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Repetitive transcranial magnetic stimulation in Alzheimer’s disease:effects on neural and synaptic rehabilitation

Neural Regeneration Research 2025年第2期20卷 326-342页

作者： Yi Ji Chaoyi Yang Xuerui Pang Yibing Yan Yue Wu Zhi Geng Wenjie Hu Panpan Hu Xingqi Wu Kai Wang Department of Neurology The First Affiliated Hospital of Anhui Medical UniversityHefeiAnhui ProvinceChina Anhui Province Key laboratory of Cognition and neuropsychiatric Disorders HefeiAnhui ProvinceChina Collaborative Innovation Center of neuropsychiatric Disorders and Mental Health HefeiAnhui ProvinceChina Institute of Artificial Intelligence Hefei Comprehensive National Science CenterHefeiAnhui ProvinceChina Department of Psychology and Sleep Medicine The Second Affiliated Hospital of Anhui Medical UniversityHefeiAnhui ProvinceChina

Alzheimer’s disease is a neurodegenerative disease resulting from deficits in synaptic transmission and *** Alzheimer’s disease brain tends to be hyperexcitable and hypersynchronized,thereby causing neurodegeneration and ultimately disrupting the operational abilities in daily life,leaving patients *** transcranial magnetic stimulation is a cost-effective,neuro-modulatory technique used for multiple neurological *** the past two decades,it has been widely used to predict cognitive decline;identify pathophysiological markers;promote neuroplasticity;and assess brain excitability,plasticity,and *** has also been applied to patients with dementia,because it can yield facilitatory effects on cognition and promote brain recovery after a neurological ***,its therapeutic effectiveness at the molecular and synaptic levels has not been elucidated because of a limited number of *** study aimed to characterize the neurobiological changes following repetitive transcranial magnetic stimulation treatment,evaluate its effects on synaptic plasticity,and identify the associated *** review essentially focuses on changes in the pathology,amyloidogenesis,and clearance pathways,given that amyloid deposition is a major hypothesis in the pathogenesis of Alzheimer’s *** mechanisms associated with repetitive transcranial magnetic stimulation procedures and different pathways mediating gene transcription,which are closely related to the neural regeneration process,are also ***,we discuss the outcomes of animal studies in which neuroplasticity is modulated and assessed at the structural and functional levels by using repetitive transcranial magnetic stimulation,with the aim to highlight future directions for better clinical translations.

关键词： Alzheimer’s disease amyloid deposition apoptotic mechanisms biomarker neural regeneration neurodegeneration repetitive transcranial magnetic stimulation synaptic plasticity

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Loss of VAPB Regulates Autophagy in a Beclin 1-Dependent Manner

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Neuroscience Bulletin 2018年第6期34卷 1037-1046页

作者： Dan Wu Zongbing Hao Haigang Ren Guanghui Wang laboratory of Molecular Neuropathology Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences Soochow University

Autophagy is an evolutionarily-conserved selfdegradative process that maintains cellular homeostasis by eliminating protein aggregates and damaged ***, vesicle-associated membrane protein-associated protein B(VAPB), which is associated with the familial form of amyotrophic lateral sclerosis, has been shown to regulate autophagy. In the present study, we demonstrated that knockdown of VAPB induced the up-regulation of beclin 1 expression, which promoted LC3(microtubuleassociated protein light chain 3) conversion and the formation of LC3 puncta, whereas overexpression of VAPB inhibited these processes. The regulation of beclin1 by VAPB was at the transcriptional level. Moreover,knockdown of VAPB increased autophagic flux, which promoted the degradation of the autophagy substrate p62 and neurodegenerative disease proteins. Our study provides evidence that the regulation of autophagy by VAPB is associated with the autophagy-initiating factor beclin 1.

关键词： VAPB Autophagy Beclin 1 ALS Autophagic flux LC3

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The Multiple Roles of Autophagy in Neural Function and diseases

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Neuroscience Bulletin 2024年第3期40卷 363-382页

作者： Yan-Yan Li Zheng-Hong Qin Rui Sheng Department of Pharmacology and laboratory of Aging and Nervous diseases Jiangsu Key laboratory of Neuropsychiatric DiseasesCollege of Pharmaceutical Sciences of Soochow UniversitySuzhou 215123China

Autophagy involves the sequestration and delivery of cytoplasmic materials to lysosomes,where proteins,lipids,and organelles are degraded and *** to the way the cytoplasmic components are engulfed,autophagy can be divided into macroautophagy,microautophagy,and chaperone-mediated ***,many studies have found that autophagy plays an important role in neurological diseases,including Alzheimer's disease,Parkinson's disease,Huntington's disease,neuronal excitotoxicity,and cerebral *** maintains cell homeostasis in the nervous system via degradation of misfolded proteins,elimination of damaged organelles,and regulation of apoptosis and ***-mTOR,Beclin 1,TP53,endoplasmic reticulum stress,and other signal pathways are involved in the regulation of autophagy and can be used as potential therapeutic targets for neurological ***,we discuss the role,functions,and signal pathways of autophagy in neurological diseases,which will shed light on the pathogenic mechanisms of neurological diseases and suggest novel targets for therapies.

关键词： Autophagy Neurodegenerative diseases Cerebral ischemia AMPK mTOR Beclin 1 TP53 Endoplasmic reticulum stress

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Poly-PR in C9ORF72-Related Amyotrophic Lateral Sclerosis/Frontotemporal Dementia Causes Neurotoxicity by Clathrin-Dependent Endocytosis

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Neuroscience Bulletin 2019年第5期35卷 889-900页

作者： Rui Wang Xingyun Xu Zongbing Hao Shun Zhang Dan Wu Hongyang Sun Chenchen Mu Haigang Ren Guanghui Wang laboratory of Molecular Neuropathology Jiangsu Key Laboratory of Neuropsychiatric Diseases and Department of Pharmacology College of Pharmaceutical SciencesSoochow University

GGGGCC repeat expansions in the C9 ORF72 gene are the most common cause of amyotrophic lateral sclerosis and frontotemporal dementia(c9 ALS/FTD). It has been reported that hexanucleotide repeat expansions in C9 ORF72 produce five dipeptide repeat(DPR) proteins by an unconventional repeat-associated non-ATG(RAN)translation. Within the five DPR proteins, poly-PR and poly-GR that contain arginine are more toxic than the other DPRs(poly-GA, poly-GP, and poly-PA). Here, we demonstrated that poly-PR peptides transferred into cells by endocytosis in a clathrin-dependent manner, leading to endoplasmic reticulum stress and cell death. In SH-SY5 Y cells and primary cortical neurons, poly-PR activated JUN amino-terminal kinase(JNK) and increased the levels of p53 and Bax. The uptake of poly-PR peptides by cells was significantly inhibited by knockdown of clathrin or by chlorpromazine, an inhibitor that blocks clathrin-mediated endocytosis. Inhibition of clathrin-dependent endocytosis by chlorpromazine significantly blocked the transfer of poly-PR peptides into cells, and attenuated poly-PRinduced JNK activation and cell death. Our data revealed that the uptake of poly-PR undergoes clathrin-dependentendocytosis and blockade of this process prevents the toxic effects of synthetic poly-PR peptides.

关键词： Amyotrophic lateral sclerosis C9ORF72 Poly-PR Clathrin ER stress

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Enterochromaffin Cell:Friend or Foe for Human Health?

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Neuroscience Bulletin 2023年第11期39卷 1732-1734页

作者： Yang Yu Yong-Chang Li Fu-Chao Zhang Guang-Yin Xu Jiangsu Key laboratory of neuropsychiatric diseases and Institute of Neuroscience Soochow UniversitySuzhou 215123China

Enterochromaffin(EC)cells are a type of enteroendocrine cells that reside in the epithelial lining of the gastrointestinal *** function as sensory transducers of stimuli present in the intestinal lumen,as afferent nerves do not protrude into the lumen,but have been shown to act as a friend or a foe depending on various *** has been well-described that EC cells play their role by releasing 5-HT to activate neighboring afferent nerves in a paracrine fashion,while emerging evidence suggests the existence of synaptic-like connections between enteroendocrine cells and adjacent afferent nerves based on in vitro co-culture and in vivo viral tracing studies.

关键词： nerves releasing Human

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H_(2)S-based therapies for ischaemic stroke:opportunities and challenges

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Stroke & Vascular Neurology 2019年第2期4卷 63-66页

作者： Jia Jia Jie Li Jian Cheng Jiangsu Key laboratory of neuropsychiatric diseases and College of Pharmaceutical Sciences Soochow UniversitySuzhouJiangsuChina Jiangsu Key laboratory of neuropsychiatric diseases and Institute of Neuroscience Soochow UniversitySuzhouJiangsuChina

Stroke is a cerebrovascular disease displaying high mortality and morbidity. Despite extensive efforts, only very few therapies are available for stroke patients as yet. Hydrogen sulfide (H2S) is thought to be a signalling molecule that is endogenously produced and plays functional roles in the central nervous system. Currently, numerous studies show that H2S impacts stroke outcomes in animal and cellular models. Here, we review the recent research regarding the effects of endogenously produced H2S as well as exogenous H2S donors on stroke pathology, focusing on the potential of H2S-based therapies in treating ischaemic stroke. We also discuss the several issues that hinder the clinical translation of H2S-based therapies from the bench. Taken together, we think that H2S-based therapies are promising strategies for treating cerebral ischaemia if we successfully address these issues.

关键词： therapies endogenous mortality

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Role of the C9ORF72 Gene in the Pathogenesis of Amyotrophic Lateral Sclerosis and Frontotemporal Dementia

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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

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α-Synuclein aggregation and transmission in Parkinson’s disease: a link to mitochondria and lysosome

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Science China(Life Sciences) 2020年第12期63卷 1850-1859页

作者： Rui Wang Hongyang Sun Haigang Ren Guanghui Wang laboratory of Molecular Neuropathology Jiangsu Key Laboratory of Neuropsychiatric Diseases&Department of PharmacologyCollege of Pharmaceutical SciencesSoochow UniversitySuzhou 215123China

The presence of intraneuronal Lewy bodies(LBs) and Lewy neurites(LNs) in the substantia nigra(SN) composed of aggregatedα-synuclein(α-syn) has been recognized as a hallmark of pathological changes in Parkinson’s disease(PD). Numerous studies have shown that aggregated α-syn is necessary for neurotoxicity. Meanwhile, the mitochondrial and lysosomal dysfunctions are associated with α-syn pathogenicity. The hypothesis that α-syn transmission in the human brain contributes to the instigation and progression of PD has provided insights into PD pathology. This review will provide a brief overview of increasing researches that shed light on the relationship of α-syn aggregation with mitochondrial and lysosomal dysfunctions, and highlight recent understanding of α-syn transmission in PD pathology.

关键词： α-synuclein Lewy pathology mitochondria lysosome aggregation transmission

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Local Circuits in the Cerebellum Interact with Biochemical Events

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Neuroscience Bulletin 2023年第4期39卷 710-712页

作者： Hongyang Sun Guanghui Wang laboratory of Molecular Neuropathology Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical SciencesSoochow UniversitySuzhou215123JiangsuChina

In a recent study published in Signal Transduction and Targeted Therapy,Liu et al.[1]studied a particular circuit from lobules IV/V in the cerebellar vermis to neurons within the fastigial nucleus(FN),which regulates ... 详细信息

关键词： Local sensor

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Small-molecule inhibitor of smoothend suppress neuroinflammation through hedgehog signaling independent mechanisms

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中国药理学与毒理学杂志 2018年第9期32卷 706-707页

作者： CAO Zhong-qiang ZHEN Xue-chu ZHENG Long-tai Jiangsu Key laboratory of neuropsychiatric diseases and College of Pharmaceutical Sciences Soochow University Suzhou 215123 China

OBJECTIVE Microglial activation mediated neuroinflammation plays an important role in the progression of neurodegerative *** purpose of this study was to investigate the effect of small-molecule inhibitors of smoothend(Smo) on microglial activation mediate *** To search for the novel anti-neuroinflammatory agents,the BV-2 cel-based nitric oxide(NO) assay was used to screen a series of small-molecule inhibitors of *** production of NO and cell viability were detected by Griess and MTT assay *** expression of inflammatory factors were evaluated by Real-time quantitative PCR or Western blotting or ELISA assay,and activation of signal molecules were detected by Western *** dopaminergic neuronal cell apoptosis were measured by flow *** stereotaxic injection of LPS into the mice Substantia Nigra(SN) were employed to establish animal model of neuroinflammation and immunofluorescence staining on brain slices sections were used to verify microglial activation and dopaminergic cell *** To search for the compounds that inhibit microglial activation,we have screened a series of Smo inhibitors(0.01-40 μmol·L^(-1)) for the activity to inhibit NO production in BV-2 microglia *** the Smo inhibitors tested,Hh-079 strongly inhibited LPS-induced microglial NO production without affecting the cell ***-079 significantly inhibited the expression of proinflammatory factors in LPSstimulated BV-2 microglial ***-079 inhibited phosphorylation of IKKα/β,phosphorylation and degradation of IκBα,phosphorylation of P65 subunit of NF-κB and NF-κB transcriptional activity in LPS-stimulated BV-2 microglial ***-079 reduced cytotoxicity of conditioned media of activated microglia toward HT-22 neuroblastoma cells in a co-culture *** studies demonstrated that among the Shh-Ptch-Gli pathway,microglia cells did not express detectable levels of Shh,Smo and ***,neither Smo inhibit

关键词： smoothend inhibitor Hh-079 neuroinflammation microglia

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