Explore the vast range of titles available.

Autism spectrum disorders (ASDs) are characterized by deficits in social and communication processes. Recent data suggest that altered functional connectivity (FC), i.e. synchronous brain activity, might contribute to these deficits. Of specific interest is the FC integrity of the default mode network (DMN), a network active during passive resting states and cognitive processes related to social deficits seen in ASD, e.g. Theory of Mind. We investigated the role of altered FC of default mode sub-networks (DM-SNs) in 16 patients with high-functioning ASD compared to 16 matched healthy controls of short resting fMRI scans using independent component analysis (ICA). ICA is a multivariate data-driven approach that identifies temporally coherent networks, providing a natural measure of FC. Results show that compared to controls, patients showed decreased FC between the precuneus and medial prefrontal cortex/anterior cingulate cortex, DMN core areas, and other DM-SNs areas. FC magnitude in these regions inversely correlated with the severity of patients' social and communication deficits as measured by the Autism Diagnostic Observational Schedule and the Social Responsiveness Scale. Importantly, supplemental analyses suggest that these results were independent of treatment status. These results support the hypothesis that DM-SNs under-connectivity contributes to the core deficits seen in ASD. Moreover, these data provide further support for the use of data-driven analysis with resting-state data for illuminating neural systems that differ between groups. This approach seems especially well suited for populations where compliance with and performance of active tasks might be a challenge, as it requires minimal cooperation. ► Three default mode sub-networks (DM-SNs) were identified from resting state fMRI scans of 16 patients with high-functioning autism spectrum disorders (ASD) and 16 matched healthy controls (HC) using independent component analysis (ICA). ► Compared to HC, patients with ASD showed decreased functional connectivity between the precuneus and medial prefrontal cortex/anterior cingulate cortex and other DM-SNs areas. ► FC magnitude in these regions inversely correlated with the severity of patients’ social and communication deficits as measured by the Autism Diagnostic Observational Schedule and the Social Responsiveness Scale. ► Supplemental analyses suggest that these results were independent of treatment status.

Background/ObjectivesObesity has been ascribed to corticostriatal regions taking control over homeostatic areas. To test this assumption, we applied an effective connectivity approach to reveal the direction of information flow between brain regions and the valence of connections (excitatory versus inhibitory) as a function of increased BMI and homeostatic state.Subjects/MethodsForty-one participants (21 overweight/obese) underwent two resting-state fMRI scans: after overnight fasting (hunger) and following a standardised meal (satiety). We used spectral dynamic causal modelling to unravel hunger and increased BMI-related changes in directed connectivity between cortical, insular, striatal and hypothalamic regions.ResultsDuring hunger, as compared to satiety, we found increased excitation of the ventromedial prefrontal cortex over the ventral striatum and hypothalamus, suggesting enhanced top-down modulation compensating energy depletion. Increased BMI was associated with increased excitation of the anterior insula over the hypothalamus across the hunger and satiety conditions. The interaction of hunger and increased BMI yielded decreased intra-cortical excitation from the dorso-lateral to the ventromedial prefrontal cortex.ConclusionsOur findings suggest that excess weight and obesity is associated with persistent top-down excitation of the hypothalamus, regardless of homeostatic state, and hunger-related reductions of dorso-lateral to ventromedial prefrontal inputs. These findings are compatible with eating without hunger and reduced self-regulation views of obesity.

Specific learning disabilities (SLDs) are estimated to affect up to 10% of the population, and they co-occur far more often than would be expected, given their prevalences. We need to understand the complex etiology of SLDs and their co-occurrences in order to underpin the training of teachers, school psychologists, and clinicians, so that they can reliably recognize SLDs and optimize the learning contexts for individual learners.

Patients with hippocampal amnesia play a central role in memory neuroscience but the neural underpinnings of amnesia are hotly debated. We hypothesized that focal hippocampal damage is associated with changes across the extended hippocampal system and that these, rather than hippocampal atrophy per se, would explain variability in memory between patients. We assessed this hypothesis in a uniquely large cohort of patients (n = 38) after autoimmune limbic encephalitis, a syndrome associated with focal structural hippocampal pathology. These patients showed impaired recall, recognition and maintenance of new information, and remote autobiographical amnesia. Besides hippocampal atrophy, we observed correlatively reduced thalamic and entorhinal cortical volume, resting-state inter-hippocampal connectivity and activity in posteromedial cortex. Associations of hippocampal volume with recall, recognition, and remote memory were fully mediated by wider network abnormalities, and were only direct in forgetting. Network abnormalities may explain the variability across studies of amnesia and speak to debates in memory neuroscience.

The occipital lobe contains a substantial part of the neural machinery involved in visual perception. Mutations in the LAMC3 gene have recently been shown to cause complex bilateral occipital cortical gyration abnormalities. However, to what extent these structural changes impact visual behavior is not known. We recorded responses for two screening test batteries targeting visual function (Leuven - Perceptual Organization Screening Test, Cortical Vision Screening Test) and measured eye fixation performance in a visual attention experiment from a patient with homozygous LAMC3 gene mutation. Using voxel-based morphometry (VBM) we quantitatively assessed the extent of structural changes brought on by the genetic mutation by comparing mean cortical curvature, cortical thickness, and gray matter volume in 34 cortical areas between patient and an age-, sex-, and education-matched control group. Anatomical connectivity between these cortical areas was investigated by a structural covariance analysis. Visual screening-, and behavioral results revealed that the patient's impairments were predominantly in visuo-spatial attention. Consistent with this, VBM and structural connectivity results revealed significant structural changes in cortical regions subserving attentional functions. We conclude that the LAMC3 gene mutation affects cortical areas beyond the occipital lobe and primarily those visual functions that involve heavily distributed networks – such as visuo-spatial attention. •LAMC3 gene mutation links to cortical structural changes beyond the occipital lobe.•LAMC3 gene mutation links to deficits in visual attention.•Structural changes primarily in cortical areas subserving visual attention.•Spared object and face recognition despite compromised cortical architecture.

The survival rates of infants born prematurely have improved as a result of advances in neonatal care, although there remains an increased risk of subsequent disability. Accurate measurement of the shape and appearance of the very preterm brain at term-equivalent age may guide the development of predictive biomarkers of neurological outcome. We demonstrate in 92 preterm infants (born at an average gestational age of 27.0±2.7weeks) scanned at term equivalent age (scanned at 40.4±1.74weeks) that the cortical sulcation ratio varies spatially over the cortical surface at term equivalent age and correlates significantly with gestational age at birth (r=0.49,p<0.0001). In the underlying white matter, fractional anisotropy of local white matter regions correlated significantly with gestational age at birth at term equivalent age (for the genu of the corpus callosum r=0.26,p=0.02 and for the splenium r=0.52,p<0.001) and in addition the fractional anisotropy in these local regions varies according to location. Finally, we demonstrate that connectivity measurements from tractography correlate significantly and specifically with the sulcation ratio of the overlying cortical surface at term equivalent age in a subgroup of 20 infants (r={0.67,0.61,0.86}, p={0.004,0.01,0.00002}) for tract systems emanating from the left and right corticospinal tracts and the corpus callosum respectively). Combined, these results suggest a close relationship between the cortical surface phenotype and underlying white matter structure assessed by diffusion weighted MRI. The spatial surface pattern may allow inference on the connectivity and developmental trajectory of the underlying white matter complementary to diffusion imaging and this result may guide the development of biomarkers of functional outcome. •Survival rates of infants born prematurely have improved recently.•Accurate measurement of the shape of the brain may guide the development of predictive biomarkers.•We show in 92 infants that the cortical folding pattern varies with gestational age at birth.•In preterm WM, connectivity measurements correlate with the overlying cortical surface pattern.•Cortical folding may allow inference on the connectivity and developmental trajectory of WM

Diffusion tensor imaging (DTI) was applied to 12 patients with focal cortical dysplasia (FCD) in frontal or occipital cortex. Fiber tractography was obtained from seeding points in superior longitudinal fasciculus or posterior corona radiata. Mean fractional anisotropy of fiber bundles around the affected cortex was decreased in comparison to the contralateral hemisphere with statistical significance (paired t test, P = 0.0274). On visual analysis, tractography depicted decreased volume of fiber bundles connected to the dysplastic cortex invariably even in those with a normal T2 signal intensity of underlying white matter adjacent to FCD. DTI has high potential to be applied to localize the FCD and to provide a better understanding of the pathological changes in the white matter.

An extremely rare variation of the (left) middle meningeal artery (MMA) originating from the basilar artery, detected incidentally during cerebral angiography, is reported. The right MMA was normal and an accessory meningeal artery arising from the maxillary artery was present on both the sides. The foramen spinosum on the variant side was absent. This abnormal origin of the MMA can be explained by the presence of a perineural arterial network in the region of the Gasserian ganglion, formed by branches of the developing basilar and stapedial arterial systems; the middle meningeal–basilar arterial channel opening up in the absence of a normally developing MMA.

Parkinson's disease presents several practical challenges: it can be difficult to distinguish from atypical parkinsonian syndromes, clinical ratings can be insensitive as markers of disease progression, and its non-motor manifestations are not readily assessed in animal models. These challenges, along with others, are beginning to be addressed by innovative imaging methods to characterise Parkinson's disease-specific functional networks across the whole brain and measure their expression in each patient. These signatures can help improve differential diagnosis, guide selection of patients for clinical trials, and quantify treatment responses and placebo effects in individual patients. The primary Parkinson's disease-related metabolic pattern has been replicated in multiple patient populations and used as an outcome measure in clinical trials. It can also be used as a predictor of near-term phenoconversion in prodromal syndromes, such as rapid eye movement sleep behaviour disorder. Functional network imaging holds great promise for future clinical use in the management of neurodegenerative disorders.

The developing brain initially makes more synapses than it needs. With further development, excess synapses are pruned away, leaving mature circuits. Synapses can be eliminated by microglia, which engulf and destroy them. Vainchtein et al. found that the microglia are called into action by astrocytes, supportive cells on which neurons rely. Astrocytes near a redundant synapse release the cytokine interleukin-33 (IL-33), which recruits microglia to the site. In mice, disruptions in this process, as caused by deficiency in IL-33, led to too many excitatory synapses and overactive brain circuitry. Science , this issue p. 1269 Astrocytes use microglia to prune redundant neuronal synapses. Neuronal synapse formation and remodeling are essential to central nervous system (CNS) development and are dysfunctional in neurodevelopmental diseases. Innate immune signals regulate tissue remodeling in the periphery, but how this affects CNS synapses is largely unknown. Here, we show that the interleukin-1 family cytokine interleukin-33 (IL-33) is produced by developing astrocytes and is developmentally required for normal synapse numbers and neural circuit function in the spinal cord and thalamus. We find that IL-33 signals primarily to microglia under physiologic conditions, that it promotes microglial synapse engulfment, and that it can drive microglial-dependent synapse depletion in vivo. These data reveal a cytokine-mediated mechanism required to maintain synapse homeostasis during CNS development.