Neuropathology of the Down syndrome cerebral cortex includes fewer interneurons in upper cortical layers.
To test the hypothesis that cognitively unimpaired individuals with Alzheimer disease (AD) neuropathology differ from individuals with AD dementia on biomarkers of neurodegeneration, synaptic dysfunction, and glial activation.
Title: Associations of prenatal maternal depression and anxiety symptoms with infant white matter microstructure Legend: Decreased frontal neurite density in the prefrontal white matter (blue highlighted regions) of 1-month old infants was associated with higher prenatal …
When we speak, we are able to use what we hear about that speech (auditory feedback) to alter our speech movements both in real time within a single word (feedback control) as well as over longer time scales across multiple utterances (feedforward control).
Disorders of speech production may be accompanied by abnormal processing of speech sensory feedback. Here, we introduce a semi-automated analysis designed to assess the degree to which speakers use natural online feedback to decrease acoustic variability in spoken words.
Adult neural stem cells in mouse models of fragile X syndrome (FXS) have elevated histone acetylation, leading to reduced neurogenesis. Treatment with either Nutlin-3 or Curcumin rebalances histone acetylation and rescues cognitive functions
A single-word identification test was used to study speech production in children and adults with Down syndrome (DS) to determine the developmental pattern of speech intelligibility with an emphasis on vowels.
The current study investigated the relation between postural balance and performance of daily living skills (DLS) in youth with autism spectrum disorder (ASD). Fifty-two youth with ASD (6–17 years; IQ ≥ 67) completed standardized balance testing and parent-reported DLS measures.
Children who cannot effectively read print because of a visual, physical, perceptual, developmental, cognitive or learning disability, are considered to have a print disability.
Our goal was to define the genetic cause of the profound hypomyelination in the taiep rat model and determine its relevance to human white matter disease.