and significantly alleviated cognitive impairments,including exploration and spatial and non-spatial memory abilities.Tissue examinations demonstrated that RMF reduced amyloid plaque accumulation,attenuated microglial activation,and reduced oxidative stress in the APP/PS1 mouse brain.These findings suggest that RMF holds considerable potential as a non-invasive,high-penetration physical approach for AD treatment. 展开更多
关键词 lzheimer’s disease Rotating magnetic field Amyloid-β Cognitive function alzheimer’s disease animal models
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Efficacy of Chinese herbal compound GAPT for the treatment of Alzheimer’s disease during mouse/rat studies:A systematic review and meta-analysis
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作者 Qingling Sun Jing Shi +6 位作者 Jingnian Ni Mingqing Wei Xuekai Zhang Ting Li Pengwen Wang Baoqiang Guo Jinzhou Tian 《Journal of Traditional Chinese Medical Sciences》 2019年第4期294-307,共14页
Objective:To evaluate the efficacy of the Chinese herbal compound GAPT for the treatment of Alzheimer’s disease(AD)and to provide current evidence for potential treatment mechanisms.Methods:A comprehensive search of ... Objective:To evaluate the efficacy of the Chinese herbal compound GAPT for the treatment of Alzheimer’s disease(AD)and to provide current evidence for potential treatment mechanisms.Methods:A comprehensive search of PubMed,Embase,Web of Science,SinoMed,China Network Knowledge Infrastructure,Wanfang Data,and Chinese Scientific Journals Database was performed to identify GAPT mouse/rat studies published from inception to July 2019.The outcomes extracted were Morris water maze results and molecular biological quantifications.Results:A total of 19 studies were included in this analysis.The analysis indicated that GAPT was able to significantly improve learning and memory abilities compared with model mice/rats,as assessed by Morris water maze,and showed similar efficacy as donepezil.Subgroup analyses showed that low,medium,and high doses resulted in no obvious dose-dependent effects.Additionally,the GAPT group had significantly reduced expression levels of amyloid-beta peptide,presenilin 1,phosphorylated tau,acetylcholinesterase,and glycogen synthase kinase-3b,but increased expression levels of Shank1,and protein phosphatase-2A,and improved synapses structures compared with the model group,and subgroup analyses showed the medium dose of GAPT was superior to the low and high doses.Conclusions:Based on the pooled analysis,GAPT improved the learning and memory abilities and regulated the expression levels of related proteins during the progression of AD in mouse/rat studies.Notably,the medium dose of GAPT exhibited better performance than the other two doses,providing experimental evidence for further applications of GAPT during clinical practice. 展开更多
关键词 Chinese herbal compound alzheimer’s disease mouse systematic review META-ANALYsIs
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Exploring the role of N-acetyltransferases in diseases:a focus on N-acetyltransferase 9 in neurodegeneration
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作者 Prajakta Deshpande Anuradha Venkatakrishnan Chimata Amit Singh 《Neural Regeneration Research》 SCIE CAS 2025年第10期2862-2871,共10页
Acetyltransferases,required to transfer an acetyl group on protein are highly conserved proteins that play a crucial role in development and disease.Protein acetylation is a common post-translational modification pivo... Acetyltransferases,required to transfer an acetyl group on protein are highly conserved proteins that play a crucial role in development and disease.Protein acetylation is a common post-translational modification pivotal to basic cellular processes.Close to 80%-90%of proteins are acetylated during translation,which is an irreversible process that affects protein structure,function,life,and localization.In this review,we have discussed the various N-acetyltransferases present in humans,their function,and how they might play a role in diseases.Furthermore,we have focused on N-acetyltransferase 9 and its role in microtubule stability.We have shed light on how N-acetyltransferase 9 and acetylation of proteins can potentially play a role in neurodegenerative diseases.We have specifically discussed the N-acetyltransferase 9-acetylation independent function and regulation of c-Jun N-terminal kinase signaling and microtubule stability during development and neurodegeneration. 展开更多
关键词 acetyl-coenzyme A alzheimer’s disease animal models cell death DROsOPHILA eye human disease c-Jun N-terminal kinase signaling N-Acetyltransferases N-acetyltransferase 9 NEURODEGENERATION
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Animal models of Alzheimer’s disease: Applications, evaluation, and perspectives 被引量:14
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作者 Zhi-Ya Chen Yan Zhang 《Zoological Research》 SCIE CAS CSCD 2022年第6期1026-1040,共15页
Although great advances in elucidating the molecular basis and pathogenesis of Alzheimer’s disease(AD)have been made and multifarious novel therapeutic approaches have been developed,AD remains an incurable disease.E... Although great advances in elucidating the molecular basis and pathogenesis of Alzheimer’s disease(AD)have been made and multifarious novel therapeutic approaches have been developed,AD remains an incurable disease.Evidence shows that AD neuropathology occurs decades before clinical presentation.AD is divided into three stages:preclinical stage,mild cognitive impairment(MCI),and AD dementia.In the natural world,some animals,such as non-human primates(NHPs)and canines,can develop spontaneous AD-like dementia.However,most animals do not develop AD.With the development of transgenic techniques,both invertebrate and vertebrate animals have been employed to uncover the mechanisms of AD and study treatment methods.Most AD research focuses on early-onset familial AD(FAD)because FAD is associated with specific genetic mutations.However,there are no well-established late-onset sporadic AD(SAD)animal models because SAD is not directly linked to any genetic mutation,and multiple environmental factors are involved.Moreover,the widely used animal models are not able to sufficiently recapitulate the pathological events that occur in the MCI or preclinical stages.This review summarizes the common models used to study AD,from yeast to NHP models,and discusses the different applications,evaluation methods,and challenges related to AD animal models,as well as prospects for the evolution of future studies. 展开更多
关键词 alzheimer’s disease Animal models NEUROINFLAMMATION Amyloid-β Tau protein
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Melatonin ameliorates microvessel abnormalities in the cerebral cortex and hippocampus in a rat model of Alzheimer’s disease 被引量:8
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作者 Pan Wang Hai-Juan Sui +3 位作者 Xiao-Jia Li Li-Na Bai Jing Bi Hong Lai 《Neural Regeneration Research》 SCIE CAS CSCD 2021年第4期787-794,共8页
Melatonin can attenuate cardiac microvascular ischemia/reperfusion injury,but it remains unclear whether melatonin can also ameliorate cerebral microvascular abnormalities.Rat models of Alzheimer’s disease were estab... Melatonin can attenuate cardiac microvascular ischemia/reperfusion injury,but it remains unclear whether melatonin can also ameliorate cerebral microvascular abnormalities.Rat models of Alzheimer’s disease were established by six intracerebroventricular injections of amyloidbeta 1–42,administered once every other day.Melatonin(30 mg/kg)was intraperitoneally administered for 13 successive days,with the first dose given 24 hours prior to the first administration of amyloid-beta 1–42.Melatonin ameliorated learning and memory impairments in the Morris water maze test,improved the morphology of microvessels in the cerebral cortex and hippocampus,increased microvessel density,alleviated pathological injuries of cerebral neurons,and decreased the expression of vascular endothelial growth factor and vascular endothelial growth factor receptors 1 and 2.These findings suggest that melatonin can improve microvessel abnormalities in the cerebral cortex and hippocampus by lowering the expression of vascular endothelial growth factor and its receptors,thereby improving the cognitive function of patients with Alzheimer’s disease.This study was approved by the Animal Care and Use Committee of Jinzhou Medical University,China(approval No.2019015)on December 6,2018. 展开更多
关键词 alzheimer’s disease brain central nervous system factor in vivo model pathways protein RAT
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Amelioration of Alzheimer's disease pathology and cognitive deficits by immunomodulatory agents in animal models of Alzheimer's disease 被引量:7
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作者 Bridget Martinez Philip V.Peplow 《Neural Regeneration Research》 SCIE CAS CSCD 2019年第7期1158-1176,共19页
The most common age-related neurodegenerative disease is Alzheimer's disease(AD) characterized by aggregated amyloid-β(Aβ) peptides in extracellular plaques and aggregated hyperphosphorylated tau protein in intr... The most common age-related neurodegenerative disease is Alzheimer's disease(AD) characterized by aggregated amyloid-β(Aβ) peptides in extracellular plaques and aggregated hyperphosphorylated tau protein in intraneuronal neurofibrillary tangles,together with loss of cholinergic neurons,synaptic alterations,and chronic inflammation within the brain.These lead to progressive impairment of cognitive function.There is evidence of innate immune activation in AD with microgliosis.Classically-activated microglia(M1 state) secrete inflammatory and neurotoxic mediators,and peripheral immune cells are recruited to inflammation sites in the brain.The few drugs approved by the US FDA for the treatment of AD improve symptoms but do not change the course of disease progression and may cause some undesirable effects.Translation of active and passive immunotherapy targeting Aβ in AD animal model trials had limited success in clinical trials.Treatment with immunomodulatory/anti-inflammatory agents early in the disease process,while not preventive,is able to inhibit the inflammatory consequences of both Aβ and tau aggregation.The studies described in this review have identified several agents with immunomodulatory properties that alleviated AD pathology and cognitive impairment in animal models of AD.The majority of the animal studies reviewed had used transgenic models of early-onset AD.More effort needs to be given to creat models of late-onset AD.The effects of a combinational therapy involving two or more of the tested pharmaceutical agents,or one of these agents given in conjunction with one of the cell-based therapies,in an aged animal model of AD would warrant investigation. 展开更多
关键词 alzheimer’s disease NEUROPATHOLOGY cognitive deficits behavioral deficits IMMUNOMODULATORY agents animal models AMYLOID deposits GLIOsIs
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Effects of Panax notoginseng saponins in a rat model of Alzheimer's disease 被引量:5
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作者 Zhenguo Zhong Zeqiang Qu +3 位作者 Yunping Bao Naiping Wang Fengfen Zhang Wenyan Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2008年第1期37-40,共4页
BACKGROUND: Modem pharmacological studies have demonstrated that Panax notoginseng saponins (PNS) can ameliorate and protect from neuropathological impairment. Whether PNS can improve the abnormality in memory and ... BACKGROUND: Modem pharmacological studies have demonstrated that Panax notoginseng saponins (PNS) can ameliorate and protect from neuropathological impairment. Whether PNS can improve the abnormality in memory and behavior of rats with Alzheimer's disease (AD) remains unclear. OBJECTIVE: Based on a Morris water maze test, this study aimed to measure improvements of spatial learning and memory by PNS in a rat model of AD, and to compare effects with huperzine A. DESIGN: A completely randomized grouping design, controlled animal experiment. SETTING: Center of Research & Development of New Drugs, Guangxi Traditional Chinese Medical University. MATERIALS: Ninety healthy Wistar rats of both genders, 15-month-old (n =75) and 3-month-old rats as young controls (n =15), were used for this study. The study was performed in accordance with animal ethics guidelines for the use and care of animals. PNS was provided by Weihe Pharmaceutical Co., Ltd (permission No. Z53021485, Yuxi, Yunan Province, China). Morris water maze equipment was provided by the Institute of Physiology, Chinese Academy of Science. METHODS: This study was performed at the Center of Research & Development of New Drugs, Guangxi Traditional Chinese Medical University from June 2003 to April 2005. Of the included rats, 15 healthy aged rats were randomly chosen as aged controls, and the remaining 60 aged rats were randomly divided into 4 groups with 15 rats in each: model group, PNS high- and low-dose groups, and an huperzine A group. Rats in the model group and the 3 treated groups were treated with intraperitoneal infusion of 9.6 g/L D-galactose (5 mL/kg) every day for 6 weeks successively to induce a subacute aging model. During week 7, animals received 1 μ L ibotenic acid (5 g/L) bilaterally into the nucleus basalis of Meynert to create a rat model of AD. The young and old rat controls received, in parallel, a corresponding volume of saline. Two weeks later, rats in the PNS high- and low-dose groups were gavaged with 200 and 100 mg/kg PNS suspension, respectively. Huperzine A suspension (0.3 mg/kg) was used in the huperzine A group. Rats in the other 3 groups were gavaged with a corresponding volume of normal saline. In each group, administration was carried out once per day for 4 consecutive weeks. MAIN OUTCOME MEASURES: After administration, learning and memory abilities were measured by place navigation and spatial probe tests. Recording indices consisted of escape latency (time-to-platform), number of times to find the platform within 2 minutes, number of times the animal crosses the original platform location, and the percent of swimming time in each quadrant. RESULTS: Several rats died due to inflammatory reactions following brain lesion or intragastric administration; therefore, 61 rats were included in the final analysis. Results of spatial navigation test: Escape latency of rats in the model group was significantly prolonged, and number of times to find the platform within 2 minutes were significantly reduced compared with other groups (both P 〈 0.05). No significant differences in these two indices were measured among the administration groups (all P 〉 0.05). Results of spatial probe test: Times for crossing the original platform location and percent of time spent in the quadrant of original platform location were significantly less in the model group than in the other groups (P 〈 0.05). There were no significant differences in these two indices among the administration groups (P 〉 0.05). CONCLUSION: PNS can remarkably improve spatial learning and memory abilities of rats with AD. The therapeutic effect of PNS is not dose-dependent and is equivalent to the effect of huperzine A. 展开更多
关键词 alzheimers disease Panax notoginseng saponins animal model Morris water maze LEARNING MEMORY
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