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BACKGROUND Pediatric obstructive sleep apnea (OSA) is associated with neurocognitive deficits. However, the neural substrates underlying such deficits remain unknown. METHODS To examine executive control and emotional processing in OSA, 10 children age 7 to 11 y with polysomnographically diagnosed OSA and 7 age- and sex-matched controls underwent a color-word Stroop task and an empathy task consisting of dynamic visual scenarios depicting interpersonal harm or neutral actions in a magnetic resonance imaging (MRI) scanner. Functional MRI data were processed using MATLAB 7.12 with SPM8 for region of interest (ROI) analyses, and a general linear model was used with regressors for each trial type in each task. RESULTS For the Stroop task, accuracy was similar in the two groups, with no differences in the effect of incongruency on success rates. OSA showed greater neural activity than controls in eight ROI clusters for incongruent versus congruent trials (P < 0.001). Within the a priori ROIs, the anterior cingulate cortex was significantly different between groups (P < 0.05). For perceiving harm versus neutral actions, ROI analysis revealed a significant correlation between apnea-hypopnea index and left amygdala activity in harm versus neutral actions (r = -0.71, P < 0.05). CONCLUSIONS These results provide the first functional MRI evidence that cognitive and empathetic processing is influenced by obstructive sleep apnea (OSA) in children. Children with OSA show greater neural recruitment of regions implicated in cognitive control, conflict monitoring, and attentional allocation in order to perform at the same level as children without OSA. When viewing empathy-eliciting scenarios, the severity of OSA predicted less sensitivity to harm in the left amygdala.

In this paper, we propose a multi-view learning method using Magnetic Resonance Imaging (MRI) data for Alzheimer’s Disease (AD) diagnosis. Specifically, we extract both Region-Of-Interest (ROI) features and Histograms of Oriented Gradient (HOG) features from each MRI image, and then propose mapping HOG features onto the space of ROI features to make them comparable and to impose high intra-class similarity with low inter-class similarity. Finally, both mapped HOG features and original ROI features are input to the support vector machine for AD diagnosis. The purpose of mapping HOG features onto the space of ROI features is to provide complementary information so that features from different views can not only be comparable (i.e., homogeneous) but also be interpretable. For example, ROI features are robust to noise, but lack of reflecting small or subtle changes, while HOG features are diverse but less robust to noise. The proposed multi-view learning method is designed to learn the transformation between two spaces and to separate the classes under the supervision of class labels. The experimental results on the MRI images from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) dataset show that the proposed multi-view method helps enhance disease status identification performance, outperforming both baseline methods and state-of-the-art methods.

Background and Purpose— Intraventricular hemorrhage (IVH) is a common complication of prematurity that results in neurological sequelae, including cerebral palsy, posthemorrhagic hydrocephalus, and cognitive deficits. Despite this, there is no standardized animal model exhibiting neurological consequences of IVH in prematurely delivered animals. We asked whether induction of moderate-to-severe IVH in premature rabbit pups would produce long-term sequelae of cerebral palsy, posthemorrhagic hydrocephalus, reduced myelination, and gliosis. Methods— The premature rabbit pups, delivered by cesarean section, were treated with intraperitoneal glycerol at 2 hours postnatal age to induce IVH. The development of IVH was diagnosed by head ultrasound at 24 hours of age. Neurobehavioral, histological, and ultrastructural evaluation and diffusion tensor imaging studies were performed at 2 weeks of age. Results— Although 25% of pups with IVH (IVH pups) developed motor impairment with hypertonia and 42% developed posthemorrhagic ventriculomegaly, pups without IVH (non-IVH) were unremarkable. Immunolabeling revealed reduced myelination in the white matter of IVH pups compared with saline- and glycerol-treated non-IVH controls. Reduced myelination was confirmed by Western blot analysis. There was evidence of gliosis in IVH pups. Ultrastructural studies in IVH pups showed that myelinated and unmyelinated fibers were relatively preserved except for focal axonal injury. Diffusion tensor imaging showed reduction in fractional anisotropy and white matter volume confirming white matter injury in IVH pups. Conclusion— The rabbit pups with IVH displayed posthemorrhagic ventriculomegaly, gliosis, reduced myelination, and motor deficits, like humans. The study highlights an instructive animal model of the neurological consequences of IVH, which can be used to evaluate strategies in the prevention and treatment of posthemorrhagic complications.

The organization of sensory maps in the cerebral cortex depends on experience, which drives homeostatic and long-term synaptic plasticity of cortico-cortical circuits. In the mouse primary somatosensory cortex (S1) afferents from the higher-order, posterior medial thalamic nucleus (POm) gate synaptic plasticity in layer (L) 2/3 pyramidal neurons via disinhibition and the production of dendritic plateau potentials. Here we address whether these thalamocortically mediated responses play a role in whisker map plasticity in S1. We find that trimming all but two whiskers causes a partial fusion of the representations of the two spared whiskers, concomitantly with an increase in the occurrence of POm-driven N-methyl-D-aspartate receptor-dependent plateau potentials. Blocking the plateau potentials restores the archetypical organization of the sensory map. Our results reveal a mechanism for experience-dependent cortical map plasticity in which higher-order thalamocortically mediated plateau potentials facilitate the fusion of normally segregated cortical representations. Significance Here we describe a mechanism for cortical map plasticity. Classically, representational map changes are thought to be driven by changes within cortico-cortical circuits, e.g., Hebbian plasticity of synaptic circuits that lost vs. maintained an excitatory drive from the first-order thalamus, possibly steered by neuromodulatory forces from deep brain regions. Our work provides evidence for an additional gating mechanism, provided by plateau potentials, which are driven by higher-order thalamic feedback. Higher-order thalamic neurons are characterized by broad receptive fields, and the plateau potentials that they evoke strongly facilitate long-term potentiation and elicit spikes. We show that these features combined constitute a powerful driving force for the fusion or expansion of sensory representations within cortical maps.

Mood and anxiety disorders are complex heterogeneous syndromes that manifest in dysfunctions across multiple brain regions, cell types, and circuits. Biomarkers using brain-wide activity patterns in humans have proven useful in distinguishing between disorder subtypes and identifying effective treatments. In order to improve biomarker identification, it is crucial to understand the basic circuitry underpinning brain-wide activity patterns. Leveraging a large repertoire of techniques, animal studies have examined roles of specific cell types and circuits in driving maladaptive behavior. Recent advances in multiregion recording techniques, data-driven analysis approaches, and machine-learning-based behavioral analysis tools can further push the boundary of animal studies and bridge the gap with human studies, to assess how brain-wide activity patterns encode and drive emotional behavior. Together, these efforts will allow identifying more precise biomarkers to enhance diagnosis and treatment.

AbstractLittle is known about factors that promote optimal development of executive function (EF) skills. The focus of this study was associations among early maternal behaviors, infant frontal brain electrical activity, and child EF at age 4 and following kindergarten. Infant frontal electroencephalogram was collected from 56 infants at 10 months of age and maternal positive affect was observed. Children completed EF measures in the research laboratory at age 4; parental‐reported EF was obtained following children's kindergarten year. Maternal positive affect and infant frontal brain electrical activity measured when the children were 10 months jointly and uniquely predicted both preschool and post‐kindergarten EF. Findings suggest parenting behavior and brain development in infancy are precursors of later self‐regulatory EF abilities. © 2012 Wiley Periodicals, Inc. Dev Psychobiol 55: 530–538, 2013

Background: A previous phase 2 trial has suggested that statins might delay brain atrophy in secondary progressive multiple sclerosis. Objectives: The objective of this study was to evaluate the effect of atorvastatin add-on therapy on cerebral atrophy in relapsing–remitting multiple sclerosis. Methods: This randomised, placebo-controlled study compared atorvastatin 40 mg or placebo add-on therapy to interferon β1b for 24 months. Brain magnetic resonance imaging, multiple sclerosis functional composite score, Rao neuropsychological battery and expanded disability status scale were evaluated over 24 months. Results: A total of 154 patients were randomly assigned, 75 in the atorvastatin and 79 in the placebo arms, with a comparable drop-out rate (overall 23.4%). Brain atrophy over 2 years was not different in the two arms (−0.38% and −0.32% for the atorvastatin and placebo groups, respectively). Relapse rate, expanded disability status scale, multiple sclerosis functional composite score or cognitive changes were not different in the two arms. Patients withdrawing from the study had a higher number of relapses in the previous 2 years ( P=0.04) and a greater probability of relapsing within 12 months. Conclusions: Our results suggest that the combination of atorvastatin and interferon β1b is not justified in early relapsing–remitting multiple sclerosis and adds to the body of evidence indicating an absence of significant radiological and clinical benefit of statins in relapsing–remitting multiple sclerosis.