Jun Huang, Jianping Song, Meijie Qu, Yang Wang, Qinzhu An, Yaying Song, Wei Yan, Bingshun Wang, Xiaojin Wang, Song Zhang, Xi Chen, Bing Zhao, Peixi Liu, Tongyi Xu, Zhijun Zhang, David A. Greenberg, Yongting Wang, Pingjin Gao, Wei Zhu, Guo-Yuan Yang September 3, 2017

Abstract

Objectives: Brain arteriovenous malformations (AVMs) are the most common cause of non-traumatic intracerebral hemorrhage in young adults. The genesis of brain AVM remains enigmatic. We investigated microRNA (miRNA) expression and its contribution to the pathogenesis of brain AVMs.

Methods: We used a large-scale miRNA analysis on 16 samples including AVMs, hemangioblastoma, and controls to identify a distinct AVM miRNA signature.

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Ahmed A. Hawash, Andrew A. Voss, Mark M. Rich September 3, 2017

Abstract

Objective: Patients with myotonia congenita have muscle hyperexcitability due to loss-of-function mutations in the ClC-1 chloride channel in skeletal muscle, which causes involuntary firing of muscle action potentials (myotonia), producing muscle stiffness. The excitatory events that trigger myotonic action potentials in the absence of stabilizing ClC-1 current are not fully understood.

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Bernhard Gesslbauer, Laura A. Hruby, Aidan D. Roche, Dario Farina, Roland Blumer, Oskar C. Aszmann September 3, 2017

ABSTRACT

Objective: Axons travelling within the brachial plexus are responsible for the dexterous control of human arm and hand movements. Despite comprehensive knowledge on the topographical anatomy of nerves innervating the human upper limb, the definite quantity of sensory and motor axons within this neural network remains elusive.

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Ruthger Righart, Viola Biberacher, Laura E Jonkman, Roel Klaver, Paul Schmidt, Dorothea Buck, Achim Berthele, Jan S Kirschke, Claus Zimmer, Bernhard Hemmer, Jeroen JG Geurts, Mark Mühlau September 3, 2017

Abstract

Objective

In multiple sclerosis, neuropathological studies have shown widespread changes in the cerebral cortex. In vivo imaging is critical since the histopathological substrate of most measurements is unknown.

Method

Using a novel MRI analysis technique, based on the ratio of T1- and T2-weighted signal intensities, we studied the cerebral cortex of a large cohort of patients in early stages of multiple sclerosis.

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Kunio Nakamura, Jacqueline T. Chen, Daniel Ontaneda, Robert J. Fox, Bruce D. Trapp September 3, 2017

Abstract

Detecting cortical demyelination in patients with multiple sclerosis (MS) is difficult. Using magnetic resonance imaging (MRI), ratio maps of T1-weighted and T2-weighted images (T1w/T2w) may be sensitive to cortical myelin levels. In this MRI-histological study, postmortem in situ scans were acquired from six cadavers with MS on a 3 Tesla MRI.

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Richard L. Yates, Margaret M. Esiri, Jacqueline Palace, Benjamin Jacobs, Rafael Perera, Gabriele C. DeLuca September 3, 2017

Objective

Neuronal loss, a key substrate of irreversible disability in multiple sclerosis (MS), is a recognized feature of MS cortical pathology of which the cause remains unknown. Fibrin(ogen) deposition is neurotoxic in animal models of MS, but has not been evaluated in human progressive MS cortex.

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Gareth Ball, Paul Aljabar, Phumza Nongena, Nigel Kennea, Nuria Gonzalez-Cinca, Shona Falconer, Andrew T.M. Chew, Nicholas Harper, Julia Wurie, Mary A. Rutherford, Serena J. Counsell, A. David Edwards September 3, 2017

Objective

Premature birth is associated with numerous complex abnormalities of white and gray matter and a high incidence of long-term neurocognitive impairment. An integrated understanding of these abnormalities and their association with clinical events is lacking. The aim of this study was to identify specific patterns of abnormal cerebral development and their antenatal and postnatal antecedents.

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David J. Irwin, Alberto Lleó, Sharon X. Xie, Corey T. McMillan, David A. Wolk, Edward B. Lee, Viviana M. Van Deerlin, Leslie M. Shaw, John Q. Trojanowski, Murray Grossman September 3, 2017

Objective

To test the hypotheses that (1) antemortem cerebrospinal fluid (CSF) tau levels correlate with postmortem tau pathology in frontotemporal lobar degeneration (FTLD) and (2) tauopathy patients have higher phosphorylated-tau levels compared to transactivation response element DNA-binding protein 43 (TDP-43) proteinopathy patients while accounting for Alzheimer’s disease (AD) copathology.

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