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December 2015 Volume 11 Number 12 | |||||||||||||||||||||||||||||||||||||
In this issue Research Highlights News and Views Reviews Correspondence
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NEWS AND VIEWS | Top | ||||||||||||||||||||||||||||||||||||
Alzheimer disease: Solanezumab—prospects for meaningful interventions in AD? Sam Gandy & Mary Sano Published online: 03 November 2015 p669 | doi:10.1038/nrneurol.2015.218 A treatment trial of the monoclonal anti-amyloid antibody solanezumab showed slight benefits in people with dementia due to mild Alzheimer disease. Drug effects on several neuropsychological testing outcomes were statistically significant, but the effect sizes were unlikely to manifest as meaningful functional benefits. Here, we discuss the implications and possible molecular underpinnings. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
Neurodegenerative disease: C9orf72 repeats compromise nucleocytoplasmic transport Marka van Blitterswijk & Rosa Rademakers Published online: 03 November 2015 p670 | doi:10.1038/nrneurol.2015.219 The molecular mechanisms of neurodegeneration due to a repeat expansion in C9orf72, the most common cause of frontotemporal dementia and amyotrophic lateral sclerosis, are unknown. Three reports now link compromised nucleocytoplasmic transport to disease pathogenesis. Whether RNA structures or dipeptide repeat proteins are most toxic in humans remains open to question. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
Stroke: Preventive antibiotics for stroke-associated pneumonia Andreas Meisel & Craig J. Smith Published online: 03 November 2015 p672 | doi:10.1038/nrneurol.2015.220 Pneumonia impedes recovery from acute stroke and contributes to poor clinical outcomes. Two recent clinical trials demonstrate that antibiotics commonly used to treat stroke-associated pneumonia (SAP) neither reduce the frequency of pneumonia nor improve outcome after stroke when administered in a preventive manner. These findings necessitate fundamental reassessment of our current concepts of SAP. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
Alzheimer Disease: Alzheimer dementia with sparse amyloid—AD mimic or variant? Alberto Serrano-Pozo & Bradley T. Hyman Published online: 10 November 2015 p674 | doi:10.1038/nrneurol.2015.221 In a new study, one-quarter of individuals with a clinical diagnosis of mild to moderate Alzheimer dementia had no or only sparse neuritic amyloid plaques in their brains, and most were also at a low or an intermediate neurofibrillary tangle stage. The findings have enormous implications for clinical trials of anti-amyloid-[beta] and anti-tau therapies. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
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REVIEWS | Top | ||||||||||||||||||||||||||||||||||||
Nonconventional MRI and microstructural cerebral changes in multiple sclerosis Christian Enzinger, Frederik Barkhof, Olga Ciccarelli, Massimo Filippi, Ludwig Kappos, Maria A. Rocca, Stefan Ropele, Àlex Rovira, Torben Schneider, Nicola de Stefano, Hugo Vrenken, Claudia Wheeler-Kingshott, Jens Wuerfel, Franz Fazekas & on behalf of the MAGNIMS study group Published online: 03 November 2015 p676 | doi:10.1038/nrneurol.2015.194 In our third and final installment from the MAGNIMS study group, Enzinger et al. consider how dramatic progress in MRI has enabled nonconventional structural imaging techniques to shed new light on the pathophysiology of multiple sclerosis. The authors discuss the present use of these techniques in the disease, and consider their future application to clinical research and practice. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||
A novel diagnostic approach to patients with myoclonus Rodi Zutt, Martje E. van Egmond, Jan Willem Elting, Peter Jan van Laar, Oebele F. Brouwer, Deborah A. Sival, Hubertus P. Kremer, Tom J. de Koning & Marina A. Tijssen Published online: 10 November 2015 p687 | doi:10.1038/nrneurol.2015.198 Myoclonus is characterized by sudden, involuntary jerks, and can be caused by a variety of acquired and genetic disorders. Identification of the aetiology of myoclonus is paramount, because treatment should be based on the underlying disorder. The authors propose a novel eight-step diagnostic algorithm for myoclonus, incorporating—for the first time—next-generation sequencing. The algorithm should aid clinical decision-making and facilitate mechanism-based treatment. Abstract | Full Text | PDF | Supplementary information | |||||||||||||||||||||||||||||||||||||
Remote ischaemic conditioning—a new paradigm of self-protection in the brain David C. Hess, Rolf A. Blauenfeldt, Grethe Andersen, Kristina D. Hougaard, Md Nasrul Hoda, Yuchuan Ding & Xunming Ji Published online: 20 November 2015 p698 | doi:10.1038/nrneurol.2015.223 Harnessing self-protective pathways in the brain could protect against neurological disease, but pharmacological attempts at such an approach have failed. In this Review, Hess et al. consider the neurological potential of remote ischaemic conditioning (RIC), a procedure in which brief ischaemia induced by vascular occlusion in the limb activates self-protective pathways and protects distant organs against longer episodes of ischaemia. Clinical trials in cardiological settings have been successful, and trials in neurological conditions suggest that RIC is a feasible option for patients with ischaemic neurological conditions. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||
Synaptopathy connects inflammation and neurodegeneration in multiple sclerosis Georgia Mandolesi, Antonietta Gentile, Alessandra Musella, Diego Fresegna, Francesca De Vito, Silvia Bullitta, Helena Sepman, Girolama A. Marfia & Diego Centonze Published online: 20 November 2015 p711 | doi:10.1038/nrneurol.2015.222 Inflammation-driven synaptic dysfunction is emerging as a prominent pathogenic mechanism in multiple sclerosis (MS). Importantly, synaptic alterations and synaptic loss are potentially reversible, making them potential therapeutic targets. This Review draws on studies in patients with MS and in animal models of the disease to discuss the synaptic alterations in MS and the most promising drugs to restore synaptic function and intervene in the disease progression. Abstract | Full Text | PDF | Supplementary information | |||||||||||||||||||||||||||||||||||||
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CORRESPONDENCE | Top | ||||||||||||||||||||||||||||||||||||
Bumetanide for neonatal seizures—back from the cotside Ronit M. Pressler, Geraldine B. Boylan, Neil Marlow, Linda S. de Vries, Mats Blennow, Catherine Chiron, J. Helen Cross, Boubou Hallberg, Lena Hellström-Westas, Vincent Jullien, Barry Mangum, Brendan Murphy, Deirdre Murray, Gerard Pons, Janet Rennie, Mona C. Toet & Sarah Zohar Published online: 03 November 2015 p724 | doi:10.1038/nrneurol.2015.116 Full Text | PDF | |||||||||||||||||||||||||||||||||||||
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*Journal Citation Reports, Thomson, 2015. Nature Reviews Neurology was previously published as Nature Clinical Practice Neurology. |
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