Tuesday, 6 August 2013

Nature Reviews Neurology - Table of Contents alert Volume 9 Issue 8

Nature Reviews Neurology

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TABLE OF CONTENTS
 
August 2013 Volume 9 Number 8Advertisement

Nature Reviews Neurology cover
Impact Factor 15.518 *
In this issue
Research Highlights
News and Views
Correction
Reviews
Perspectives

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 Web collection:
Slowing down neurodegeneration


 
Just one of many high quality articles Frontiers in Neurology has to offer: 

Clinico-pathological correlations of the most common neurodegenerative dementias (open access)
In this review, Ricardo Taipa and colleagues describe the key neuropathological features of the most common neurodegenerative dementias and the relationship with the clinical syndromes described in clinico-pathological studies.


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New Impact Factor
We are pleased to announce that the new impact factor for Nature Reviews Neurology is 15.518*. This places the journal first among all monthly review journals in the Clinical Neurology category!
*2012 Journal Citation Reports® (Thomson Reuters, 2013)
 
RESEARCH HIGHLIGHTS

Top

Neurodegenerative disease: Defective mitochondrial dynamics in the hot seat—a therapeutic target common to many neurological disorders?
Published online: 23 July 2013
p417 | doi:10.1038/nrneurol.2013.138

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Movement disorders: Novel FUS gene variants linked to essential tremor
Published online: 23 July 2013
p418 | doi:10.1038/nrneurol.2013.143

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Migrane: New susceptibility loci associated with migraine
Published online: 09 July 2013
p419 | doi:10.1038/nrneurol.2013.136

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Alzheimer disease: CSF levels of mitochondrial DNA—a new biomarker for preclinical Alzheimer disease?
Published online: 09 July 2013
p420 | doi:10.1038/nrneurol.2013.134

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Neuro-oncology: BCAT1 promotes cell proliferation in aggressive gliomas
Published online: 09 July 2013
p420 | doi:10.1038/nrneurol.2013.135

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IN BRIEF

Alzheimer disease: Increased risk of falls in preclinical Alzheimer disease | Cerebrovascular malformations: Endothelial-to-mesenchymal transition—role in cerebral cavernous malformation | Neurometabolic disease: Pioglitazone for treatment of X-linked adrenoleukodystrophy? | Amyotrophic lateral sclerosis: Histone deacetylase 4—accelerator of progression in ALS? | White matter disease: 'Bright spotty lesions'—a novel NMO-specific MRI feature? | Neurodevelopmental disorders: New brain imaging measure for early diagnosis of autism | Motor neuron disease: Neurotransmitter imbalance identified in ALS | Parkinson disease: Medical therapy versus deep brain stimulation for advanced PD—long-term outcomes
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NEWS AND VIEWS

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Neurodegenerative disease: 'Fifty shades of grey' in the Huntington disease gene
Ferdinando Squitieri
Published online: 25 June 2013
p421 | doi:10.1038/nrneurol.2013.128
Huntington disease is caused by a CAG repeat expansion in the huntingtin gene. A repeat length of 35 CAGs has long been accepted as the cut-off point beyond which the expansion becomes pathological, but recent findings indicate that intermediate expansions (27-35 repeats) are associated with either a distinct behavioural phenotype or an endophenotype.
Full Text | PDF


Alzheimer disease: 'Generation Next' in Alzheimer disease genetic studies
Liana G. Apostolova
Published online: 16 July 2013
p422 | doi:10.1038/nrneurol.2013.133
A recent study has used whole-exome sequencing, an 'extreme trait' design and imaging genetics to identify coding variants associated with hippocampal volume loss in Alzheimer disease. The research highlights the utility of next-generation sequencing and association studies involving quantitative traits for discovery of disease-related variants in neurodegeneration.
Full Text | PDF


Neuro-oncology: In search of molecular markers of glioma in elderly patients
Monika E. Hegi & Roger Stupp
Published online: 02 July 2013
p424 | doi:10.1038/nrneurol.2013.127
Elderly patients represent a growing proportion of individuals with malignant glioma, but are often excluded from trials owing to their poor prognosis. In a new study, researchers have investigated molecular markers of glioma specifically in elderly patients—are these markers of clinical use?
Full Text | PDF


Neurodegenerative disease: Can synucleinopathy and tauopathy be identified during life?
Shin-ichiro Kubo & Nobutaka Hattori
Published online: 16 July 2013
p426 | doi:10.1038/nrneurol.2013.137
Data on the incidence of synucleinopathies and tauopathies are limited, and a recently published study has attempted to address this deficit. Confirmation of these proteinopathies currently relies on pathological findings at autopsy, but the new findings raise the possibility of diagnosis during life in some cases.
Full Text | PDF


 
CORRECTION

Top
Ushering in the study and treatment of preclinical Alzheimer disease
Langbaum, J. B. et al.
Published online: 16 July 2013
p418 | doi:10.1038/nrneurol.2013.145

Full Text | PDF


 
REVIEWS

Top
The clinical maze of mitochondrial neurology
Salvatore DiMauro, Eric A. Schon, Valerio Carelli & Michio Hirano
Published online: 09 July 2013
p429 | doi:10.1038/nrneurol.2013.126
Mitochondrial diseases are a complex and clinically heterogeneous group of disorders, which— together with our poor understanding of the underlying pathology—makes their diagnosis difficult. Here, DiMauro et al. review current knowledge of defects of the mitochondrial respiratory complex that lead to neurological mitochondrial disorders, outlining diagnostic clues for each disorder, and discussing current therapeutic approaches for these often devastating diseases.
Abstract | Full Text | PDF


Advances in the genetics of Parkinson disease
Joanne Trinh & Matt Farrer
Published online: 16 July 2013
p445 | doi:10.1038/nrneurol.2013.132
Over the past 15 years, the contribution of genetic factors to development of Parkinson disease has been increasingly recognized. In their Review, Trinh and Farrer summarize the latest findings in this field, highlighting overlapping results from diverse genetics studies. Together, the genes identified suggest a key role for impaired vesicle and mitochondrial dynamics in neurons, which could represent promising targets for novel therapies in Parkinson disease.
Abstract | Full Text | PDF


The spectrum of MOG autoantibody-associated demyelinating diseases
Markus Reindl, Franziska Di Pauli, Kevin Rostásy & Thomas Berger
Published online: 25 June 2013
p455 | doi:10.1038/nrneurol.2013.118
In this Review, Reindl et al. discuss a range of CNS disorders that are known to be associated with autoantibodies against myelin oligodendrocyte glycoprotein (MOG). They examine the experimental evidence for a role for MOG autoantibodies in the pathogenesis of demyelinating CNS disorders such as multiple sclerosis and acute disseminated encephalomyelitis, and explore the potential of MOG to function as a biomarker in these diseases.
Abstract | Full Text | PDF | Supplementary information


Chronic low back pain: pharmacological, interventional and surgical strategies
Bart Morlion
Published online: 02 July 2013
p462 | doi:10.1038/nrneurol.2013.130
Chronic low back pain (CLBP) is a highly prevalent and debilitating disorder. Despite progress in understanding the aetiology of CLBP in recent years, this knowledge has not been translated into decreased prevalence or new therapies. In this Review, Morlion discusses interventional pain management, as well as surgical and pharmacotherapy approaches, and reviews the current evidence for the efficacy of these treatments in CLBP.
Abstract | Full Text | PDF



 
PERSPECTIVES

Top
OPINION
New treatments for mitochondrial disease—no time to drop our standards
Gerald Pfeffer, Rita Horvath, Thomas Klopstock, Vamsi K. Mootha, Anu Suomalainen, Saskia Koene, Michio Hirano, Massimo Zeviani, Laurence A. Bindoff, Patrick Yu-Wai-Man, Michael Hanna, Valerio Carelli, Robert McFarland, Kari Majamaa, Douglas M. Turnbull, Jan Smeitink & Patrick F. Chinnery
Published online: 02 July 2013
p474 | doi:10.1038/nrneurol.2013.129
Despite recent advances in our understanding of the pathophysiology of mitochondrial disease, beneficial treatments for these disorders are lacking. In this Perspectives article, Pfeffer et al. retrospectively review data from clinical trials in mitochondrial disease, and find that many problems arise from publication bias and poor trial design. After discussing these issues, the authors make recommendations for the design of future treatment trials in mitochondrial diseases.
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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