检索结果-南通市图书馆

Tau truncation in the pathogenesis of Alzheimer's disease: a narrative review

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Neural Regeneration Research 2024年第6期19卷 1221-1232页

作者： Dandan Chu Xingyue Yang Jing Wang Yan Zhou Jin-Hua Gu Jin Miao Feng Wu Fei Liu Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products Coinnovation Center of Neuroregeneration Nantong University 2. Department of Pharmacology School of Pharmacy Nantong University 3. Department of Biochemistry and Molecular Biology School of Medicine Nantong University 4. Department of Clinical Pharmacy Affiliated Maternity and Child Health Care Hospital of Nantong University Nantong University 5. Laboratory of Animal Center Nantong University Department of neurochemistry Inge Grundke-Iqbal Research Floor New York State Institute for Basic Research in Developmental Disabilities

Alzheimer’s disease is characterized by two major neuropathological hallmarks—the extracellular β-amyloid plaques and intracellular neurofibrillary tangles consisting of aggregated and hyperphosphorylated Tau protein. Recent studies suggest that dysregulation of the microtubuleassociated protein Tau, especially specific proteolysis, could be a driving force for Alzheimer’s disease neurodegeneration. Tau physiologically promotes the assembly and stabilization of microtubules, whereas specific truncated fragments are sufficient to induce abnormal hyperphosphorylation and aggregate into toxic oligomers, resulting in them gaining prion-like characteristics. In addition, Tau truncations cause extensive impairments to neural and glial cell functions and animal cognition and behavior in a fragment-dependent manner. This review summarizes over 60 proteolytic cleavage sites and their corresponding truncated fragments, investigates the role of specific truncations in physiological and pathological states of Alzheimer’s disease, and summarizes the latest applications of strategies targeting Tau fragments in the diagnosis and treatment of Alzheimer’s disease.

关键词： Alzheimer's disease cleavage site diagnosis marker neurofibrillary tangles phosphorylation Tau Tau aggregation therapy truncation

Plasticity of callosal neurons in the contralesional cortex following traumatic brain injury

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Neural Regeneration Research 2023年第6期18卷 1257-1258页

作者： Alexandra Chovsepian Laura Empl Florence M.Bareyre Institute of clinical neuroimmunology Biomedical Building and Clinic of the Ludwig-Maximilians Universität MünchenMunichGermany

Traumatic brain injury(TBI) represents a significant cause of disability worldwide.It creates a vast array of damaging macro-and microscopic changes in the affected brain area(s),ranging from neuronal cell death,changes in structural spine integrity and dynamics to axonal injury and ove rall neuronal circuit disruption,ultimately leading to functional and cognitive deficits in both humans and animal models(N udo,2013).

关键词： injury traumatic cortex

Semaphorin7A:its role in the control of serotonergic circuits and functional recovery following spinal cord injury

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2022年第5期17卷 959-962页

作者： Julie Fourneau Florence M.Bareyre Institute of clinical neuroimmunology Ludwig-Maximilians Universität MünchenMunichGermany Munich Cluster of Systems Neurology(SyNergy) MunichGermany

Serotonin is a monoamine neurotransmitter synthetized in various populations of brainstem neurons.In the spinal cord,descending serotonergic projections regulate postural muscle tone,locomotion and rhythm and coordination of movements via the Central Pattern Generator.Following a spinal cord injury,serotonergic projections to the lumbar spinal cord,where the Central Pattern Generators are located,are interrupted resulting in devastating locomotor impairments and changes in the expression and activation of serotonin and its spinal receptors.The molecular cues that control the precise patterning and targeting of serotonergic inputs onto Central Pattern Generator networks in healthy animals or after injury are still unknown.In our recent research work,we have been particularly interested in Semaphorin7A,which belongs to the Semaphorins family involved in guiding growing axons and controlling plasticity of synaptic connections.In this review,we discuss the role of Semaphorin7A signaling as an important molecular actor that instructs the patterning of serotonin inputs to spinal Central Pattern Generator networks.We show that Semaphorin7A controls the wiring of descending serotonin axons in the spinal cord.Our results reveal that mistargetting of serotonin fibers in the spinal cord is compensated in healthy uninjured Semaphorin7A deficient mice so that their gross locomotion proceeds accurately.We also demonstrate that when the system is challenged with a spinal lesion,the pattern of post-injury serotonin expression is significantly altered in Semaphorin7A deficient mice with specific ectopic targeting of serotonin fibers in the lumbar spinal cord.Compensatory mechanisms in place in uninjured Semaphorin7A deficient mice are lost and injured Semaphorin7A deficient mice exhibit a worsening of their post-injury locomotor abilities.Our findings identify Semaphorin7A as a critical determinant of serotonergic circuit formation in healthy or spinal cord injured mice.

关键词： central pattern generator guidance molecule locomotion recovery rewiring semaphorin7A serotonergic patterning serotonin spinal cord injury

Mesenchymal stem cells require the peripheral immune system for immunomodulating effects in animal models of multiple sclerosis

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2016年第1期11卷 90-91页

作者： Laura Salinas Tejedor Thomas Skripuletz Martin Stangel Viktoria Gudi clinical neuroimmunology and neurochemistry Department of NeurologyHannover Medical SchoolHanoverGermany Center for Systems Neuroscience HannoverGermany

Multiple sclerosis（MS）is a chronic inflammatory disease of the central nervous system（CNS）that affects oligodendrocytes and myelin.Loss of myelin leads to progressive axonal damage and neuronal death resulting in neurodenegeration and functional disability.Several inflammatory factors influence the development of this neurological disorder.

关键词： disability migrate myelin axonal neuronal neurological progressive affects interleukin amyotrophic

Regulation of neuroinflammatory properties of glial cells by T cell effector molecules

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2018年第2期13卷 234-236页

作者： chittappen k.prajeeth jochen huehn martin stangel clinical neuroimmunology and neurochemistry department of neurologyhannover medical schoolHannoverGermany experimental immunology helmholtz centre for infection researchBraunschweigGermany center of systems neuroscience hannover medical schoolGermany

Multiple sclerosis （MS） is a chronic inflammatory and neurodegenerative disorder that is thought to be mediated by autoreactive T lymphocytes that find their way into the central nervous system （CNS）. The pathological mechanism of MS is still being elucidated but it involves complex interactions between infiltrating immune cells and resi- dent glial cells within the CNS that culminate into strong neuroinflammation and axonal damage.

关键词： Regulation of neuroinflammatory properties of glial cells by T cell effector molecules Th CNS

Rehabilitation following spinal cord injury:how animal models can help our understanding of exercise-induced neuroplasticity

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2019年第3期14卷 405-412页

作者： Kristina Loy Florence M.Bareyre Institute of clinical neuroimmunology Ludwig-Maximilians Universitat Munchen Munich Cluster of Systems Neurology (SyNergy)

Spinal cord injury is a devastating condition that is followed by long and often unsuccessful recovery after trauma. The state of the art approach to manage paralysis and concomitant impairments is rehabilitation, which is the only strategy that has proven to be effective and beneficial for the patients over the last decades. How rehabilitation influences the remodeling of spinal axonal connections in patients is important to understand, in order to better target these changes and define the optimal timing and onset of training. While clinically the answers to these questions remain difficult to obtain, rodent models of rehabilitation like bicycling, treadmill training, swimming, enriched environments or wheel running that mimic clinical rehabilitation can be helpful to reveal the axonal changes underlying motor recovery. This review will focus on the different animal models of spinal cord injury rehabilitation and the underlying changes in neuronal networks that are improved by exercise and rehabilitation.

关键词： remodeling exercise wheel running treadmill detour circuit propriospinal neuron corticospinal tract raphespinal tract reticulospinal tract activity recovery central nervous system

A novel viewpoint in glaucoma therapeutics: enriched environment

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2022年第7期17卷 1431-1439页

作者： María F.González Fleitas Damián Dorfman Ruth E.Rosenstein Laboratory of Retinal neurochemistry and Experimental Ophthalmology Department of Human BiochemistrySchool of Medicine/CEFyBOUniversity of Buenos Aires/CONICETBuenos AiresArgentina

Glaucoma is one of the world’s most frequent visual impairment causes and leads to selective damage to retinal ganglion cells and their axons.Despite glaucoma’s most accepted risk factor is increased intraocular pressure(IOP),the mechanisms behind the disease have not been fully elucidated.To date,IOP lowering remains the gold standard;however,glaucoma patients may still lose vision regardless of effective IOP management.Therefore,the exclusive IOP control apparently is not enough to stop the disease progression,and developing new resources to protect the retina and optic nerve against glaucoma is a goal of vast clinical importance.Besides pharmacological treatments,environmental conditions have been shown to prevent neurodegeneration in the central nervous system.In this review,we discuss current concepts on key pathogenic mechanisms involved in glaucoma,the effect of enriched environment on these mechanisms in different experimental models,as well as recent evidence supporting the preventive and therapeutic effect of enriched environment exposure against experimental glaucomatous damage.Finally,we postulate that stimulating vision may become a non-invasive and rehabilitative therapy that could be eventually translated to the human disease,preventing glaucoma-induced terrible sequelae resulting in permanent visual disability.

关键词： brain-derived neurotrophic factor chondroitin sulfate enriched environment glaucoma optic nerve axons optic nerve glia retinal ganglion cells visual stimulation

Regulation of axonal remodeling following spinal cord injury

在线全文

学校读者我要写书评

暂无评论

Neural Regeneration Research 2015年第10期10卷 1555-1557页

作者： Anne Jacobi Florence M.Bareyre Institute of clinical neuroimmunology Ludwig-Maximilians Universit?t München Munich Cluster of Systems Neurology (Sy Nergy)

Central nervous system injuries,such as spinal cord injury（SCI）,are a leading cause of disability in young adults.SCIs generally have severe clinical consequences and often lead to loss of motor or sensory input bel... 详细信息

关键词： Regulation of axonal remodeling following spinal cord injury STAT FGFR Figure CST

Promoting remyelination for the treatment of multiple sclerosis:opportunities and challenges

在线全文

学校读者我要写书评

暂无评论

Neuroscience Bulletin 2013年第2期29卷 144-154页

作者： Yueting Zhang Taylor B.Guo Hongtao Lu neuroimmunology Discovery Performance Unit GlaxoSmithKline Research and Development Center

Multiple sclerosis （MS） is a chronic and devastating autoimmune demyelinating disease of the central nervous system. With the increased understanding of the pathophysiology of this disease in the past two decades, many disease-modifying therapies that primarily target adaptive immunity have been shown to prevent exacerbations and new lesions in patients with relapsing-remitting MS. However, these therapies only have limited efficacy on the progression of disability. Increasing evidence has pointed to innate immunity, axonal damage and neuronal loss as important contributors to disease progression. Remyelination of denuded axons is considered an effective way to protect neurons from damage and to restore neuronal function. The identification of several key molecules and pathways controlling the differentiation of oligodendrocyte progenitor cells and myelination has yielded clues for the development of drug candidates that directly target remyelination and neuroprotection. The long-term efficacy of this strategy remains to be evaluated in clinical trials. Here, we provide an overview of current and emerging therapeutic concepts, with a focus on the opportunities and challenges for the remyelination approach to the treatment of MS.

关键词： multiple sclerosis myelination neurodegeneration oligodendrocytes disease progression disease modifying therapy drug target animal models