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Gamma-glutamyl transferase 5 overexpression in cerebrovascular endothelial cells improves brain pathology,cognition,and behavior in app/ps1 mice

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Neural Regeneration Research 2025年第2期20卷 533-547页

作者： Yanli Zhang Tian Li Jie Miao Zhina Zhang Mingxuan Yang Zhuoran Wang Bo Yang Jiawei Zhang Haiting Li Qiang Su Junhong 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 Department of Physiology Key Laboratory of Cellular PhysiologyMinistry of EducationShanxi Medical UniversityTaiyuanShanxi ProvinceChina Department of Hernia and Abdominal Wall Surgery Shanxi Bethune HospitalShanxi Academy of Medical SciencesTongji Shanxi HospitalThird Hospital of Shanxi Medical UniversityTaiyuanShanxi ProvinceChina Department of Laboratory Medicine of Fenyang College Shanxi Medical UniversityFenyangShanxi ProvinceChina

In patients with Alzheimer’s disease,gamma-glutamyl transferase 5(GGT5)expression has been observed to be downregulated in cerebrovascular endothelial ***,the functional role of GGT5 in the development of Alzheimer’s disease remains *** study aimed to explore the effect of GGT5 on cognitive function and brain pathology in an app/ps1 mouse model of Alzheimer’s disease,as well as the underlying *** observed a significant reduction in GGT5 expression in two in vitro models of Alzheimer’s disease(Aβ_(1-42)-treated hCMEC/D3 and bEnd.3 cells),as well as in the app/ps1 mouse ***,injection of app/ps1 mice with an adeno-associated virus encoding GGT5 enhanced hippocampal synaptic plasticity and mitigated cognitive ***,increasing GGT5 expression in cerebrovascular endothelial cells reduced levels of both soluble and insoluble amyloid-βin the brains of app/ps1 *** effect may be attributable to inhibition of the expression ofβ-site app cleaving enzyme 1,which is mediated by nuclear factor-kappa *** findings demonstrate that GGT5 expression in cerebrovascular endothelial cells is inversely associated with Alzheimer’s disease pathogenesis,and that GGT5 upregulation mitigates cognitive deficits in app/ps1 *** findings suggest that GGT5 expression in cerebrovascular endothelial cells is a potential therapeutic target and biomarker for Alzheimer’s disease.

关键词： Alzheimer’s disease amyloid-β app/ps1 mice cerebrovascular endothelial cells cognitive deficits gamma-glutamyl transferase 5 neurovascular unit nuclear factor‐kappa B synaptic plasticity β-site app cleaving enzyme 1

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AAV mediated carboxyl terminus of Hsp70 interacting protein overexpression mitigates the cognitive and pathological phenotypes of app/ps1 mice

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Neural Regeneration Research 2025年第1期20卷 253-264页

作者： Zhengwei Hu Jing Yang Shuo Zhang Mengjie Li Chunyan Zuo Chengyuan Mao Zhongxian Zhang Mibo Tang Changhe Shi Yuming Xu Department of Neurology The First Affiliated Hospital of Zhengzhou UniversityZhengzhou UniversityZhengzhouHenan ProvinceChina Academy of Medical Sciences of Zhengzhou University ZhengzhouHenan ProvinceChina NHC Key Laboratory of Prevention and treatment of Cerebrovascular Diseases The First Affiliated Hospital of Zhengzhou UniversityZhengzhou UniversityZhengzhouHenan ProvinceChina Henan Key Laboratory of Cerebrovascular Diseases The First Affiliated Hospital of Zhengzhou UniversityZhengzhou UniversityZhengzhouHenan ProvinceChina Institute of Neuroscience Zhengzhou UniversityZhengzhouHenan ProvinceChina Sino-British Research Centre for Molecular Oncology National Centre for International Research in Cell and Gene TherapySchool of Basic Medical SciencesAcademy of Medical SciencesZhengzhou UniversityZhengzhouHenan ProvinceChina Department of Gerontology The First Affiliated Hospital of Zhengzhou UniversityZhengzhou UniversityZhengzhouHenan ProvinceChina

The E3 ubiquitin ligase,carboxyl terminus of heat shock protein 70(Hsp70)interacting protein(CHIP),also functions as a co-chaperone and plays a crucial role in the protein quality control *** this study,we aimed to investigate the neuroprotective effect of overexpressed CHIP on Alzheimer’s *** used an adeno-associated virus vector that can cross the blood-brain barrier to mediate CHIP overexpression in app/ps1 mouse *** overexpression significantly ameliorated the performance of app/ps1 mice in the Morris water maze and nest building tests,reduced amyloid-βplaques,and decreased the expression of both amyloid-βand phosphorylated *** also alleviated the concentration of microglia and astrocytes around *** app/ps1 mice of a younger age,CHIP overexpression promoted an increase in ADAM10 expression and inhibitedβ-site app cleaving enzyme 1,insulin degrading enzyme,and neprilysin *** of HSP70 and HSP40,which have functional relevance to CHIP,were also *** nuclei transcriptome sequencing in the hippocampus of CHIP overexpressed mice showed that the lysosomal pathway and oligodendrocyte-related biological processes were up-regulated,which may also reflect a potential mechanism for the neuroprotective effect of *** research shows that CHIP effectively reduces the behavior and pathological manifestations of app/ps1 ***,overexpression of CHIP could be a beneficial approach for the treatment of Alzheimer’s disease.

关键词： adeno-associated virus Alzheimer’s disease app/ps1 mice carboxyl terminus of Hsp70 interacting protein gene therapy

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Ketogenic diet alleviates cognitive dysfunction and neuroinflammation in app/ps1 mice via the Nrf2/HO-1 and NF-κB signaling pathways

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Neural Regeneration Research 2023年第12期18卷 2767-2772页

作者： Jingwen Jiang Hong Pan Fanxia Shen Yuyan Tan Shengdi Chen Department of Neurology and Institute of Neurology Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghaiChina Lab of Translational Research of Neurodegenerative Diseases Institute of ImmunochemistryShanghaiTech UniversityShanghaiChina

Alzheimer's disease is a progressive neurological disorder characterized by cognitive decline and chronic inflammation within the *** ketogenic diet,a widely recognized therapeutic intervention for refractory epilepsy,has recently been proposed as a potential treatment for a variety of neurological diseases,including Alzheimer's ***,the efficacy of ketogenic diet in treating Alzheimer's disease and the underlying mechanism remains *** current investigation aimed to explore the effect of ketogenic diet on cognitive function and the underlying biological mechanisms in a mouse model of Alzheimer's *** amyloid precursor protein/presenilin 1(app/ps1)mice were randomly assigned to either a ketogenic diet or control diet group,and received their respective diets for a duration of 3 *** findings show that ketogenic diet administration enhanced cognitive function,attenuated amyloid plaque formation and proinflammatory cytokine levels in app/ps1 mice,and augmented the nuclear factor-erythroid 2-p45 derived factor 2/heme oxygenase-1 signaling pathway while suppressing the nuclear factor-kappa B ***,these data suggest that ketogenic diet may have a therapeutic potential in treating Alzheimer's disease by ameliorating the neurotoxicity associated with Aβ-induced *** study highlights the urgent need for further research into the use of ketogenic diet as a potential therapy for Alzheimer's disease.

关键词： Alzheimer's disease app/ps1 mice cognitive impairment ketogenic diet neuroinflammation nuclear factor-kappa B pathway nuclear factor-erythroid 2-p45 derived factor 2/heme oxygenase-1 therapeutic benefits

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Long-term exercise training inhibits inflammation by suppressing hippocampal NLRP3 in app/ps1 mice

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Sports Medicine and Health Science 2023年第4期5卷 329-335页

作者： Xue Li Yu Jin Xianyi Ding Tongyang Zhu Changling Wei Li Yao School of Sports Medicine and Health Chengdu Sport UniversityChengduSichuanChina

Behavioral experiments have demonstrated that long-term physical exercise can be beneficial for learning and memory dysfunction caused by neuroinflammation in Alzheimer's disease(AD).However,the molecular mechanism remains poorly understood due to a lack of sufficient pertinent biochemical *** investigated the potential effect of long-term physical exercise on cognition and hippocampal gene and protein expression changes in a transgenic AD mouse *** twenty weeks of treadmill exercise,transgenic AD mice showed improvement in cognitive functions and downregulation of Nod-like receptor protein 3(NLRP3)(p1),interleukin-1beta(IL-1β)(p1-42(Aβ1-42)(pmice(p1),which might be a result of the downregulation of NLRP3-mediated signaling and neuroinflammatory *** neuronal damage due to inflammation might be a likely cause of AD-associated cognitive *** results suggested that the anti-inflammatory effects of exercise training involved downregulating the expression of key inflammatory factors and might play an important role in protecting hippocampal neurons against damage during the course of AD.

关键词： Exercise NLRP3 Neuroinflammation Hippocampus app/ps1 mice Alzheimer's

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The role of MS/vDB-hippocampus cholinergic pathway in app/ps1 mice at early stage

The role of MS/vDB-hippocampus cholinergic pathway in APP/PS...

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中国神经科学学会第十二届全国学术会议

作者： Xi Chen Li Yang Cheng Long School of Life Sciences South China Normal University School of psychology South China Normal University Institute of Brain Science and Rehabilitation Medicine South China Normal University

The two main pathological manifestation of Alzheimer’s disease（AD） are senile plaques（Aβ） and neurofibrillary tangle（the major component is the abnormally phosphorylated microtubule binding protein tau）. Although presenilin（ps） and apolipoprotein E（ApoE） are also of concern, the mainstream direction of AD research has been focused on the Aβand tau. However, there is growing evidence that abnormal synaptic transmission disorder before Aβphosphate deposition and tau in the pathological features of AD in the central nervous system, the damage of cholinergic synaptic activity is particularly significant. The studies in AD patients also found that synaptic damage and dysfunction were the major factors affecting dementia, and that the association with cognitive impairment was more pronounced than amyloid plaques and neuronal loss. This suggests that there may be other mechanisms mediated by early onset AD. Neurons in the medial septum（MS） and vertical diagonal band of Broca（v DB） predominantly extend their axons to the hippocampus, forming the MS/v DB-hippocampal pathway, which play an important role in spatial memory. So,we study on whether young AD mice show cognitive behavioral abnormalities and what the role of cholinergic system plays in it. Material 3.5-5 month-old app/ps1 mice and age-matched littermate wild-type mice were used. app/ps1 mice expressing mouse/human chimeric app gene（appswe） and mutant psEN1（Delta E9）, suitable for the study of AD effect especially in early stage of neurodegeneration and synaptic activity disorder, is an ideal animal model of internationally recognized, widely used in research related to the AD. According to reports, app/ps1 mice showed decreased learning ability with increasing age, it is similar to AD cognitive impairment, moreover, the structure and function of synaptic connections in the hippocampus of the brain are abnormal. Methods In vivo double channel extracellular recording and Morris water maze test were employed. Results（

关键词： Alzheimer’s disease app/ps1 mice water maze Ms/vDB-hippocampus extracellular recording

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The neuroprotective effects of fluoxetine on the neurons and synapses in the hippocampus of the middle-aged app/ps1 mice

The neuroprotective effects of fluoxetine on the neurons and...

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中国神经科学学会第十二届全国学术会议

作者： Jing Ma Yuan Gao Lin Jiang Feng-lei Chao Wei Huang Chun-ni Zhou Wei Tang Lei Zhang Chun-xia Huang Yi Zhang Yan-min Luo Qian Xiao Hua-rong Yu Yong Tang Department of Histology and Embryology Chongqing Medical University Laboratory of Stem Cells and Tissue Engineering Chongqing Medical University Department of Geriatrics The First Affiliated Hospital Chongqing Medical University Department of Physiology Chongqing Medical University

Objective In order to understand the reasons for the neuroprotective effect of fluoxetine（FLX） on Alzheimer’s disease（AD）, the current study investigated the effects of FLX on the neurons and synapses of the hippocampus in the middle-aged app/ps1 mice. Methods Forty 16-17 month-old male app/ps1 mice were respectively randomly assigned to control group（app/ps1） or treated group（app/ps1+FLX）. Meanwhile, the wild-type（WT） mice with the same age were considered as normal control group. All mice in three groups were randomly assigned to receive systemic administration of either fluoxetine（10 mg/kg i.p. dissolved in 0.9 % Na Cl） or vehicle（equivalent 0.9 % Na Cl i.p.） once per day in the morning between 9 AM and 10 AM for 5 consecutive weeks. In the 5 th week, the Morris water maze was performed to assess the spatial learning and memory abilities. Immunohistochemical staining was used to examine the effect of FLX on the deposition of beta amyloid in middle-aged app/ps1 mice. Western blotting technique was conducted to investigate the effect of FLX on the protein expressions of Tau and Phospho-Tau（Ser396） in the middle-aged app/ps1 mice. Immunohistochemical staining and the stereological analyses were performed to investigate the effect of FLX on the number of neurons and dendritic spine synapses in the hippocampus of middleaged app/ps1 mice. Results In the hidden platform trials, the middle-aged app/ps1 mice revealed significantly higher increasing escape latencies compared with the WT mice（p ＜ 0.01）, while the escape latency of the app/ps1 mice in the FLX-treated（app/ps1+FLX） group was markedly lower than the latency of the mice in the app/ps1 group（p ＜ 0.05）. In the subsequent probe task, the frequency at which the mice crossed the platform location was not statistically different among the three groups. There was hardly any aggregation of beta amyloid in the hippocampus in the WT mice, but in the app/ps1 and app/ps1+FLX mice, beta amyloid was found to have aggregated i

关键词： app/ps1 mice Hippocampus Fluoxetine Stereology

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Ceftriaxone improves learning and memory deficits of app/ps1 transgenic mice in early stage of Alzheimer’s disease

Ceftriaxone improves learning and memory deficits of APP/PS1...

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中国神经科学学会第十二届全国学术会议

作者： Shu-Juan Fan Xiao-Hui Xian Yu-Yan Hu Min Zhang Wen-Bin Li Department of Pathophysiology Hebei Medical University

Objective Glial glutamate transporter-1（GLT-1） is impaired in Alzheimer’s disease（AD）. Ceftriaxone（Cef） has been reported to up-regulate the expression and uptake activity of GLT-1. The present study was undertaken to explore whether Cef upregulate the expression of GLT-1 and proteins associated with glutamate-glutamine cycle and then alleviate the cognitive deficits in 6-and 7-month app/ps1 mice. Methods The cognitive function, expression of GLT-1 and proteins related to glutamate-glutamine cycle and level of Aβ in hippocampus were assayed by Novel object recognition and Morris water maze tests, immunohistochemistry, western blot and ELISA, respectively. Results Cef treatment（200 mg/kg and 300 mg/kg） markedly improved cognitive deficits of app/ps1 mice and up-regulated the expression of GLT-1 in hippocampus. Moreover, Cef up-regulated the activity of glutamine synthetase, the expression of system N glutamine transporter SN1, system A transporter GlnT and vesicular glutamate transporters, which were related to the glutamate-glutamine cycle. Conclusion Cef could improve cognitive deficits of app/ps1 mice in early stage of AD by up-regulating GLT-1 expression and the effectiveness of glutamate-glutamine cycle.

关键词： Ceftriaxone app/ps1 mice GLT-1 Morris water maze Alzheimer’s disease Glutamate-glutamine cycle

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Lamotrigine protects against cognitive deficits,synapse and nerve cell damage,and hallmark neuropathologies in a mouse model of Alzheimer’s disease

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Neural Regeneration Research 2023年第1期18卷 189-193页

作者： Xin-Xin Fu Rui Duan Si-Yu Wang Qiao-Quan Zhang Bin Wei Ting Huang Peng-Yu Gong Yan E Teng Jiang Ying-Dong Zhang School of Basic Medicine and Clinical Pharmacy China Pharmaceutical UniversityNanjingJiangsu ProvinceChina Department of Neurology Nanjing First HospitalNanjing Medical UniversityNanjingJiangsu ProvinceChina Department of Pathology Nanjing Brain HospitalNanjing Medical UniversityNanjingJiangsu ProvinceChina

Lamotrigine(LTG)is a widely used drug for the treatment of *** clinical evidence suggests that LTG may improve cognitive function in patients with Alzheimer’s ***,the underlying molecular mechanisms remain *** this study,amyloid precursor protein/presenilin 1(app/ps1)double transgenic mice were used as a model of Alzheimer’s ***-month-old app/ps1 mice were intragastrically administered 30 mg/kg LTG or vehicle once per day for 3 successive *** cognitive functions of animals were assessed using Morris water *** tau and markers of synapse and glial cells were detected by western blot *** cell damage in the brain was investigated using hematoxylin and eosin *** levels of amyloid-βand the concentrations of interleukin-1β,interleukin-6 and tumor necrosis factor-αin the brain were measured using enzyme-linked immunosorbent *** expressed genes in the brain after LTG treatment were analyzed by high-throughput RNA sequencing and real-time polymerase chain *** found that LTG substantially improved spatial cognitive deficits of app/ps1 mice;alleviated damage to synapses and nerve cells in the brain;and reduced amyloid-βlevels,tau protein hyperphosphorylation,and inflammatory ***-throughput RNA sequencing revealed that the beneficial effects of LTG on Alzheimer’s disease-related neuropathologies may have been mediated by the regulation of Ptgds,Cd74,Map3k1,Fosb,and Spp1 expression in the *** findings revealed potential molecular mechanisms by which LTG treatment improved Alzheimer’s ***,these data indicate that LTG may be a promising therapeutic drug for Alzheimer’s disease.

关键词： Alzheimer’s disease Alzheimer’s disease-related neuropathologies amyloid-βpathology app/ps1 mice cognitive deficits damage of synapses and nerve cells high-throughput RNA sequencing lamotrigine neuroinflammation tau protein hyperphosphorylation

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The relationship among amyloid-βdeposition,sphingomyelin level,and the expression and function of P-glycoprotein in Alzheimer’s disease pathological process

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Neural Regeneration Research 2023年第6期18卷 1300-1307页

作者： Zi-Kang Xing Li-Sha Du Xin Fang Heng Liang Sheng-Nan Zhang Lei Shi Chun-Xiang Kuang Tian-Xiong Han Qing Yang State Key Laboratory of Genetic Engineering School of Life SciencesShanghai Engineering Research Center of Industrial MicroorganismsFudan UniversityShanghaiChina Shanghai Key Lab of Chemical Assessment and Sustainability School of Chemical Science and EngineeringTongji UniversityShanghaiChina Department of Traditional Chinese Medicine Tenth People’s Hospital of Tongji UniversityShanghaiChina

In Alzheimer’s disease,the transporter P-glycoprotein is responsible for the clearance of amyloid-βin the ***-βcorrelates with the sphingomyelin metabolism,and sphingomyelin participates in the regulation of *** amyloid cascade hypothesis describes amyloid-βas the central cause of Alzheimer’s disease *** understanding of the change of P-glycoprotein and sphingomyelin along with amyloid-βand their potential association in the pathological process of Alzheimer’s disease is ***,we found that the expression of P-glycoprotein in app/ps1 mice tended to increase with age and was significantly higher at 9 and 12 months of age than that in wild-type mice at comparable *** functionality of P-glycoprotein of app/ps1 mice did not change with age but was significantly lower than that of wild-type mice at 12 months of *** sphingomyelin levels,increased ceramide levels,and the increased expression and activity of neutral sphingomyelinase 1 were observed in app/ps1 mice at 9 and 12 months of age compared with the levels in wild-type *** results were observed in the Alzheimer’s disease mouse model induced by intracerebroventricular injection of amyloid-β1-42 and human cerebral microvascular endothelial cells treated with amyloid-β*** human cerebral microvascular endothelial cells,neutral sphingomyelinase 1 inhibitor interfered with the changes of sphingomyelin metabolism and P-glycoprotein expression and functionality caused by amyloid-β1-42 *** sphingomyelinase 1 regulated the expression and functionality of P-glycoprotein and the levels of sphingomyelin and ***,these findings indicate that neutral sphingomyelinase 1 regulates the expression and function of P-glycoprotein via the sphingomyelin/ceramide *** studies may serve as new pursuits for the development of anti-Alzheimer’s disease drugs.

关键词： Alzheimer’s disease amyloid-β app/ps1 mice ceramide ezrin-radixin-moesin human cerebral microvascular endothelial cells neutral sphingomyelinase 1 P-glycoprotein sphingomyelin synthase sphingomyelin

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The Alzheimer's disease-associated gene TREML2 modulates inflammation by regulating microglia polarization and NLRP3 inflammasome activation

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Neural Regeneration Research 2023年第2期18卷 434-438页

作者： Si-Yu Wang Xin-Xin Fu Rui Duan Bin Wei Hai-Ming Cao Yan E Shuai-Yu Chen Ying-Dong Zhang Teng Jiang Department of Neurology Nanjing First HospitalNanjing Medical UniversityNanjingJiangsu ProvinceChina Department of Clinical Pharmacy School of Basic Medicine and Clinical PharmacyChina Pharmaceutical UniversityNanjingJiangsu ProvinceChina

Triggering receptor expressed on myeloid cells-like 2(TREML2)is a newly identified susceptibility gene for Alzheimer's disease(AD).It encodes a microglial inflammation-associated *** date,the potential role of mic roglial TREML2 in neuroinflammation in the context of AD remains *** this study,app/ps1 mice were used to investigate the dynamic changes of TREML2 levels in brain during AD *** addition,lipopolysaccharide(Lps)stimulation of primary microglia as well as a lentivirus-mediated TREML2 overexpression and knockdown were employed to explore the role of TREML2 in neuroinflammation in the context of *** res ults show that TREML2 levels gradually increased in the brains of AP P/ps1 mice during disease *** stimulation of primary microglia led to the release of inflammato ry cytokines including interleukin-1β,inte rleukin-6,and tumor necrosis factor-a in the culture *** Lps-induced mic roglial release of inflammatory cytokines was enhanced by TREML2 overexpression and was attenuated by TREML2 knoc *** increased the levels of mic roglial M1-type polarization marker inducible nitric oxide *** effect was enhanced by TREML2 overexpression and ameliorated by TREML2 ***,the levels of microglial M2-type polarization markers CD206 and ARG1 in the primary microglia were reduced by TREML2 overexpression and elevated by TREML2 *** stimulation increased the levels of NLRP3 in primary *** Lps-induced increase in NLRP3 was further elevated by TREML2 overexpression and alleviated by TREML2 *** summary,this study provides the first evidence that TREML2 modulates inflammation by regulating microglial polarization and NLRP3 inflammasome *** findings reveal the mechanisms by which TREML2 regulates microglial inflammation and suggest that TREML2 inhibition may represent a novel therapeutic strategy for AD.

关键词： Alzheimer's disease app/ps1 mice inflammatory cytokine lipopolysaccharide microglia neuroinflammation NLRP3 inflammasome polarization susceptibility gene TREML2

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