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Neuroscience Bulletin 2020年第9期36卷 1057-1070页

作者： Zongbing Hao Rui Wang Haigang Ren Guanghui Wang laboratory of Molecular Neuropathology Jiangsu Key Laboratory of Neuropsychiatric Diseases and Department of PharmacologyCollege of Pharmaceutical SciencesSoochow UniversitySuzhou 215123China

Since the discovery of the C9ORF72 gene in2011,great advances have been achieved in its genetics and in identifying its role in disease models and pathological mechanisms;it is the most common genetic cause of amyotrophic lateral sclerosis(ALS) and frontotemporal dementia(FTD).ALS patients with C9ORF72 expansion show heterogeneous *** who are C9ORF72 expansion carriers have shorter survival after disease onset than non-C9ORF72 expansion *** and clinical features of C9ORF72 patients have been well mimicked via several models,including induced pluripotent stem cell-derived neurons and transgenic mice that were embedded with bacterial artificial chromosome construct and that overexpressing dipeptide repeat *** mechanisms implicated in C9ORF72 pathology include DNA damage,changes of RNA metabolism,alteration of phase separation,and impairment of nucleocytoplasmic transport,which may underlie C9ORF72 expansion-related ALS/FTD and provide insight into nonC9ORF72 expansion-related ALS,FTD,and other neurodegenerative diseases.

关键词： Amyotrophic lateral sclerosis Frontotemporal dementia C9ORF72 Dipeptide repeat proteins Pathological inclusions

APOE interacts with ACE2 inhibitingg SARS-CoV-2 cellular entry and inflammation in COVID-19 patients

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Signal Transduction and Targeted Therapy 2022年第9期7卷 3459-3467页

作者： Hongsheng Zhang Lin Shao Zhihao Lin Quan-Xin Long Huilong Yuan Lujian Cai Guangtong Jiang Xiaoyi Guo Renzhi Yang Zepeng Zhang Bingchang Zhang Fan Liu Zhiyong Li Qilin Ma Yun-Wu Zhang Ai-Long Huang Zhanxiang Wang Yingjun Zhao Huaxi Xu Center for Brain Sciences the First Aliated Hospital of Xiamen UniversityInstitute of NeuroscienceFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging ResearchXiamen UniversityXiamenChina Institute for Brain Science and Disease Chongqing Medical UniversityChongqingChina school of Medicine Xiamen UniversityXiamenChina Key laboratory of Molecular Biology for Infectius diseases(Minstry of Educatio) Chongqing Medical UniversityChongqingChina

Apolipoprotein E(APOE)plays a pivotal role in lipid including cholesterol *** APOE 4(APOE4)allele is a major genetic risk factor for Alzheimer's and cardiovascular *** APOE has recently been associated with increased susceptibility to infections of several viruses,whether and how APOEand its isoforms affect SARS-CoV-2 infection remains ***,we show that serum concentrations of APOE correlate inversely with levels of cytokine/chemokine in 73 COVID-19 *** multiple protein interaction assays,we demonstrate that APOE3 and APOE4 interact with the SARS-CoV-2 receptor ACE2;and APOE/ACE2 interactions require zinc metallopeptidase domain of ACE2,a key docking site for SARS-CoV-2 Spike *** addition,immuno-imaging assays using confocal,super-resolution,and transmission electron microscopies reveal that both APOE3 and APOE4 reduce ACE2/Spikemediated viral entry into ***,while having a comparable binding affinity to ACE2,APOE4 inhibits viral entry to a lesser extent compared to APOE3,which is likely due to APOE4's more compact structure and smaller spatial obstacle to compete against Spike binding to ***,APOE e4 carriers clinically correlate with increased SARS-CoV-2 infection and elevated serum inflammatory factors in 142 COVID-19 patients *** study suggests a regulatory mechanism underlying SARS-CoV-2 infection through APOE interactions with ACE2,which may explain in part increased COVID-19 infection and disease severity in APOE e4 carriers.

关键词： ACE2 patients inflammation

Glutamate receptor delocalization in postsynaptic membrane and reduced hippocampal synaptic plasticity in the early stage of Alzheimer's disease

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Neural Regeneration Research 2019年第6期14卷 1037-1045页

作者： Ning Li Yang Li Li-Juan Li Ke Zhu Yan Zheng Xiao-Min Wang Department of Neurobiology Capital Medical University Key laboratory for neurodegenerative Disorders of the Ministry of Education Capital Medical University Beijing Institute for Brain Disorders Department of Physiology Capital Medical University

Mounting evidence suggests that synaptic plasticity provides the cellular biological basis of learning and memory, and plasticity deficits play a key role in dementia caused by Alzheimer's disease. However, the mechanisms by which synaptic dysfunction contributes to the pathogenesis of Alzheimer's disease remain unclear. In the present study, Alzheimer's disease transgenic mice were used to determine the relationship between decreased hippocampal synaptic plasticity and pathological changes and cognitive-behavioral deterioration, as well as possible mechanisms underlying decreased synaptic plasticity in the early stages of Alzheimer's disease-like diseases. APP/PS1 double transgenic(5 XFAD; Jackson laboratory) mice and their littermates(wild-type, controls) were used in this study. Additional 6-weekold and 10-week-old 5 XFAD mice and wild-type mice were used for electrophysiological recording of hippocampal dentate gyrus. For10-week-old 5 XFAD mice and wild-type mice, the left hippocampus was used for electrophysiological recording, and the right hippocampus was used for biochemical experiments or immunohistochemical staining to observe synaptophysin levels and amyloid beta deposition levels. The results revealed that, compared with wild-type mice, 6-week-old 5 XFAD mice exhibited unaltered long-term potentiation in the hippocampal dentate gyrus. Another set of 5 XFAD mice began to show attenuation at the age of 10 weeks, and a large quantity of amyloid beta protein was accumulated in hippocampal cells. The location of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor and N-methyl-D-aspartic acid receptor subunits in synaptosomes was decreased. These findings indicate that the delocalization of postsynaptic glutamate receptors and an associated decline in synaptic plasticity may be key mechanisms in the early onset of Alzheimer's disease. The use and care of animals were in strict accordance with the ethical standards of the Animal Ethics Committee of Ca

关键词： nerve regeneration Alzheimer’s disease synaptic plasticity hippocampus learning and memory long-term potentiation βamyloid glutamate receptor synaptic strength neural regeneration

Protective effect of melatonin on soluble Aβ1-42-induced Notch1 signaling pathway in the rat cortex

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Protective effect of melatonin on soluble Aβ1-42-induced No...

Possible mechanisms of lycopene amelioration of learning and memory impairment in rats with vascular dementia

中国解剖学会2019年年会

作者： Wang Pan Zhang Shuman Ren Lili Bi Jing Department of Neurobiology and Key laboratory of neurodegenerative diseases of Liaoning Province Jinzhou Medical University

＜正＞Oligomeric forms ofβ-amyloid [Aβ（42）] peptides have been thought to be implicated in the progression of Alzheimer’s disease （AD）.Alterations in proteolysis of the Notch by gamma-secretase could be involve...

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Neural Regeneration Research 2020年第2期15卷 332-341页

作者： Ning-Wei Zhu Xiao-Lan Yin Ren Lin Xiao-Lan Fan Shi-Jie Chen Yuan-Ming Zhu Xiao-Zhen Zhao Department of Human Anatomy Histology and EmbryologySchool of Basic Medical SciencesFujian Medical UniversityFuzhouFujian ProvinceChina Department of Pharmacy Zhejiang Pharmaceutical CollegeNingboZhejiang ProvinceChina Key laboratory of Brain Aging and neurodegenerative diseases School of Basic Medical SciencesFujian Medical UniversityFuzhouFujian ProvinceChina

Oxidative stress is involved in the pathogenesis of vascular dementia. Studies have shown that lycopene can significantly inhibit oxidative stress;therefore, we hypothesized that lycopene can reduce the level of oxidative stress in vascular dementia. A vascular dementia model was established by permanent bilateral ligation of common carotid arteries. The dosage groups were treated with lycopene(50, 100 and 200 mg/kg) every other day for 2 months. Rats without bilateral carotid artery ligation were prepared as a sham group. To test the ability of learning and memory, the Morris water maze was used to detect the average escape latency and the change of search strategy. Hematoxylin-eosin staining was used to observe changes of hippocampal neurons. The levels of oxidative stress factors, superoxide dismutase and malondialdehyde, were measured in the hippocampus by biochemical detection. The levels of reactive oxygen species in the hippocampus were observed by dihydroethidium staining. The distribution and expression of oxidative stress related protein, neuron-restrictive silencer factor, in hippocampal neurons were detected by immunofluorescence histochemistry and western blot assays. After 2 months of drug administration,(1) in the model group, the average escape latency was longer than that of the sham group, and the proportion of straight and tend tactics was lower than that of the sham group, and the hippocampal neurons were irregularly arranged and the cytoplasm was hyperchromatic.(2) The levels of reactive oxygen species and malondialdehyde in the hippocampus of the model group rats were increased, and the activity of superoxide dismutase was decreased.(3) Lycopene(50, 100 and 200 mg/kg) intervention improved the above changes, and the lycopene 100 mg/kg group showed the most significant improvement effect.(4) Neuron-restrictive silencer factor expression in the hippocampus was lower in the sham group and the lycopene 100 mg/kg group than in the model group.(5) Th

关键词： bilateral carotid artery ligation lycopene hippocampus learning and memory malondialdehyde neuron neuron-restrictive silencer factor reactive oxygen species superoxide dismutase

Melatonin ameliorates microvessel abnormalities in the cerebral cortex and hippocampus in a rat model of Alzheimer’s disease

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Neural Regeneration Research 2021年第4期16卷 787-794页

作者： Pan Wang Hai-Juan Sui Xiao-Jia Li Li-Na Bai Jing Bi Hong Lai Department of Anatomy China Medical UniversityShenyangLiaoning ProvinceChina Department of Neurobiology and Key laboratory of neurodegenerative diseases of Liaoning Province Jinzhou Medical UniversityJinzhouLiaoning ProvinceChina Department of Neurobiology Jinzhou Medical UniversityJinzhouLiaoning ProvinceChina Department of Pharmacology Jinzhou Medical UniversityJinzhouLiaoning ProvinceChina

Melatonin can attenuate cardiac microvascular ischemia/reperfusion injury,but it remains unclear whether melatonin can also ameliorate cerebral microvascular *** models of Alzheimer’s disease were established by six intracerebroventricular injections of amyloidbeta 1–42,administered once every other ***(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–*** 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 *** 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 *** study was approved by the Animal Care and Use Committee of Jinzhou Medical University,China(approval No.2019015)on December 6,2018.

关键词： Alzheimer’s disease brain central nervous system factor in vivo model pathways protein rat

Protective Role of Melatonin against Soluble Aβ1-42-induced Neurotoxicity in the Cerebral Cortex of Rats

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Progress of research in the application of ultrasound technology for the treatment of Alzheimer’s disease

中国神经科学学会第十二届全国学术会议

作者： Pan Wang Shuman Zhang Xiaojie Chen Lili Ren Jing Bi Department of Neurobiology Key Laboratory of Neurodegenerative Diseases of Liaoning Province Jinzhou Medical University

Amyloid-beta(Aβ) plays an important role in Alzheimer’s disease(AD) pathogenesis, and soluble Aβoligomers are more cytotoxic than Aβ fibrils. Recent studies suggest that Notch1 signaling is affected by AD and other brain diseases. Melatonin exerts many beneficial effects on AD and may protect against myocardial ischemia via Notch1 signaling regulation. Therefore, we hypothesized that the Notch1 signaling pathway is involved in the neuroprotective role of melatonin against soluble Aβ1–42. By using a established soluble Aβ1–42 repeated intracerebroventricular injection rat model, we found soluble Aβ1–42 increased neurodegeneration, neurotoxicity and activation of astrocyte in cerebral cortex. Melatonin intraperitoneal injection could significantly reduce the effect of soluble Aβ1–42 in cerebral cortex. Furthermore, our in vitro studies indicated that Notch1 signaling pathway may be involved in regulating the neuroprotective role of Melatonin against soluble Aβ-induced neurotoxicity in the cerebral cortex. These findings suggest that melatonin may prevent the soluble Aβ1–42-induced neurotoxicity through Notch1 signaling pathway.

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Neural Regeneration Research 2025年第10期20卷 2823-2837页

作者： Qiuquan Cai Lianghui Meng Meina Quan Ling Wang Jing Ren Chenguang Zheng Jiajia Yang Dong Ming Academy of Medical Engineering and Translational Medicine Tianjin UniversityTianjinChina Innovation Center for Neurological Disorders Xuanwu HospitalCapital Medical UniversityBeijingChina Brain-Computer Interaction and Human-Machine Fusion Haihe laboratory Tianjin UniversityTianjinChina Tianjin Key laboratory of Brain Science and Neural Engineering Tianjin UniversityTianjinChina

Alzheimer’s disease is a common neurodegenerative disorder defined by decreased reasoning abilities,memory loss,and cognitive *** presence of the blood-brain barrier presents a major obstacle to the development of effective drug therapies for Alzheimer’s *** use of ultrasound as a novel physical modulation approach has garnered widespread attention in recent *** a safe and feasible therapeutic and drug-delivery method,ultrasound has shown promise in improving cognitive *** article provides a summary of the application of ultrasound technology for treating Alzheimer’s disease over the past 5 years,including standalone ultrasound treatment,ultrasound combined with microbubbles or drug therapy,and magnetic resonance imaging-guided focused ultrasound *** is placed on the benefits of introducing these treatment methods and their potential *** found that several ultrasound methods can open the blood-brain barrier and effectively alleviate amyloid-βplaque *** believe that ultrasound is an effective therapy for Alzheimer’s disease,and this review provides a theoretical basis for future ultrasound treatment methods.

关键词： Alzheimer’s disease blood-brain barrier drugs magnetic resonance imaging-guided focused ultrasound microbubbles scanning ultrasound ultrasound ultrasound stimulation

Potassium Channels: A Potential Therapeutic Target for Parkinson's Disease

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Neuroscience Bulletin 2018年第2期34卷 341-348页

作者： Xiaoyan Chen Bao Xue Jun Wang Haixia Liu Limin Shi Junxia Xie Collaborative Innovation Center for Brain Science Department of Physiology Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders Key Laboratory of Pathogenesis and Prevention of Neurological Disorders Medical College of Qingdao University

The pathogenesis of the second major neurodegenerative disorder, Parkinson’s disease(PD), is closely associated with the dysfunction of potassium(K~+ ) channels. Therefore, PD is also considered to be an ion channel disease or neuronal channelopathy. Mounting evidence has shown that K~+ channels play crucial roles in the regulations of neurotransmitter release, neuronal excitability, and cell volume. Inhibition of K~+ channels enhances the spontaneous firing frequency of nigral dopamine(DA)neurons, induces a transition from tonic firing to burst discharge, and promotes the release of DA in the ***, three K~+ channels have been identified to protect DA neurons and to improve the motor and non-motor symptoms in PD animal models: small conductance(SK)channels, A-type K~+ channels, and KV7/KCNQ *** this review, we summarize the physiological and pharmacological effects of the three K~+ channels. We also describe in detail the laboratory investigations regarding K~+ channels as a potential therapeutic target for PD.

关键词： Parkinson’s disease A-type K+ channels SK channels KV7/KCNQ channels Dopamine