Theta and alpha connectivity in children with autism spectrum disorder.

Spontaneous electroencephalography (EEG) measurements have demonstrated putative variations in the neural connectivity of subjects with autism spectrum disorder, as compared to neurotypical individuals. However, the exact nature of these connectivity differences has remained unknown, a question that we now address. Resting-state, eyes-open EEG data were recorded over 20 min from a cohort of 13 males aged 3-5 years with autism spectrum disorder, and nine neurotypical individuals as a control group.

Acceptability and Feasibility of a Taekwondo Mindful Movement Intervention in Dialectical Behavior Therapy.

Borderline personality disorder (BPD) is often comorbid with disordered eating behaviors. Effective treatments are critically needed for this complex population. Mindful movement interventions may represent a promising, adjunctive treatment option for individuals with BPD symptoms, especially those with co-occurring disordered eating.

A Hypothesis: Metabolic Contributions to 16p11.2 Deletion Syndrome.

16p11.2 deletion syndrome is a severe genetic disorder associated with the deletion of 27 genes from a Copy Number Variant region on human chromosome 16. Symptoms associated include cognitive impairment, language and motor delay, epilepsy or seizures, psychiatric disorders, autism spectrum disorder (ASD), changes in head size and body weight, and dysmorphic features, with a crucial need to define genes and mechanisms responsible for symptomatology.

Listening-in-noise difficulties following stroke: a scoping review protocol.

Introduction: Across different populations, listening difficulties have been shown to adversely impact social interactions and work performance, and substantively contribute to poorer quality of life. Following a stroke, people also report listening difficulties in noisy, everyday environments such as cafes and workplaces. Despite the prevalence of these challenges, there is limited understanding of this issue, which means the listening needs of stroke survivors remain under-recognised and unmet.

Non-ionotropic signaling through the NMDA receptor GluN2B carboxy-terminal domain drives dendritic spine plasticity and reverses fragile X phenotypes.

N-methyl-D-aspartate (NMDA)-induced spine shrinkage proceeds independently of ion flux and requires the initiation of de novo protein synthesis. Using subtype-selective pharmacological and genetic tools, we find that structural plasticity is dependent on ligand binding to GluN2B-containing NMDA receptors (NMDARs) and signaling via the GluN2B carboxy-terminal domain (CTD). Disruption of non-ionotropic signaling by replacing the GluN2B CTD with the GluN2A CTD leads to an increase in spine density, dysregulated basal protein synthesis, exaggerated long-term depression mediated by G-protein-coupled metabotropic glutamate receptors (mGluR-LTD), and epileptiform activity reminiscent of phenotypes observed in the Fmr1 knockout (KO) model of fragile X syndrome.