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

{"title":"Neurosurgical Treatment of Intractable Tourette’s Syndrome: A Scientific Clinical Review of Literatures","authors":"M. Meratee,&nbsp;J. Chung,&nbsp;J. Schweitzer","doi":"10.1016/j.nurx.2006.05.013","DOIUrl":"10.1016/j.nurx.2006.05.013","url":null,"abstract":"<div><h3>Background</h3><p>Tourette’s syndrome (TS) is an inherited neuropsychiatric disorder characterized by fluctuating motor and vocal tics that starts in childhood. Diagnostic criteria for TS include the presence of multiple motor tics and one or more vocal tics, both of which must exceed a year’s duration. Pharmacotherapy has been the mainstay of the treatment. However, some TS patients will not respond to conventional medications. They might develop residual debilitating symptoms. The current article examines the reported experience with neurosurgical treatment of intractable Tourette’s syndrome.</p></div><div><h3>Design/Method</h3><p>All articles and textbooks containing descriptions of Tourette’s syndrome and its surgical treatment were reviewed. All related articles in PubMed were searched using these words: Tourette’s syndrome, TS, Tourette, Gilles de la Tourette, tic, tics, surgical treatment of tic disorders, surgical intervention of Tourrete’s syndrome, ablative surgery in Tourette’s syndrome, stereotactic surgery of Tourette’s syndrome. Only articles published in English were reviewed. In total, 11 articles and 2 textbooks were found describing the experimental surgery of refractory Tourette’s syndrome. All data about patient’s history, surgical treatment, outcome and side effects were collected and reviewed.</p></div><div><h3>Results</h3><p>Intractable Tourette’s syndrome may represent a special subgroup of the tic range. A variety of experimental procedures have been performed in an attempt to treat intractable Tourette’s syndrome, including: 1) frontal lobe operation (i.e., frontal lobotomy and bimedial frontal leucotomy), 2) limbic system operation (i.e., anterior cingulotomy, limbic leucotomy), 3) a novel multisite operation (i.e., anterior cingulotomy combined with infrathalamic lesions), 4) thalamic operation (i.e., bilateral coagulation of rostral infrathalamic and medial thalamic nuclei), and 5) a cerebellar operation (i.e., bilateral cerebellar dentatomy). There are serious uncertainties regarding any experimental neurosurgical procedures. However, in the case of severe, intractable Tourette’s syndrome, these appropriate concerns must be weighed against the risks of conventional therapies, including tardive dyskinesia. Patients who suffer from severe Tourette’s syndrome, and are debilitated by their symptoms, and have failed an exhaustive range of conventional pharmacologic therapies could be candidates for an experimental treatment.</p></div><div><h3>Conclusion</h3><p>Case reports in the literature provide only anecdotal evidence supporting the efficacy and safety of neurosurgical treatment of Tourette’s syndrome. There is no convincing evidence showing that any particular neurosurgical procedure is best for Tourette’s syndrome. If experimental neurosurgery for Tourette’s syndrome is to continue, then guidelines should be developed regarding patient and operation selection. Also, accurate clinical measurement should be a","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 3","pages":"Page 408"},"PeriodicalIF":0.0,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.05.013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54958859","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":"Androstenol (5α-androst-16-en-3α-ol) Is a Novel Neurosteroid Positive Modulator of GABAA Receptors: In Vitro and In Vivo Studies","authors":"R.M. Kaminski ,&nbsp;H. Marini ,&nbsp;P.I. Ortinski ,&nbsp;W. Yonekawa ,&nbsp;S. Vicini ,&nbsp;M.A. Rogawski","doi":"10.1016/j.nurx.2006.05.030","DOIUrl":"10.1016/j.nurx.2006.05.030","url":null,"abstract":"<div><p>Androstenol (5α-androst-16-en-3α-ol) is a volatile steroid compound belonging to the group of 16-androstenes found in human plasma. It is structurally similar to endogenous A-ring reduced steroids that act as positive modulators of GABA_A receptors, i.e., neurosteroids. Thus, we have hypothesized that androstenol may have electrophysiological and behavioral traits characteristic for neurosteroids.</p><p>The influence of androstenol on GABA_A receptors currents under voltage clamp conditions in mouse cerebellar granule cell cultures, rat brain slices, and HEK cells expressing human GABA_A receptor subunits has been assessed. Additionally, the effect of androstenol on 4-aminopyridine–induced epileptiform activity in rat hippocampal slices was studied. Assessment of anticonvulsant, anxiolytic, and antidepressant effects of androstenol in the 6 Hz, PTZ, open field, and forced swim models has also been performed.</p><p>We have found that androstenol potentiates GABA-evoked currents in HEK cells as well as in cerebellar cultures and slices. Androstenol inhibited epileptiform activity induced by 4-aminopyridine in rat brain slices and had strong anticonvulsant effects against PTZ- and 6 Hz-induced seizures in mice. In addition, we have found that androstenol has anxiolytic and antidepressant effects in animal models.</p><p>These results for the first time demonstrate that androstenol acts as a positive modulator of GABA_A receptors and has behavioral properties compatible with this physiological action. Androstenol may act as an endogenous modulator of GABA_A receptors, and it may be useful in treatment of epilepsy and possibly other neurological disorders, i.e., anxiety and depression.</p></div>","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 3","pages":"Pages 413-414"},"PeriodicalIF":0.0,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.05.030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54959846","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 Microarray Data Analysis Process: From Raw Data to Biological Significance","authors":"N. Eric Olson","doi":"10.1016/j.nurx.2006.05.005","DOIUrl":"10.1016/j.nurx.2006.05.005","url":null,"abstract":"<div><h3>Summary</h3><p>Despite advances in microarray technology that have led to increased reproducibility and substantial reductions in the cost of microarrays, the successful use of this technology is still elusive for many researchers, and microarray data analysis in particular presents a substantial bottleneck for many biomedical researchers. There are many reasons for this, including the expense of and a lack of adequate training in the use of analysis software. An additional reason is that microarray data analysis has largely been treated in the past as a set of separate steps, with the majority of emphasis being placed on statistical analysis and visualization of the data. For many biomedical researchers determining the biological significance of the data has been the greatest challenge and in the last several years more emphasis has been placed on this aspect of the analysis process. Despite this broadening of the scope of analysis there are still several aspects of the process that continue to be neglected, including additional related and interdependent aspects, such as experimental design, data accessibility, and platform selection. Though not traditionally thought of as integral to the data analysis process, these factors have profound effects on the analysis process. This article will discuss the importance of these additional aspects, as well as statistical analysis and determination of biological significance of microarray data. A summary of currently available software options will also be presented with a focus on the aspects discussed.</p></div>","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 3","pages":"Pages 373-383"},"PeriodicalIF":0.0,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.05.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26122304","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":"Imaging of Neurotransmitter Deficits: New Potential Biomarkers for Alzheimer’s Disease?","authors":"K. Herholz,&nbsp;A. Nordberg,&nbsp;J. Masdeu,&nbsp;A. Gerhard,&nbsp;K. Ebmeier,&nbsp;S. Pappata,&nbsp;D. Perani,&nbsp;K. van Laere,&nbsp;C. Halldin,&nbsp;E. Salmon,&nbsp;G. Knudsen","doi":"10.1016/j.nurx.2006.05.026","DOIUrl":"10.1016/j.nurx.2006.05.026","url":null,"abstract":"<div><p>There is growing agreement that early diagnosis of Alzheimer’s disease (AD) prior to onset of dementia is required for efficient clinical trials of neuroprotective interventions. In the past years, substantial progress has been made in that respect by refining clinical and neuropsychological assessment and quantitative evaluation of structural and functional brain imaging (mainly MRI and PET). It is also hoped that quantitative imaging will provide more efficient means to monitor disease progression than repeated neuropsychological testing. Alzheimer’s disease is likely to be a common clinical manifestation with diverse and multifactorial etiology, and it also needs to be distinguished from other dementias, such as fronto-temporal dementia (FTD), dementia with Lewy bodies (DLB), and vascular dementia (VD). Yet, currently available clinical tools do not yet allow identifying specific etiologies and distinguishing between different dementing diseases at the clinical stage of mild cognitive impairment.</p><p>To address these needs, we have formed a multicentre network to compare molecular and neurotransmitter imaging in mild cognitive impairment. Within this network we are including normal controls and patients with mild cognitive impairment using harmonized longitudinal study protocols that share common neuropsychological and clinical assessment (MMSE, DemTect, CDR, Rey auditory verbal learning and complex figure, digit span, verbal fluency, trail making, IADL, Geriatric depression scale, NPI). Participating laboratories have established positron emission tomography (PET) or single photon emission computed tomography (SPECT) procedures to assess <em>in vivo</em> key molecular events, specifically amyloid deposition (C-11-PIB) and microglial activiation (C-11-PK11195), and assessment of neurotransmitter deficits, specifically acetylcholine esterase (C-11-MP4A, C-11-MP4P), nicotinic receptors (I-123-A85380), serotonin and benzodiazepine receptors, and dopamine transporters.</p><p>Preliminary results and evidence from postmortem studies suggest that amyloid deposition and cholinergic deficits occur early in AD but not in FTD, serotonergic deficits may be present in AD and FTD, whereas a dopaminergic deficit is seen in DLB only. The ongoing studies in MCI patients should provide more information on whether early differential diagnosis is possible and could become available for testing of drugs that target specific molecular mechanisms and transmitter systems.</p></div>","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 3","pages":"Page 412"},"PeriodicalIF":0.0,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.05.026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54959655","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":"Prolonged Attenuation of Amygdla Kindled Seizures by Local Delivery of Large Molecular Weight Therapeutic Agents by Convection-Enhanced Delivery in Rats","authors":"M. Gasior,&nbsp;R. Tang,&nbsp;N. White,&nbsp;M.A. Rogawski","doi":"10.1016/j.nurx.2006.05.031","DOIUrl":"10.1016/j.nurx.2006.05.031","url":null,"abstract":"<div><p>Many patients with temporal lobe epilepsy (TLE) respond inadequately to antiepileptic drugs, necessitating resective surgery as a last resort. An alternative less invasive approach is site-specific delivery of therapeutic agents into the epileptic focus. However, conventional intraparenchymal injection produces localized tissue damage and there is poor control over the drug distribution. Convection-enhanced delivery (CED) is an alternative infusion technique that allows for the nondestructive and well-controlled localized delivery of solutes, including high molecular weight agents (e.g., peptides, proteins, and even viral vectors). The present study examined whether long-term changes in amygdala-kindled seizure susceptibility can be produced by a one-time CED infusion into the amygdala. Agents selected for study were presynaptic neurotoxins capable of producing long-term attenuation of neurotransmitter release either by inhibiting N-type calcium channels (i.e., ω-conotoxins GVIA and MVIIA) or cleaving intracellular proteins involved in exocytosis (i.e., botulinum toxins type A and B). A conventional, small-molecule antiepileptic drug, carbamazepine, was used for comparison.</p><p>Each rat was implanted with a combination infusion cannula and stimulation electrode into the right basolateral amygdala. Daily stimulations were carried out until the animals were fully kindled (stage 5 seizures for at least five consecutive days). Then, the rats received infusions of vehicle alone or ω-conotoxins (5-500 pmol), botulinum toxins (7-67 fmol), or carbamazepine (500 nmol) through the cannula whose tip was adjacent to the stimulation site. Each dose was delivered in a volume of 5 μL at a rate of 0.25 μL/min. Electrophysiological (afterdischarge threshold and duration) and behavioral (seizure stage and duration) measures of amygdala-kindled seizures were recorded daily for up to 64 days after the infusion.</p><p>There were no changes in any of the kindling parameters in rats that had received vehicle infusions. In contrast, infusions of ω-conotoxins and botulinum toxins resulted in a dose- and time-dependent increase in the afterdischarge threshold and a decrease in seizure stage and duration, indicting an inhibitory effect on kindled seizure expression. The protective effects of ω-conotoxins reached a maximum at 48 h postinfusion and then gradually dissipated within the next five days; in contrast, effects of botulinum toxins lasted for several weeks. Infusions of each toxin appeared well tolerated and devoid of any immediate or long-term side effects. In marked contrast to the long-lasting effects produced by ω-conotoxins and botulinum toxins, attenuation of seizures produced by carbamazepine lasted only a few hours after the infusion.</p><p>These results indicate that local CED-mediated delivery of high molecular weight presynaptic toxins can produce long-lasting anticonvulsant effects that persist for weeks. Whether this approach will be useful in","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 3","pages":"Page 414"},"PeriodicalIF":0.0,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.05.031","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54959882","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":"Dose Decrease and Other Correlates of Relapse in Patients with Schizophrenia or Schizoaffective Disorder During Olanzapine Drug Therapy","authors":"W. Deberdt,&nbsp;J. Csernansky,&nbsp;P. Buckley,&nbsp;J. Peiskens,&nbsp;I. Lipkovich,&nbsp;S. Kollack-Walter,&nbsp;J. Houston,&nbsp;Y. Zhang,&nbsp;H. Liu-Siefert","doi":"10.1016/j.nurx.2006.05.017","DOIUrl":"10.1016/j.nurx.2006.05.017","url":null,"abstract":"<div><h3>Purpose</h3><p>To assess dose decrease and other variables as correlates of relapse during olanzapine treatment.</p></div><div><h3>Methods</h3><p>In two 28-week, randomized, double-blind clinical trials, a Cox proportional hazards model was used for <em>post hoc</em> analysis of potential correlates of relapse (defined as ≥20% worsening on PANSS total and CGI-Severity ≥ 3) among patients (<em>N</em> = 271) who responded to 8 weeks of olanzapine treatment (10-20 mg/day). Variables examined included demographics, illness characteristics, baseline symptoms, symptom changes, dose, adverse events, and functioning.</p></div><div><h3>Results</h3><p>Patients with a lower last dose relative to that of the preceding visit interval were 4 times more likely to relapse during that visit interval than patients without a lower dose (<em>p</em> &lt; 0.001). A similar finding was observed for a decrease in interval modal dose and risk for relapse, although this relationship was more predictive of relapse in the next visit interval (<em>p</em> = 0.027). A dose decrease in women was not associated with relapse (<em>p</em> = 0.922), whereas a dose decrease in men did predict relapse (<em>p</em> &lt; 0.001). Relapse also correlated with the emergence or worsening of a psychiatric adverse event during the same visit interval as relapse (<em>p</em> &lt; 0.001), and during the preceding visit interval (<em>p</em> = 0.007). The occurrence of a nonpsychiatric adverse event was not associated with relapse.</p></div><div><h3>Conclusion</h3><p>Dose decrease was a significant predictor of relapse in male patients. Psychiatric adverse events were also a significant predictor of relapse. Symptom worsening and dose decrease are both clinical measures that call for closer monitoring of patients due to increased likelihood of relapse.</p></div>","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 3","pages":"Page 409"},"PeriodicalIF":0.0,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.05.017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54959069","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":"Prediction of Combined Symptomatic and Functional Outcome in Patients with Schizophrenia or Schizoaffective Disorder","authors":"I. Lipkovich ,&nbsp;W. Deberdt ,&nbsp;P.F. Buckley ,&nbsp;J.G. Csernansky ,&nbsp;J. Peuskens ,&nbsp;S. Kollack-Walker ,&nbsp;J.P. Houston ,&nbsp;M. Rotelli","doi":"10.1016/j.nurx.2006.05.018","DOIUrl":"10.1016/j.nurx.2006.05.018","url":null,"abstract":"<div><h3>Purpose</h3><p>An earlier analysis of data from six randomized, active-control studies involving 1449 patients identified five distinct clusters characterized by different combinations of psychiatric and functional outcomes. We explored baseline demographics, disease characteristics, early symptom response, treatment, and adverse events as possible predictors of clusters representing best and worst clinical outcomes.</p></div><div><h3>Methods</h3><p>At 6-month endpoint in combined treatment groups, good outcome (Cluster A) was associated with good functioning and limited psychopathology. Poor outcome was associated with poor functioning and moderate (Cluster D) or severe (Cluster E) psychopathology. Stepwise logistic regression was used to construct predictive models of cluster membership (<em>N</em> = 1260) for baseline predictors and with 2/4/8 weeks of treatment. Odds ratios were adjusted for study effects.</p></div><div><h3>Results</h3><p>Cluster A baseline predictors included female gender and higher levels of occupational and psychosocial functioning. Greater improvement across PANSS factors during early treatment also predicted good outcome. Cluster D baseline predictors included earlier onset of illness, older age, pseudoparkinsonism, and worse occupational and psychosocial functioning; subsequent worsening in PANSS depression and positive factor scores and in functioning predicted poor outcome for Cluster D. Predictors of Cluster E included earlier onset of illness, non-olanzapine treatment, and higher scores on the PANSS depression, hostility, and positive factors; subsequent worsening in PANSS disorganization, negative, and positive factor scores was predictive of poor outcome for Cluster E.</p></div><div><h3>Conclusion</h3><p>Early symptom improvement/worsening was predictive of outcome. Early monitoring of psychiatric symptoms and functioning may lead to better therapeutic decisions based on individual characteristics.</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.2006.05.018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54959106","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":"Duloxetine in the Management of Diabetic Peripheral Neuropathic Pain: Response Profile","authors":"Y. Pritchett,&nbsp;B. McCarberg,&nbsp;J. Watkin,&nbsp;A. Chappell,&nbsp;M. Robinson","doi":"10.1016/j.nurx.2006.05.011","DOIUrl":"10.1016/j.nurx.2006.05.011","url":null,"abstract":"<div><h3>Introduction</h3><p>Analyses examine the response rate at endpoint, as well as time course of response, in patients receiving duloxetine for management of diabetic peripheral neuropathic pain (DPNP).</p></div><div><h3>Methods</h3><p>Data were pooled from 3 double-blind, randomized, placebo-controlled 12-week trials in patients with DPNP ≥ 6 months duration, and without depression. Study 1 (<em>N</em> = 457) compared duloxetine 20 mg once daily (QD), 60 mg QD, 60 mg twice daily (BID), and placebo; Studies 2 (<em>N</em> = 334) and 3 (<em>N</em> = 348) compared duloxetine 60 mg QD and 60 mg BID with placebo. Ethics committees approved the study protocol in accordance with Declaration of Helsinki principles. Patients provided written informed consent prior to study participation. Treatment response was defined a priori as 30% reduction in the primary efficacy measure, 24-hour average pain severity. Analysis was replicated using alternative criteria (50% reduction or 2-point reduction).</p></div><div><h3>Results</h3><p>Endpoint response rates were significantly higher among patients receiving duloxetine (60 mg QD or 60 mg BID) than those receiving placebo, regardless of chosen response criterion. The proportion of patients responding (30% reduction in 24-hour average pain severity) to duloxetine was statistically greater than to placebo Week 1 and all subsequent visits. Similar results were obtained for the visitwise sustained response rate. Within the group with a sustained response at Week 12, the proportion of patients first exhibiting a response at Weeks 1 or 2 was higher in the duloxetine groups (60 mg QD, 65.0%; 60 mg BID, 62.0%) when compared with the placebo group (40.2%).</p></div><div><h3>Conclusion</h3><p>Patients with DPNP receiving duloxetine 60 mg QD or 60 mg BID had significantly higher treatment response rates compared with patients receiving placebo, regardless of response criterion. Response to duloxetine treatment tended to occur early, with approximately 30% of patients responding at Week 1. Among duloxetine-treated patients with a sustained treatment response at Week 12, over 60% had maintained responder status for 10 to 11 weeks.</p></div>","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 3","pages":"Page 407"},"PeriodicalIF":0.0,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.05.011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129328813","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":"Systems Biology: A Primer","authors":"Howard J. Federoff M.D., Ph.D. (Guest Editor),&nbsp;Timothy R. Mhyre Ph.D. (Guest Editor)","doi":"10.1016/j.nurx.2006.05.035","DOIUrl":"10.1016/j.nurx.2006.05.035","url":null,"abstract":"","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 3","pages":"Pages 293-294"},"PeriodicalIF":0.0,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.05.035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26124207","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":"Microarrays in Parkinson’s Disease: A Systematic Approach","authors":"Renee M. Miller ,&nbsp;Howard J. Federoff","doi":"10.1016/j.nurx.2006.05.008","DOIUrl":"10.1016/j.nurx.2006.05.008","url":null,"abstract":"<div><h3>Summary</h3><p>Neurological disease (ND) is one of the greatest challenges facing our population, from medical, financial, and social perspectives. The application of new research approaches to understand the underlying pathogenesis of ND is critical. In this article, we review the use of microarray analysis in Parkinson’s disease (PD). Microarrays have tremendous power, simultaneously querying the expression of tens of thousands of genes from a given biological sample. Coupled with impressive advances in statistical tools for analyzing large, complex data sets, well-designed microarray experiments are poised to make a big impact in the field of ND. Parkinson’s disease is a devastating neurodegenerative disease well suited to a systems-based microarray analysis. Genetic and environmental rodent models of PD emulate many of the cardinal features of human PD, providing the unique opportunity to compare gene expression profiles from different etiologies of the same disease. The elucidation of important gene expression patterns during disease will make possible identification of genetic susceptibility markers, biomarkers of disease progression, and new therapeutic targets.</p></div>","PeriodicalId":87195,"journal":{"name":"NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics","volume":"3 3","pages":"Pages 319-326"},"PeriodicalIF":0.0,"publicationDate":"2006-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nurx.2006.05.008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26124209","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}