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The burden of clinical neurophysiology for the neurological prognosis of coma 昏迷神经预后的临床神经生理学负担
IF 1.3
Future Neurology Pub Date : 2018-08-01 DOI: 10.2217/FNL-2018-0013
M. Scarpino, A. Grippo, G. Lanzo, F. Lolli
{"title":"The burden of clinical neurophysiology for the neurological prognosis of coma","authors":"M. Scarpino, A. Grippo, G. Lanzo, F. Lolli","doi":"10.2217/FNL-2018-0013","DOIUrl":"https://doi.org/10.2217/FNL-2018-0013","url":null,"abstract":"","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":"13 1","pages":"127-129"},"PeriodicalIF":1.3,"publicationDate":"2018-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47395816","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}
引用次数: 18
Intravenous phenytoin in convulsive status epilepticus: the devil we (think we) know 静脉注射苯妥英治疗惊厥癫痫持续状态:我们(自认为)知道的魔鬼
IF 1.3
Future Neurology Pub Date : 2018-08-01 DOI: 10.2217/FNL-2018-0011
Francesco Brigo, S. Lattanzi
{"title":"Intravenous phenytoin in convulsive status epilepticus: the devil we (think we) know","authors":"Francesco Brigo, S. Lattanzi","doi":"10.2217/FNL-2018-0011","DOIUrl":"https://doi.org/10.2217/FNL-2018-0011","url":null,"abstract":"","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":"1 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2018-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42952896","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}
引用次数: 2
Advancing personalized treatment of Alzheimer's disease: a call for the N-of-1 trial design 推进阿尔茨海默病的个性化治疗：对1选N试验设计的呼吁
IF 1.3
Future Neurology Pub Date : 2018-08-01 DOI: 10.2217/FNL-2018-0004
J. Galvin
{"title":"Advancing personalized treatment of Alzheimer's disease: a call for the N-of-1 trial design","authors":"J. Galvin","doi":"10.2217/FNL-2018-0004","DOIUrl":"https://doi.org/10.2217/FNL-2018-0004","url":null,"abstract":"There has not been a new treatment for Alzheimer's disease (AD) for over a decade, with a large number of Phase II/III randomized clinical trials failing. Randomized clinical trials examine group effects that may be difficult to extrapolate to the individual patient given the multifactorial pathogenic processes associated with AD, and are increasingly long in duration, expensive to run, requiring large sample sizes that are difficult to recruit. An alternative approach is to consider N-of-1 trial designs. The N-of-1 trial is ideal to evaluate effectiveness of interventions for chronic conditions combining the rigor of a randomized trial with the tailoring of therapy to an individual. This review examines the N-of-1 design, its benefits and limitations, and how it could be implemented to investigate new therapies for AD.","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2018-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45538435","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}
引用次数: 9
Motor neuron biology and disease: A current perspective on infantile-onset spinal muscular atrophy. 运动神经元生物学与疾病:婴儿期脊髓性肌萎缩的最新研究进展。
IF 1.3
Future Neurology Pub Date : 2018-07-06 DOI: 10.2217/FNL-2018-0008
Narendra N. Jha, Jeong-Ki Kim, U. Monani
{"title":"Motor neuron biology and disease: A current perspective on infantile-onset spinal muscular atrophy.","authors":"Narendra N. Jha, Jeong-Ki Kim, U. Monani","doi":"10.2217/FNL-2018-0008","DOIUrl":"https://doi.org/10.2217/FNL-2018-0008","url":null,"abstract":"Infantile-onset spinal muscular atrophy (SMA) is a prototypical disease in which to investigate selective neurodegenerative phenotypes. Caused by low levels of the ubiquitously expressed Survival Motor Neuron (SMN) protein, the disease mainly targets the spinal motor neurons. This selective phenotype remains largely unexplained, but has not hindered the development of SMN repletion as a means to a treatment. Here we chronicle recent advances in the area of SMA biology. We provide a brief background to the disease, highlight major advances that have shaped our current understanding of SMA, trace efforts to treat the condition, discuss the outcome of two promising new therapies and conclude by considering contemporary as well as new challenges stemming from recent successes within the field.","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":"13 3 1","pages":"161-172"},"PeriodicalIF":1.3,"publicationDate":"2018-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48693954","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}
引用次数: 9
Pathological human astroglia in Alzheimer's disease: Opening new horizons with stem cell technology 阿尔茨海默病中的病理性人类星形胶质细胞：用干细胞技术开辟新视野
IF 1.3
Future Neurology Pub Date : 2018-05-01 DOI: 10.2217/FNL-2017-0029
L. Mohamet, V. C. Jones, G. Dayanithi, A. Verkhratsky
{"title":"Pathological human astroglia in Alzheimer's disease: Opening new horizons with stem cell technology","authors":"L. Mohamet, V. C. Jones, G. Dayanithi, A. Verkhratsky","doi":"10.2217/FNL-2017-0029","DOIUrl":"https://doi.org/10.2217/FNL-2017-0029","url":null,"abstract":"Pathological remodeling, degeneration and reactivity of astrocytes are fundamental astrogliopathies contributing to all neurological diseases. In neurodegenerative disorders (including Alzheimer's disease [AD]) astroglia undergo complex changes that range from atrophy with loss of function to accumulation of reactive cells around disease-specific lesions (senile plaques in the case of AD). The cellular pathology of astroglia in the context of human AD remains enigmatic; mainly because of the severe limitations of animal models, which, although reproducing some pathological features of the disease, do not mimic its progression in full. Human-induced pluripotent stem cells technology creates a novel and potentially revolutionizing platform for studying fundamental mechanisms of the disease and for screening to identify new therapeutic compounds.","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":"13 1","pages":"87-99"},"PeriodicalIF":1.3,"publicationDate":"2018-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2017-0029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42929736","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}
引用次数: 8
Is cognitive training able to improve brain functioning with age 认知训练能随着年龄的增长而改善大脑功能吗
IF 1.3
Future Neurology Pub Date : 2018-05-01 DOI: 10.2217/FNL-2018-0007
M. Motes
{"title":"Is cognitive training able to improve brain functioning with age","authors":"M. Motes","doi":"10.2217/FNL-2018-0007","DOIUrl":"https://doi.org/10.2217/FNL-2018-0007","url":null,"abstract":"","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":"13 1","pages":"41-44"},"PeriodicalIF":1.3,"publicationDate":"2018-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47969367","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}
引用次数: 4
The mTOR pathway in treatment of epilepsy: a clinical update. mTOR通路在癫痫治疗中的应用:临床进展
IF 1.3
Future Neurology Pub Date : 2018-05-01 Epub Date: 2018-05-29 DOI: 10.2217/fnl-2018-0001
Jennifer L Griffith, Michael Wong
{"title":"The mTOR pathway in treatment of epilepsy: a clinical update.","authors":"Jennifer L Griffith,&nbsp;Michael Wong","doi":"10.2217/fnl-2018-0001","DOIUrl":"https://doi.org/10.2217/fnl-2018-0001","url":null,"abstract":"<p><p>Nearly a third of patients with epilepsy have seizures refractory to current medical therapies. In the search for novel drug targets, the mTOR pathway has emerged as key in the regulation of neuronal function, growth and survival, and other cellular processes related to epileptogenesis. Hyperactivation of the mTOR pathway has been implicated in tuberous sclerosis complex and other 'mTORopathies', clinical syndromes associated with cortical developmental malformations and drug-resistant epilepsy. Recently published clinical trials of mTOR inhibitors in tuberous sclerosis complex have shown that these drugs are effective at decreasing seizure frequency. Future studies may establish whether mTOR inhibitors can provide effective treatment for patients with diverse genetic and acquired epilepsies, including preventative, disease-modifying therapies.</p>","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":"13 2","pages":"49-58"},"PeriodicalIF":1.3,"publicationDate":"2018-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/fnl-2018-0001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36727559","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}
引用次数: 44
The use of erenumab for migraine prevention: an interview with Andreas Gantenbein 阿仑单抗预防偏头痛的应用：Andreas Gantenbein访谈
IF 1.3
Future Neurology Pub Date : 2018-05-01 DOI: 10.2217/FNL-2018-0009
A. Gantenbein
{"title":"The use of erenumab for migraine prevention: an interview with Andreas Gantenbein","authors":"A. Gantenbein","doi":"10.2217/FNL-2018-0009","DOIUrl":"https://doi.org/10.2217/FNL-2018-0009","url":null,"abstract":"","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":"13 1","pages":"45-47"},"PeriodicalIF":1.3,"publicationDate":"2018-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42344312","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}
引用次数: 0
New directions in therapeutics for Huntington disease. 亨廷顿病治疗的新方向。
IF 1.3
Future Neurology Pub Date : 2018-05-01 Epub Date: 2018-05-29 DOI: 10.2217/fnl-2017-0035
Katya T Potkin, Steven G Potkin
{"title":"New directions in therapeutics for Huntington disease.","authors":"Katya T Potkin,&nbsp;Steven G Potkin","doi":"10.2217/fnl-2017-0035","DOIUrl":"https://doi.org/10.2217/fnl-2017-0035","url":null,"abstract":"<p><p>Huntington disease (HD) is an autosomal dominantly inherited neurodegenerative disease that affects motor, cognitive and psychiatric functions, and ultimately leads to death. The pathology of the disease is based on an expansion of CAG repeats in exon 1 of the <i>huntingtin</i> gene on chromosome 4, which produces a mutant huntingtin protein (mHtt). This protein is involved in neurotoxicity and brain atrophy, and can form β-sheets and abnormal mHtt aggregates. Currently, there are no approved effective treatments for HD, although tetrabenazine (Xenazine™) and deutetrabenazine (AUSTEDO™) have been approved for treatment of the motor symptom chorea in HD. This literature review aims to address the latest research on promising therapeutics based on influencing the hypothesized pathological mechanisms.</p>","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":"13 2","pages":"101-121"},"PeriodicalIF":1.3,"publicationDate":"2018-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/fnl-2017-0035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37155544","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}
引用次数: 25
Pleiotropy and promiscuity in pharmacogenomics for the treatment of Alzheimer's disease and related risk factors 治疗阿尔茨海默病的药物基因组学中的多效性和混杂性及其相关危险因素
IF 1.3
Future Neurology Pub Date : 2018-02-05 DOI: 10.2217/FNL-2017-0038
R. Cacabelos
{"title":"Pleiotropy and promiscuity in pharmacogenomics for the treatment of Alzheimer's disease and related risk factors","authors":"R. Cacabelos","doi":"10.2217/FNL-2017-0038","DOIUrl":"https://doi.org/10.2217/FNL-2017-0038","url":null,"abstract":"Patients with Alzheimer's disease are current consumers of polypharmacy with a high risk for drug–drug interactions. Antidementia drugs and other pharmacological treatments for vascular risk factors associated with dementia exert pleiotropic effects which are promiscuously regulated by different gene products. The aim of this review is to highlight the influence of genes involved in pharmacogenetics (i.e., pathogenic, mechanistic, metabolic, transporter and pleiotropic genes) as major determinants of response to treatment in Alzheimer's disease. Patients harboring poor or ultrarapid geno-phenotypes display more irregular profiles in drug efficacy and safety than extensive or intermediate metabolizers. Polymorphic variants of genes associated with lipid metabolism influence the therapeutic response to hypolipemic agents. Understanding these effects is very useful for optimizing polytherapy in dementia.","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":"13 1","pages":"71-86"},"PeriodicalIF":1.3,"publicationDate":"2018-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2017-0038","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48195254","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}
引用次数: 14
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