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| April 2014 Volume 10 Number 4 | |||||||||||||||||||||||||||||||||||||
In this issue
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| NEWS AND VIEWS | Top | ||||||||||||||||||||||||||||||||||||
| Multiple sclerosis: TOWER confirms the efficacy of oral teriflunomide in MS Aiden Haghikia & Ralf Gold Published online: 18 March 2014 p183 | doi:10.1038/nrneurol.2014.42 Results of the TOWER phase III trial confirm the efficacy of teriflunomide in relapsing-remitting multiple sclerosis (RRMS). With seven substances now approved for RRMS, individualized treatment for the inflammatory aspect of the disease is within reach, although many questions remain unanswered, particularly concerning the neurodegenerative aspect RRMS. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Dementia: The complexities of comorbidity in dementia Christopher M. Callahan & Cathy C. Schubert Published online: 18 March 2014 p184 | doi:10.1038/nrneurol.2014.46 A large claims-based study has identified several comorbidity clusters in individuals with dementia, corroborating the notion that comorbid conditions are an important contributor to health outcomes. The complexity of comorbidities calls for a patient-centred approach for care. Importantly, good management of comorbidities can improve quality of life in progressive dementia. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Parkinson disease: Gene therapy for Parkinson disease—a hope, or a dream? C. Warren Olanow Published online: 25 March 2014 p186 | doi:10.1038/nrneurol.2014.45 Gene therapy offers the potential to deliver therapeutic proteins to a target region, and is a promising treatment for Parkinson disease. A new open-label study testing ProSavin®, which encodes three rate-limiting enzymes required for dopamine biosynthesis, showed favourable safety and efficacy results, but its therapeutic potential awaits confirmation in double-blind trials. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Alzheimer disease: Lessons from immunotherapy for Alzheimer disease Yan-Jiang Wang Published online: 18 March 2014 p188 | doi:10.1038/nrneurol.2014.44 Amyloid-β (Aβ) is suggested to have a pivotal role in the pathogenesis of Alzheimer disease (AD) and is a major therapeutic target. Recent phase III trials of the anti-Aβ monoclonal antibodies bapineuzumab and solanezumab, which failed to improve cognitive function in patients, provide valuable insights for the future development of immunotherapies. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| REVIEWS | Top | ||||||||||||||||||||||||||||||||||||
| Neuroprognostication of hypoxic-ischaemic coma in the therapeutic hypothermia era David M. Greer, Eric S. Rosenthal & Ona Wu Published online: 11 March 2014 p190 | doi:10.1038/nrneurol.2014.36 Neurological prognostication in patients who remain in hypoxic-ischaemic coma after cardiac arrest has always been challenging, and has become even more so since the advent of therapeutic hypothermia (TH). In this Review, Greer et al. consider how neurological outcomes and prognostic indicators might be influenced by the use of TH, and discuss advances in neuroimaging and electrophysiology that are expected to aid neuroprognostication in this patient population. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Huntington disease: natural history, biomarkers and prospects for therapeutics Christopher A. Ross, Elizabeth H. Aylward, Edward J. Wild, Douglas R. Langbehn, Jeffrey D. Long, John H. Warner, Rachael I. Scahill, Blair R. Leavitt, Julie C. Stout, Jane S. Paulsen, Ralf Reilmann, Paul G. Unschuld, Alice Wexler, Russell L. Margolis & Sarah J. Tabrizi Published online: 11 March 2014 p204 | doi:10.1038/nrneurol.2014.24 Huntington disease (HD) is considered to be a model neurodegenerative disorder, in that it is caused by a single genetic mutation and is amenable to predictive genetic testing, enabling the entire disease course to be studied. Ross et al. describe the natural history of HD, including the timing of emergence of motor, cognitive and emotional impairments. Building on this information, they review recent progress in the development of biomarkers for HD, and potential future roles of these biomarkers in clinical trials. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Microglial priming in neurodegenerative disease V. Hugh Perry & Clive Holmes Published online: 18 March 2014 p217 | doi:10.1038/nrneurol.2014.38 As a response to accumulation of debris and abnormally folded proteins during neurodegeneration, microglia multiply and adopt a chronically activated state. This process, referred to as priming, makes microglia susceptible to a secondary inflammatory stimulus, often arising from a systemic disorder with an inflammatory component, such as diabetes. Primed microglia react to the secondary inflammatory stimulus with an exaggarated response, which can further exacerbate neurodegeneration. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis Manuel A. Friese, Benjamin Schattling & Lars Fugger Published online: 18 March 2014 p225 | doi:10.1038/nrneurol.2014.37 Great progress has been made in elucidating the acute inflammatory components of multiple sclerosis (MS), but the pathophysiological mechanisms of the concomitant neurodegeneration are poorly understood. Friese and colleagues review the current state of knowledge regarding the pathological mechanisms of neuroaxonal dysfunction and injury in MS, highlighting evidence that axonal and neuronal impairment are early and independent contributors to disease progression. Abstract | Full Text | PDF | Supplementary information | |||||||||||||||||||||||||||||||||||||
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| *Journal Citation Reports, Thomson, 2012. Nature Reviews Neurology was previously published as Nature Clinical Practice Neurology. |
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