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| February 2013 Volume 9 Number 2 | |||||||||||||||||||||||||||||||||||||
In this issue
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| YEAR IN REVIEW | Top | ||||||||||||||||||||||||||||||||||||
| Motor neuron disease in 2012: Novel causal genes and disease modifiers Rosa Rademakers & Marka van Blitterswijk Published online: 15 January 2013 p63 | doi:10.1038/nrneurol.2012.276 In 2012, researchers published extensively on the genetic and clinicopathological characterization of patients with the newly discovered C9ORF72 repeat expansions, which cause amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Novel ALS-linked genes and genetic modifiers were identified through screening in animal models and patients. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Dementia in 2012: Further insights into Alzheimer disease pathogenesis Michael W. Weiner Published online: 22 January 2013 p65 | doi:10.1038/nrneurol.2012.275 In 2012, studies of autosomal dominant Alzheimer disease (AD), late-onset AD, and a rare genetic mutation of amyloid precursor protein provided support for the critical role of amyloid in AD pathogenesis. Increasing evidence implicated cell-to-cell transmission in the spread of tau and amyloid, highlighting novel targets for therapeutic intervention. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Epilepsy in 2012: Advances in epilepsy shed light on key questions Ingrid E. Scheffer & Saul A. Mullen Published online: 08 January 2013 p66 | doi:10.1038/nrneurol.2012.272 Research on epilepsies in 2012 has substantially advanced our knowledge of these often devastating conditions. From important discoveries that revealed causative factors and the molecular basis of disease, to major implications for surgical decision-making, these studies set the scene for future advances in the field. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Stroke in 2012: Major advances in the treatment of stroke Miguel Blanco & José Castillo Published online: 08 January 2013 p68 | doi:10.1038/nrneurol.2012.274 Several clinical trials and experimental studies that could have a major impact on the treatment of patients with ischaemic stroke were published in 2012. The studies cover all therapeutic options, including stroke prevention, recanalization and thrombolysis, neuroprotection, and promising new therapeutic approaches focused on neurorepair. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Movement disorders in 2012: Advancing research towards novel therapeutic approaches Nikolaus R. McFarland & Michael S. Okun Published online: 08 January 2013 p70 | doi:10.1038/nrneurol.2012.265 Research in movement disorders in 2012 has improved our understanding of the pathogenic mechanisms of disease and led to development of potential novel therapeutic approaches. Key advances were linked to mechanisms underlying spread of neurodegenerative pathology, immunotherapy, stem cells, genetics and deep brain stimulation in parkinsonism and related disorders. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Multiple sclerosis in 2012: Novel therapeutic options and drug targets in MS Axel Methner & Frauke Zipp Published online: 22 January 2013 p72 | doi:10.1038/nrneurol.2012.277 2012 witnessed important developments for multiple sclerosis, including successful phase III trials of novel oral therapeutics and identification of the potassium channel KIR4.1 as an autoimmune target. Additionally, the lung was highlighted as an important site for immune-cell programming, and the relevance of a TNF receptor variant was clarified. Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| REVIEWS | Top | ||||||||||||||||||||||||||||||||||||
| Eye movements in patients with neurodegenerative disorders Tim J. Anderson & Michael R. MacAskill Published online: 22 January 2013 p74 | doi:10.1038/nrneurol.2012.273 Eye movement responses are altered in patients with age-related neurodegenerative diseases such as Huntington disease or Parkinson disease. In this Review, the authors describe the oculomotor features of various neurodegenerative diseases and discuss the potential utility of laboratory and clinical assessment of eye movements in monitoring of onset and progression in patients with these disorders. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Transient amnesic syndromes Thorsten Bartsch & Christopher Butler Published online: 08 January 2013 p86 | doi:10.1038/nrneurol.2012.264 Transient amnesic syndromes, such as transient global amnesia and transient epileptic amnesia, are often difficult to diagnose. Recent studies, however, have examined the structural and functional underpinnings of these disorders. In this Review, Bartsch and Butler discuss how these studies have improved our understanding of transient amnesic syndromes, summarizing the key clinical aspects of different amnesic disorders and providing recommendations for diagnosis and patient management. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Immunotherapy in prion disease Yvonne Roettger, Yansheng Du, Michael Bacher, Inga Zerr, Richard Dodel & Jan-Philipp Bach Published online: 18 December 2012 p98 | doi:10.1038/nrneurol.2012.258 Prion diseases are a group of fatal neurodegenerative disorders caused by accumulation of misfolded prion protein. The time from infection to onset of disease symptoms can be decades, and the public health risk from infective prions is considerable. In this Review the authors discuss current research into passive and active immunization strategies against prion diseases, and the potential for effective therapy. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy Chia-Chan Liu, Takahisa Kanekiyo, Huaxi Xu & Guojun Bu Published online: 08 January 2013 p106 | doi:10.1038/nrneurol.2012.263 The ε4 allele of the apolipoprotein E (APOE) gene is the strongest genetic risk factor for Alzheimer disease (AD). Guojun Bu and colleagues describe the pathogenic links between Apo-E4 and neurodegeneration, including amyloid-β-dependent mechanisms and impairment of neurovascular function. The authors suggest potential strategies to target Apo-E, which could provide important additions to therapeutic options for AD. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||
| CORRESPONDENCE | Top | ||||||||||||||||||||||||||||||||||||
| Clarification of conclusions from the ACT NoW trial Audrey Bowen, Anne Hesketh, Emma Patchick, Alys Young, Linda Davies, Andy Vail, Andrew F. Long, Caroline Watkins, Mo Wilkinson, Gill Pearl, Matthew A. Lambon Ralph, Pippa Tyrrell (The ACT NoW Study team) & Peter Langhorne (Independent Chair of the ACT NoW Trial Steering Committee) Published online: 08 January 2013 p118 | doi:10.1038/nrneurol.2012.211-c1 Full Text | PDF | |||||||||||||||||||||||||||||||||||||
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| *Journal Citation Reports, Thomson, 2011. Nature Reviews Neurology was previously published as Nature Clinical Practice Neurology. |
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