Degenerative Neurological and Neuromuscular Disease最新文献_第8页

Use of transcranial magnetic stimulation in the treatment of selected movement disorders. 使用经颅磁刺激治疗选定的运动障碍。

Degenerative Neurological and Neuromuscular Disease Pub Date : 2014-12-04 eCollection Date: 2014-01-01 DOI: 10.2147/DNND.S70079

Katlyn E Brown, Jason L Neva, Noah Mh Ledwell, Lara A Boyd

引用次数: 11

Erratum: Epigenetic mechanisms in Alzheimer's disease [Corrigendum]. 勘误:阿尔茨海默病的表观遗传机制[勘误]。

Degenerative Neurological and Neuromuscular Disease Pub Date : 2014-09-15 eCollection Date: 2014-01-01 DOI: 10.2147/DNND.S72446

引用次数: 0

Intravenous immunoglobulin for the treatment of Alzheimer's disease: current evidence and considerations. 静脉注射免疫球蛋白治疗阿尔茨海默病：现有证据和考虑因素。

Degenerative Neurological and Neuromuscular Disease Pub Date : 2014-09-05 eCollection Date: 2014-01-01 DOI: 10.2147/DNND.S51786

Christina Schindowski, Jürgen Zimmermann, Katharina Schindowski

{"title":"Intravenous immunoglobulin for the treatment of Alzheimer's disease: current evidence and considerations.","authors":"Christina Schindowski, Jürgen Zimmermann, Katharina Schindowski","doi":"10.2147/DNND.S51786","DOIUrl":"10.2147/DNND.S51786","url":null,"abstract":"Alzheimer's disease (AD) is a devastating neurodegenerative form of dementia with increasing incidence rates in most countries. AD is characterized by amyloid plaques and neurofibrillary tangles in the brains of AD individuals accompanied by global neuronal loss. The peptide amyloid-β (Aβ) aggregates to amyloid plaques in AD brains. As a result, many therapeutic approaches target Aβ. Human plasma and the plasma product intravenous immunoglobulin (IVIG) contain naturally-occurring anti-Aβ antibodies (Nabs-Aβ) that appear to reduce risks of developing AD. IVIG sequesters Aβ and thus interferes with AD progression. This study reviews the role of different Aβ species, Nabs-Aβ, preclinical data, and clinical studies of IVIG as potential AD treatments. The focus of this study is the outcomes of a recent Gammaglobulin Alzheimer's Partnership Phase III trial that did not reach primary endpoints, as well as efforts to compare IVIG with current anti-Aβ monoclonals such as bapineuzumab, solanezumab, and BIIB037. Moreover, this study critically examines current market and ethical consequences of potential off-label uses of IVIG, limits in IVIG supply, and subsequent challenges.","PeriodicalId":11147,"journal":{"name":"Degenerative Neurological and Neuromuscular Disease","volume":"4 ","pages":"121-130"},"PeriodicalIF":0.0,"publicationDate":"2014-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/24/e1/DNND-4-121.PMC7337175.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38163220","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: 0

Optimal management of multiple sclerosis during pregnancy: current perspectives. 妊娠期多发性硬化症的最佳治疗：当前观点。

Degenerative Neurological and Neuromuscular Disease Pub Date : 2014-08-05 eCollection Date: 2014-01-01 DOI: 10.2147/DNND.S48618

Nadja Borisow, Friedemann Paul, Jan Dörr

引用次数: 0

Current and emerging treatments for relapsing multiple sclerosis in Argentinian patients: a review. 阿根廷复发性多发性硬化症患者的当前和新兴治疗方法:综述。

Degenerative Neurological and Neuromuscular Disease Pub Date : 2014-06-20 eCollection Date: 2014-01-01 DOI: 10.2147/DNND.S46557

Juan I Rojas, Liliana Patrucco, Edgardo Cristiano

引用次数: 2

Epigenetic mechanisms in Alzheimer's disease. 阿尔茨海默病的表观遗传机制。

Degenerative Neurological and Neuromuscular Disease Pub Date : 2014-05-24 eCollection Date: 2014-01-01 DOI: 10.2147/DNND.S37341

Robert Balazs

{"title":"Epigenetic mechanisms in Alzheimer's disease.","authors":"Robert Balazs","doi":"10.2147/DNND.S37341","DOIUrl":"https://doi.org/10.2147/DNND.S37341","url":null,"abstract":"The worldwide increase in life expectancy is leading to an increase in age-dependent diseases, including nonfamilial, sporadic Alzheimer's disease (AD), which is the subject of this review. The etiology and pathophysiology of the disease is not fully understood, but present observations suggest that, in addition to genetic risk factors, environmental influences may be involved via epigenetic mechanisms. Currently, there is no effective treatment, but there are indications that lifestyle has an impact on the development of the disease. This view is supported by preclinical studies not only showing that human lifestyle-equivalent interventions have a positive effect on cognitive function in animal models of AD, but also indicating the involvement of underlying epigenetic mechanisms. After a brief overview of the most characteristic chromatin modifications, ie, DNA methylation and histone modifications, epigenetic changes associated with aging are considered, given that aging is the most important risk factor for AD. This is followed by a description of some epigenetic alterations recognized in AD. The impact of environmental factors and lifestyle on the epigenome is then considered. Epigenetic treatments with HDAC inhibitors and RNA-based drugs are considered, which - while still in preclinical stages - are promising for potential benefit. It is concluded that while awaiting results from clinical trials in progress, focusing on lifestyle adjustments with an epigenetic background are the best way to prevent/delay the onset of this devastating disease.","PeriodicalId":11147,"journal":{"name":"Degenerative Neurological and Neuromuscular Disease","volume":"4 ","pages":"85-102"},"PeriodicalIF":0.0,"publicationDate":"2014-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/DNND.S37341","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38157771","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: 1

Identifying responders and nonresponders to interferon therapy in multiple sclerosis. 识别多发性硬化症干扰素疗法的应答者和非应答者。

Degenerative Neurological and Neuromuscular Disease Pub Date : 2014-04-01 eCollection Date: 2014-01-01 DOI: 10.2147/DNND.S42734

Luca Prosperini, Marco Capobianco, Costanza Giannì

{"title":"Identifying responders and nonresponders to interferon therapy in multiple sclerosis.","authors":"Luca Prosperini, Marco Capobianco, Costanza Giannì","doi":"10.2147/DNND.S42734","DOIUrl":"10.2147/DNND.S42734","url":null,"abstract":"Interferon beta is a well established disease-modifying agent used for relapsing-remitting multiple sclerosis. Despite treatment, a relevant proportion of patients continue to experience clinical (ie, relapses, worsening of disability) and magnetic resonance imaging (MRI) activity. Early identification of responders and nonresponders to interferon beta is strongly recommended to select patients who need a prompt switch to another disease-modifying agent and to ultimately avoid accumulation of fixed disability over time. Detecting responders and nonresponders to interferon beta can be challenging, mainly because of the lack of a clear and shared clinical definition of response to treatment. Clinical features at the start of treatment should be considered as prognostic factors, but MRI parameters assessed during treatment, such as contrast-enhancing lesions or new T2-hyperintense lesions, may be sensitive markers of response to interferon beta. Quantitative scoring systems derived from a combination of relapses and MRI activity have recently been proposed as practical tools for use in the everyday clinical setting. Blood biomarkers, such as neutralizing antibodies to interferon beta and Myxovirus resistance protein A, provide further useful information for detecting responders and nonresponders to interferon beta. However, since the presence of neutralizing antibodies can only partially explain the nonresponse to interferon beta, biomarkers of interferon beta activity possibly related to the pathogenesis of the disease could represent a future step toward a tailored, long-lasting effective treatment against multiple sclerosis.","PeriodicalId":11147,"journal":{"name":"Degenerative Neurological and Neuromuscular Disease","volume":"4 ","pages":"75-85"},"PeriodicalIF":0.0,"publicationDate":"2014-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a6/e7/DNND-4-75.PMC7337239.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38157769","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: 0

Neurogenic overactive bladder in spinal cord injury and multiple sclerosis: role of onabotulinumtoxinA. 脊髓损伤和多发性硬化症中神经源性膀胱过度活动:肉毒杆菌毒素的作用。

Degenerative Neurological and Neuromuscular Disease Pub Date : 2014-03-18 eCollection Date: 2014-01-01 DOI: 10.2147/DNND.S40349

K D Ethans, A R Casey, R J Bard, M P Namaka

引用次数: 4

Neurodegeneration in multiple sclerosis involves multiple pathogenic mechanisms. 多发性硬化症神经退行性变涉及多种致病机制。

Degenerative Neurological and Neuromuscular Disease Pub Date : 2014-03-12 eCollection Date: 2014-01-01 DOI: 10.2147/DNND.S54391

Michael C Levin, Joshua N Douglas, Lindsay Meyers, Sangmin Lee, Yoojin Shin, Lidia A Gardner

{"title":"Neurodegeneration in multiple sclerosis involves multiple pathogenic mechanisms.","authors":"Michael C Levin, Joshua N Douglas, Lindsay Meyers, Sangmin Lee, Yoojin Shin, Lidia A Gardner","doi":"10.2147/DNND.S54391","DOIUrl":"https://doi.org/10.2147/DNND.S54391","url":null,"abstract":"Multiple sclerosis (MS) is a complex autoimmune disease that impairs the central nervous system (CNS). The neurological disability and clinical course of the disease is highly variable and unpredictable from one patient to another. The cause of MS is still unknown, but it is thought to occur in genetically susceptible individuals who develop disease due to a nongenetic trigger, such as altered metabolism, a virus, or other environmental factors. MS patients develop progressive, irreversible, neurological disability associated with neuronal and axonal damage, collectively known as neurodegeneration. Neurodegeneration was traditionally considered as a secondary phenomenon to inflammation and demyelination. However, recent data indicate that neurodegeneration develops along with inflammation and demyelination. Thus, MS is increasingly recognized as a neurodegenerative disease triggered by an inflammatory attack of the CNS. While both inflammation and demyelination are well described and understood cellular processes, neurodegeneration might be defined by a diverse pool of any of the following: neuronal cell death, apoptosis, necrosis, and virtual hypoxia. In this review, we present multiple theories and supporting evidence that identify common biological processes that contribute to neurodegeneration in MS.","PeriodicalId":11147,"journal":{"name":"Degenerative Neurological and Neuromuscular Disease","volume":"4 ","pages":"49-63"},"PeriodicalIF":0.0,"publicationDate":"2014-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/DNND.S54391","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38157768","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: 31

Axonal transport and neurodegenerative disease: vesicle-motor complex formation and their regulation. 轴突转运与神经退行性疾病:囊泡-运动复合物的形成及其调控。

Degenerative Neurological and Neuromuscular Disease Pub Date : 2014-03-10 eCollection Date: 2014-01-01 DOI: 10.2147/DNND.S57502

Eric N Anderson, Joseph A White, Shermali Gunawardena

{"title":"Axonal transport and neurodegenerative disease: vesicle-motor complex formation and their regulation.","authors":"Eric N Anderson, Joseph A White, Shermali Gunawardena","doi":"10.2147/DNND.S57502","DOIUrl":"10.2147/DNND.S57502","url":null,"abstract":"The process of axonal transport serves to move components over very long distances on microtubule tracks in order to maintain neuronal viability. Molecular motors - kinesin and dynein - are essential for the movement of neuronal cargoes along these tracks; defects in this pathway have been implicated in the initiation or progression of some neurodegenerative diseases, suggesting that this process may be a key contributor in neuronal dysfunction. Recent work has led to the identification of some of the motor-cargo complexes, adaptor proteins, and their regulatory elements in the context of disease proteins. In this review, we focus on the assembly of the amyloid precursor protein, huntingtin, mitochondria, and the RNA-motor complexes and discuss how these may be regulated during long-distance transport in the context of neurodegenerative disease. As knowledge of these motor-cargo complexes and their involvement in axonal transport expands, insight into how defects in this pathway contribute to the development of neurodegenerative diseases becomes evident. Therefore, a better understanding of how this pathway normally functions has important implications for early diagnosis and treatment of diseases before the onset of disease pathology or behavior.","PeriodicalId":11147,"journal":{"name":"Degenerative Neurological and Neuromuscular Disease","volume":"4 ","pages":"29-47"},"PeriodicalIF":0.0,"publicationDate":"2014-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3b/ec/DNND-4-29.PMC7337264.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38157766","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: 0