NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics最新文献

{"title":"Spinal Muscular Atrophy: A Test Case for Drug Development in Orphan Diseases","authors":"Lisa J. Bain","doi":"10.1016/j.nurx.2006.07.001","DOIUrl":"10.1016/j.nurx.2006.07.001","url":null,"abstract":"","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 4","pages":"Pages 535-539"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.07.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26311373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Translational Issues in Neurorehabilitation","authors":"Michael Chopp Ph.D. (Guest Editor), Michael Weinrich M.D. (Guest Editor)","doi":"10.1016/j.nurx.2006.07.012","DOIUrl":"10.1016/j.nurx.2006.07.012","url":null,"abstract":"","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 4","pages":"Pages 418-419"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.07.012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26283933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurorestorative Treatment of Stroke: Cell and Pharmacological Approaches","authors":"Jieli Chen ,&nbsp;Michael Chopp","doi":"10.1016/j.nurx.2006.07.007","DOIUrl":"10.1016/j.nurx.2006.07.007","url":null,"abstract":"<div><p>There is a compelling need to develop cell and pharmacological therapeutic approaches to be administered beyond the hyperacute phase of stroke. These therapies capitalize on the capacity of the brain for neuroregeneration and neuroplasticity and are designed to reduce neurological deficits after stroke. This review provides an update of bone marrow–derived mesenchymal stem cells (MSCs) and select pharmacological agents in clinical use for other indications that promote the recovery process in the subacute and chronic phases after stroke. Among these agents are 3-hydroxy-3-methylglutaryl–coenzyme A reductase inhibitors (statins), erythropoietin (EPO), and phosphodiesterase type 5 (PDE-5) inhibitors and nitric oxide (NO) donors. Both the MSCs and the pharmacologic agents potentiate brain plasticity and neurobehavioral recovery after stroke.</p></div>","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 4","pages":"Pages 466-473"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.07.007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26284405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Two-photon Imaging of Synaptic Plasticity and Pathology in the Living Mouse Brain","authors":"Jaime Grutzendler ,&nbsp;Wen-Biao Gan","doi":"10.1016/j.nurx.2006.07.005","DOIUrl":"10.1016/j.nurx.2006.07.005","url":null,"abstract":"<div><p>Two–photon microscopy (TPM) has become an increasingly important tool for imaging the structure and function of brain cells in living animals. TPM imaging studies of neuronal structures over intervals ranging from seconds to years have begun to provide important insights into the structural plasticity of synapses and the modulating effects of experience in the intact brain. TPM has also started to reveal how neuronal connections are altered in animal models of neurodegeneration, acute brain injury, and cerebrovascular disease. Here, we review some of these studies with special emphasis on the degree of structural dynamism of postsynaptic dendritic spines in the adult mouse brain as well as synaptic pathology in mouse models of Alzheimer’s disease and cerebral ischemia. We also discuss technical considerations that are critical for the acquisition and interpretation of data from TPM <em>in vivo</em>.</p></div>","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 4","pages":"Pages 489-496"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.07.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26284408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changing the Name of the Journal","authors":"Alan I. Faden MD (Editor-in-Chief)","doi":"10.1016/j.nurx.2006.08.002","DOIUrl":"10.1016/j.nurx.2006.08.002","url":null,"abstract":"","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 4","pages":"Page 417"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.08.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26283932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasticity","authors":"Randolph J. Nudo","doi":"10.1016/j.nurx.2006.07.006","DOIUrl":"10.1016/j.nurx.2006.07.006","url":null,"abstract":"<div><p>Over the past 20 years, evidence has mounted regarding the capacity of the central nervous system to alter its structure and function throughout life. Injury to the central nervous system appears to be a particularly potent trigger for plastic mechanisms to be elicited. Following focal injury, widespread neurophysiological and neuroanatomical changes occur both in the peri-infarct region, as well as throughout the ipsi- and contralesional cortex, in a complex, time-dependent cascade. Since such post-injury plasticity can be both adaptive or maladaptive, current research is directed at understanding how plasticity may be modulated to develop more effective therapeutic interventions for neurological disorders, such as stroke. Behavioral training appears to be a significant contributor to adaptive plasticity after injury, providing a neuroscientific foundation for the development of physical therapeutic approaches. Adjuvant therapies, such as pharmacological agents and exogenous electrical stimulation, may provide a more receptive environment through which behavioral therapies may be imparted. This chapter reviews some of the recent results from animal models of injury and recovery that depict the complex time course of plasticity following cortical injury and implications for neurorehabilitation.</p></div>","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 4","pages":"Pages 420-427"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.07.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26283934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Drug Development in Critical Times","authors":"Lisa J. Bain","doi":"10.1016/j.nurx.2006.08.004","DOIUrl":"10.1016/j.nurx.2006.08.004","url":null,"abstract":"","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 4","pages":"Pages 540-543"},"PeriodicalIF":0.0,"publicationDate":"2006-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.08.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26311374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single Cell Gene Expression Profiling in Alzheimer’s Disease","authors":"Stephen D. Ginsberg ,&nbsp;Shaoli Che ,&nbsp;Scott E. Counts ,&nbsp;Elliott J. Mufson","doi":"10.1016/j.nurx.2006.05.007","DOIUrl":"10.1016/j.nurx.2006.05.007","url":null,"abstract":"<div><p><span><span>Development and implementation of microarray techniques to quantify expression levels of dozens to hundreds to thousands of transcripts simultaneously within select tissue samples from normal control subjects and neurodegenerative diseased brains has enabled scientists to create molecular fingerprints of vulnerable neuronal populations in Alzheimer’s disease (AD) and related disorders. A goal is to sample gene expression from homogeneous cell types within a defined region without potential contamination by expression profiles of adjacent neuronal subpopulations and </span>nonneuronal cells. The precise resolution afforded by single cell and population cell RNA analysis in combination with microarrays and </span>real-time quantitative polymerase chain reaction<span> (qPCR)–based analyses allows for relative gene expression level comparisons across cell types under different experimental conditions and disease progression. The ability to analyze single cells is an important distinction from global and regional assessments of mRNA expression and can be applied to optimally prepared tissues from animal models of neurodegeneration as well as postmortem human brain tissues. Gene expression analysis in postmortem AD brain regions including the hippocampal formation and neocortex reveals selectively vulnerable cell types share putative pathogenetic alterations in common classes of transcripts, for example, markers of glutamatergic<span> neurotransmission, synaptic-related markers, protein phosphatases and kinases, and neurotrophins/neurotrophin receptors. Expression profiles of vulnerable regions and neurons may reveal important clues toward the understanding of the molecular pathogenesis of various neurological diseases and aid in identifying rational targets toward pharmacotherapeutic interventions for progressive, late-onset neurodegenerative disorders such as mild cognitive impairment (MCI) and AD.</span></span></p></div>","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 3","pages":"Pages 302-318"},"PeriodicalIF":0.0,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.05.007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26124210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Measuring Cortical Acetylcholine Esterase Activity by PET in Dementia: Clinical Correlates","authors":"K. Herholz,&nbsp;S. Weisenbach,&nbsp;R. Hilker,&nbsp;W. Heiss","doi":"10.1016/j.nurx.2006.05.020","DOIUrl":"10.1016/j.nurx.2006.05.020","url":null,"abstract":"<div><p>The acetylcholine analogue C-11-<em>N</em>-methyl-4-piperidinyl-acetate (MP4A) is a tracer for positron emission tomography (PET) to investigate the integrity of the cerebral cholinergic system. It is a substrate of acetylcholine esterase (AChE), which is associated with cholinergic axons in human cortex. We used this technique to determine whether cortical reductions of AChE activity in dementia are associated with clinical symptoms and progression.</p><p>We examined the following age-matched subjects: 12 normal controls, 8 mild cognitive impairment (MCI, MMSE 27 ± 2), 10 mild Alzheimer’s disease (AD, MMSE 21 ± 4), 10 Parkinson’s disease dementia (PDD, MMSE 21 ± 6), and 10 non-demented PD (MMSE 27 ± 2). Cortical AChE activity was reduced significantly in all demented subjects and in those four MCI patients, who progressed to dementia within 18 months. The most severe reduction (by 30 ± 5%) was seen in PDD, followed by AD (23 ± 2%) and nondemented PD (12 ± 2%, <em>p</em> &lt; 0.01 compared to controls). Thus, the manifestation of dementia in PD was associated with a significant reduction of cortical AChE activity, which was most severe in the left inferior parietal lobule, the left precental gyrus, and the right posterior cingulate gyrus (SPM, <em>p</em> &lt; 0.001). In mild to moderate AD, regional AChE activity in temporal, parietal, and frontal association cortices was associated with attention-dependent test performance (Rey-Osterrieth figure copy, digit span forward and reverse, visual span reverse).</p><p>We conclude that a reduction of cortical AChE activity is a common feature of Alzheimer’s and Parkinson’s dementia and appears to be related mainly to impairment of attention. It is present very early during the course of the disease, even at a predementia stage. It is likely to indicate functional impairment of the synapses or of axonal transport of ascending cholinergic neurons.</p></div>","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 3","pages":"Page 410"},"PeriodicalIF":0.0,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.05.020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54959187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Application of NMR-Based Metabonomics in Neurological Disorders","authors":"Elaine Holmes ,&nbsp;Tsz M. Tsang ,&nbsp;Sarah J. Tabrizi","doi":"10.1016/j.nurx.2006.05.004","DOIUrl":"10.1016/j.nurx.2006.05.004","url":null,"abstract":"<div><h3>Summary</h3><p>Advances in postgenomic technologies have radically changed the information output from complex biological systems, generating vast amounts of high complexity data that can be interpreted by means of chemometric and bioinformatic methods to achieve disease diagnosis and prognosis. High-resolution nuclear magnetic resonance (NMR) spectroscopy of biofluids such as plasma, cerebrospinal fluid (CSF), and urine can generate robust, interpretable metabolic fingerprints that contain latent information relating to physiological or pathological status. This technology has been successfully applied to both preclinical and clinical studies of neurodegenerative diseases such as Huntington’s disease, muscular dystrophy, and cerebellar ataxia. An extension of this technology, ¹H magic-angle-spinning (HRMAS) NMR spectroscopy, can be used to generate metabolic information on small intact tissue samples, providing a metabolic link between metabolic profiling of biofluids and histology. In this review we provide a summary of high-resolution NMR studies in neurodegenerative disease and explore the potential of metabonomics in evaluating disease progression with respect to therapeutic intervention.</p></div>","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 3","pages":"Pages 358-372"},"PeriodicalIF":0.0,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.05.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26122305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}