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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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cognitive deficits and Alzheimer-like neuropathological impairments during adolescence in a rat model of type 2 diabetes mellitus

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Neural Regeneration Research 2018年第11期13卷 1995-2004页

作者： Li Jin Yi-Pei Li Qiong Feng Li Ren Fang Wang Guo-Jia Bo Li Wang Department of Pathophysiology Henan Medical College Henan Key Laboratory of Degenerative Brain Disease Henan Medical College Department of Pathophysiology School of Basic Medicine and the Collaborative Innovation Center for Brain ScienceKey Laboratory of Ministry of Education of China for Neurological DisordersTongji Medical CollegeHuazhong University of Science and Technology Department of Pathology Wuhan Children's Hospital

Numerous studies have shown that many patients who suffer from type 2 diabetes mellitus exhibit cognitive dysfunction and neuronal synaptic impairments. Therefore, growing evidence suggests that type 2 diabetes mellitus has a close relationship with occurrence and progression of neurodegeneration and neural impairment in Alzheimer＇s disease. However, the relationship between metabolic disorders caused by type 2 diabetes mellitus and neurodegeneration and neural impairments in Alzheimer＇s disease is still not fully determined. Thus, in this study, we replicated a type 2 diabetic animal model by subcutaneous injection of newborn Sprague-Dawley rats with monosodium glutamate during the neonatal period. At 3 months old, the Barnes maze assay was performed to evaluate spatial memory function. Microelectrodes were used to measure electrophysiological function in the hippocampal CA1 region. Western blot assay was used to determine expression levels of glutamate ionotropic receptor NMDA type subunit 2 A（GluN2A） and GluN2B in the hippocampus. Enzyme-linked immunosorbent assay was used to determine levels of interleukin-1β, tumor necrosis factor α, and interleukin-6 in the hippocampus and cerebral cortex, as well as hippocampal amyloid beta（Aβ）1-40 and Aβ_（1-42） levels. Our results showed that in the rat model of type 2 diabetes mellitus caused by monosodium glutamate exposure during the neonatal period, latency was prolonged and the number of errors increased in the Barnes maze. Further, latency was increased and time in the escape platform quadrant shortened. Number of times crossing the platform was also reduced in the Morris water maze. After high frequency stimulation of the hippocampus, synaptic transmission was inhibited, expression of GluN2A and GluN2B were decreased in the hippocampus, expression of interleukin 1β, interleukin 6, and tumor necrosis factor α was increased in the hippocampus and cortex, and levels of Aβ_（1-40） and Aβ_（1-42） were increased in the hippoc

关键词： nerve regeneration type 2 diabetes mellitus Alzheimer's disease monosodium glutamate neonatal period cognitive deficits hyperglycemia hyperinsulinemia insulin resistance neural regeneration

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Cold water swimming pretreatment reduces cognitive deficits in a rat model of traumatic brain injury

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Neural Regeneration Research 2017年第8期12卷 1322-1328页

作者： Zi-wei Zhou Ya-dan Li Wei-wei Gao Jie-li Chen Shu-yuan Yue Jian-ning Zhang Department of Neurosurgery Tianjin Medical University General Hospital Tianjin China Tianjin Neurological Institute Tianjin China Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System Ministry of Education Tianjin China Tianjin Key Laboratory of Injuries Variations and Regeneration of Nervous System Tianjin China Intensive Care Units Tianjin Huanhu Hospital Tianjin China Department of Neurology Henry Ford Hospital Detroit MI USA

A moderate stress such as cold water swimming can raise the tolerance of the body to potentially injurious events. However, little is known about the mechanism of beneficial effects induced by moderate stress. In this study, we used a classic rat model of traumatic brain injury to test the hypothesis that cold water swimming preconditioning improved the recovery of cognitive functions and explored the mechanisms. Results showed that after traumatic brain injury, pre-conditioned rats（cold water swimming for 3 minutes at 4℃） spent a significantly higher percent of times in the goal quadrant of cold water swim, and escape latencies were shorter than for non-pretreated rats. The number of circulating endothelial progenitor cells was significantly higher in pre-conditioned rats than those without pretreatment at 0, 3, 6 and 24 hours after traumatic brain injury. Immunohistochemical staining and Von Willebrand factor staining demonstrated that the number of CD34~＋ stem cells and new blood vessels in the injured hippocampus tissue increased significantly in pre-conditioned rats. These data suggest that pretreatment with cold water swimming could promote the proliferation of endothelial progenitor cells and angiogenesis in the peripheral blood and hippocampus. It also ameliorated cognitive deficits caused by experimental traumatic brain injury.

关键词： nerve regeneration cold water swimming cognitive deficits endothelial progenitor cells angiogenesis neural repair stress Morriswater maze fluid percussion injury model CD34 Von Willebrand factor neural regeneration

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Electroacupuncture with Bushen Jiannao improves cognitive deficits in senescence-accelerated mouse prone 8 mice by inhibiting neuroinflammation

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Journal of Traditional Chinese Medicine 2020年第5期40卷 812-819页

作者： Wang Xu Li Zhaolong Li Chunri Wang Yue Yu Song Ren Lu Mental disorders research laboratory Liaoning University of Traditional Chinese MedicineShenyang 110847China

OBJECTIVE:To investigate effect of electroacupuncture(EA)with Bushen Jiannao on learning and memory ability in senescence-accelerated mouse prone 8(SAMP8)mice and the related ***:8-month-old senescence-accelerated-resistant(SAMR1)and SAMP8 mice were treated with EA at Baihui(GV 20),Shenshu(BL 23),and Taixi(KI 3)acupoint once a week for 8 *** Morris water maze,enzyme linked immunosorbent assay,immunohistochemistry,and Western blot were used to assess Alzheimer’s disease(AD)-associated cognitive and neuroinflammatory ***:Our data showed that EA treatment decreased activation of microglia and astrocytes,decreased levels of inflammatory factors including tumor necrosis factor-α(TNF-α),interleukin(IL)-6,and IL-17,and improved spatial memory deficits in SAMP8 *** therapy with Bushen Jiannao exhibited anti-inflammatory properties and improved cognitive ***:The present study indicates that EA treatment based on the interaction between kidney and brain can improve learning and memory ability by inhibiting activation of astrocytes and microglia and decreasing expression of pro-inflammatory cytokines,TNF-αand *** treatment based on the interaction between kidney and brain may be an effective treatment for AD.

关键词： Alzheimer disease Electroacupuncture Memory and learning tests cognitive deficits Kidney and brain Neuroinflammation

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Transplantation of bone marrow mesenchymal stem cells improves cognitive deficits and alleviates neuropathology in animal models of Alzheimer’s disease: a meta-analytic review on potential mechanisms

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Translational Neurodegeneration 2020年第2期9卷 214-233页

作者： Chuan Qin Yalan Lu Kewei Wang Lin Bai Guiying Shi Yiying Huang Yongning Li Institute of Laboratory Animal Sciences Chinese Academy of Medical Sciences&Comparative Medical CenterPeking Union Medical CollegeBeijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases5 Panjiayuan Nanli StBeijing100021China Department of International Medical Service&Department of Neurosurgery Peking Union Medical College HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeShuaifuyuan 1Dong Cheng DistrictBeijing100730China

Background Alzheimer’s disease is a neurodegenerative ***,a transplantation of bone marrow mesenchymal stem cells(BMMSCs)can play a beneficial role in animal models of Alzheimer’s ***,the relevant mechanism remains to be fully *** body Subsequent to the transplantation of BMMSCs,memory loss and cognitive impairment were significantly improved in animal models with Alzheimer’s disease(AD).Potential mechanisms involved neurogenesis,apoptosis,angiogenesis,inflammation,immunomodulation,*** above mechanisms might play different roles at certain *** was revealed that the transplantation of BMMSCs could alter some gene ***,the differential expression of representative genes was responsible for neuropathological phenotypes in Alzheimer’s disease,which could be used to construct gene-specific *** Multiple signal pathways involve therapeutic mechanisms by which the transplantation of BMMSCs improves cognitive and behavioral deficits in AD *** expression profile can be utilized to establish statistical regression model for the evaluation of therapeutic *** transplantation of autologous BMMSCs maybe a prospective therapy for patients with Alzheimer’s disease.

关键词： Alzheimer's disease Bone marrow mesenchymal stem cells Meta-analysis Amyloid P peptide Memory loss cognitive deficits Animal model Neuropathology

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Protective effect of pterostilbene on cognitive deficits induced by neuroinflammation

Protective effect of pterostilbene on cognitive deficits ind...

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第十四届全国中药和天然药物学术研讨会

作者： Yue Hou Guanbo Xie Fengrong Miao Xia Liu Chunfu Wu College of Life and Health Sciences Northeastern University Department of Pharmacology Shenyang Pharmaceutical University

Neuroinflammation is considered to be associated with the progression of various neurodegenerative disorders,characterized by microglia activation and neuronal *** is known that treatment of lipopolysaccharide（LPS）,commonly used to induce neuroinflammation,can result in cognitive deficits as well as microglia activation and neuronal ***,a naturally occurring analogue of resveratrol,has recently been reported to have a beneficial effect in the protection against cognitive ***,such effect of pterostilbene on LPS-induced cognitive impairment has never been ***,the present study aims to evaluate the potential effects of pterostilbene on LPS-induced cognitive impairment as well as the possible changes of microglia and ***,cognitive function was investigated by Y-maze test and Morris water maze *** Y-maze task,pterostilbene（10,20,40 mg/kg,i.g.） significantly antagonized the decreased spontaneous alternation induced by LPS（bilaterally intrahippocampal injected,40 ug/mouse）.In the training session of Morris water maze test,pterostilbene（20 and 40mg/kg） produced a significant decrease in the escape latency and distance compared to the LPS group on the 5th day,without affecting the swimming *** the probe test,mice in the pterostilbene-treated（10,20 and 40 mg/kg） group spent more time in target quadrant and showed increased number of platform crossings and target quadrant crossings compared to the LPS ***,immunohistochemical method was used to study the changes of microglia and *** results showed that pterostilbene（10,20 and 40mg/kg） produced a significant decrease in the number of lba-1 positive cells in mouse hippocampal compared to the LPS *** of pterostilbene（10,20 and 40mg/kg） produced a significant increase in neuronal nuclear antigen（NeuN）-stained area of neurons and a significant decrease in the number of Doublecortin（DCX） positive cells compared to the LPS *** s

关键词： pterostilbene lipopolysaccharide cognitive deficits microglia neurons

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Targeting tau in Alzheimer's disease:from mechanisms to clinical therapy

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Neural Regeneration Research 2024年第7期19卷 1489-1498页

作者： Jinwang Ye Huali Wan Sihua Chen Gong-Ping Liu Shenzhen Key Laboratory of Marine Biotechnology and Ecology College of Life Sciences and OceanographyShenzhen UniversityShenzhenGuangdong ProvinceChina Department of Laboratory Medicine Guangdong Provincial People’s Hospital(Guangdong Academy of Medical Sciences)Southern Medical UniversityGuangzhouGuangdong ProvinceChina Co-innovation Center of Neurodegeneration Nantong UniversityNantongJiangsu ProvinceChina Department of Pathophysiology School of Basic Medicine and the Collaborative Innovation Center for Brain ScienceKey Laboratory of Ministry of Education of China and Hubei Province for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubei ProvinceChina

Alzheimer’s disease is the most prevalent neurodegenerative disease affecting older *** features of Alzheimer’s disease include extra cellular aggregation of amyloid-βplaques and the accumulation of neurofibrillary tangles,fo rmed by tau protein,in the *** there are amyloid-β-ta rgeting therapies for the treatment of Alzheimer’s disease,these therapies are costly and exhibit potential negative side *** evidence suggests significant involvement of tau protein in Alzheimer’s disease-related *** an important microtubule-associated protein,tau plays an important role in maintaining the stability of neuronal microtubules and promoting axonal *** fact,clinical studies have shown that abnormal phosphorylation of tau protein occurs before accumulation of amyloid-βin the *** therapeutic strategies targeting tau protein have begun to emerge,and are considered possible methods to prevent and treat Alzheimer’s ***,abnormalities in post-translational modifications of the tau protein,including aberrant phosphorylation,ubiquitination,small ubiquitin-like modifier(SUMO)ylation,acetylation,and truncation,contribute to its microtubule dissociation,misfolding,and subcellular *** causes mitochondrial damage,synaptic impairments,gliosis,and neuroinflammation,eventually leading to neurodegeneration and cognitive *** review summarizes the recent findings on the underlying mechanisms of tau protein in the onset and progression of Alzheimer’s disease and discusses tau-targeted treatment of Alzheimer’s disease.

关键词： acetylation Alzheimer’s disease cognitive deficits gliosis mitochondria damage neuroinflammation phosphorylation synaptic impairments tau tau immunotherapy

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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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Acute and chronic excitotoxicity in ischemic stroke and late-onset Alzheimer's disease

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Neural Regeneration Research 2025年第7期20卷 1981-1988页

作者： Shan Ping Yu Emily Choi Michael QJiang Ling Wei Department of Anesthesiology Emory University School of MedicineAtlantaGAUSA Center for Visual and Neurocognitive Rehabilitation Atlanta Veterans Affairs Medical CenterDecaturGAUSA

Stroke and Alzheimer's disease are common neurological disorders and often occur in the same *** comorbidity of the two neurological disorders represents a grave health threat to older *** review presents a brief background of the development of novel concepts and their clinical *** activity of glutamatergic N-methyl-D-aspartate receptors and N-methyl-D-aspartate receptor-mediated Ca^(2+)influx is critical for neuronal *** ischemic insult induces prompt and excessive glutamate release and drastic increases of intracellular Ca^(2+)mainly via N-methyl-D-aspartate receptors,particularly of those at the extrasynaptic *** Ca^(2+)-evoked neuronal cell death in the ischemic core is dominated by necrosis within a few hours and days known as acute ***,mild but sustained Ca^(2+)increases under neurodegenerative conditions such as in the distant penumbra of the ischemic brain and early stages of Alzheimer's disease are not immediately toxic,but gradually set off deteriorating Ca^(2+)-dependent signals and neuronal cell loss mostly because of activation of programmed cell death *** on the Ca^(2+)hypothesis of Alzheimer's disease and recent advances,this Ca^(2+)-activated“silent”degenerative excitotoxicity evolves from years to decades and is recognized as a unique slow and chronic *** N-methyl-D-aspartate receptor subunit GluN3A,primarily at the extrasynaptic site,serves as a gatekeeper for the N-methyl-D-aspartate receptor activity and is neuroprotective against both acute and chronic *** stroke and Alzheimer's disease,therefore,share an N-methyl-D-aspartate receptor-and Ca^(2+)-mediated mechanism,although with much different time *** is thus proposed that early interventions to control Ca^(2+)homeostasis at the preclinical stage are pivotal for individuals who are susceptible to sporadic late-onset Alzheimer's disease and Alzheimer's disease-related

关键词： Ca^(2+)hypothesis cognitive deficits hyperactivity late-onset Alzheimer's disease neurodegeneration N-methyl-D-aspartate receptors N-methyl-D-aspartate receptor subunits pathogenesis preventive treatment

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Microglia regulation of synaptic plasticity and learning and memory

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Neural Regeneration Research 2022年第4期17卷 705-716页

作者： Jessica Cornell Shelbi Salinas Hou-Yuan Huang Miou Zhou Graduate College of Biomedical Sciences Western University of Health SciencesPomonaCAUSA

Microglia are the resident macrophages of the central nervous *** possess varied morphologies and *** normal physiological conditions,microglia mainly exist in a resting state and constantly monitor their microenvironment and survey neuronal and synaptic *** the C1 q,C3 and CR3"Eat Me"and CD47 and SIRPα"Don't Eat Me"complement pathways,as well as other pathways such as CX3 CR1 signaling,resting microglia regulate synaptic pruning,a process crucial for the promotion of synapse formation and the regulation of neuronal activity and synaptic *** mediating synaptic pruning,resting microglia play an important role in the regulation of experience-dependent plasticity in the barrel cortex and visual cortex after whisker removal or monocular deprivation,and also in the regulation of learning and memory,including the modulation of memory strength,forgetfulness,and memory *** a response to brain injury,infection or neuroinflammation,microglia become activated and increase in *** microglia change to an amoeboid shape,migrate to sites of inflammation and secrete proteins such as cytokines,chemokines and reactive oxygen *** molecules released by microglia can lead to synaptic plasticity and learning and memory deficits associated with aging,Alzheimer's disease,traumatic brain injury,HIV-associated neurocognitive disorder,and other neurological or mental disorders such as autism,depression and post-traumatic stress *** a focus mainly on recently published literature,here we reviewed the studies investigating the role of resting microglia in synaptic plasticity and learning and memory,as well as how activated microglia modulate disease-related plasticity and learning and memory *** summarizing the function of microglia in these processes,we aim to provide an overview of microglia regulation of synaptic plasticity and learning and memory,and to discuss the possibility of microglia manipul

关键词： aging Alzheimer's disease cognitive deficits experience-dependent plasticity learning and memory mental disorders microglia synaptic plasticity synaptic pruning

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