Probing a neural unreliability account of auditory sensory processing atypicalities in Rett Syndrome.

Background: In the search for objective tools to quantify neural function in Rett Syndrome (RTT), which are crucial in the evaluation of therapeutic efficacy in clinical trials, recordings of sensory-perceptual functioning using event-related potential (ERP) approaches have emerged as potentially powerful tools. Considerable work points to highly anomalous auditory evoked potentials (AEPs) in RTT. However, an assumption of the typical signal-averaging method used to derive these measures is "stationarity" of the underlying responses - i.

Probing a neural unreliability account of auditory sensory processing atypicalities in Rett Syndrome.

Background In the search for objective tools to quantify neural function in Rett Syndrome (RTT), which are crucial in the evaluation of therapeutic efficacy in clinical trials, recordings of sensory-perceptual functioning using event-related potential (ERP) approaches have emerged as potentially powerful tools. Considerable work points to highly anomalous auditory evoked potentials (AEPs) in RTT. However, an assumption of the typical signal-averaging method used to derive these measures is "stationarity" of the underlying responses - i.

Probing a neural unreliability account of auditory sensory processing atypicalities in Rett Syndrome.

Background: In the search for objective tools to quantify neural function in Rett Syndrome (RTT), which are crucial in the evaluation of therapeutic efficacy in clinical trials, recordings of sensory-perceptual functioning using event-related potential (ERP) approaches have emerged as potentially powerful tools. Considerable work points to highly anomalous auditory evoked potentials (AEPs) in RTT. However, an assumption of the typical signal-averaging method used to derive these measures is "stationarity" of the underlying responses - i.

Do we all synch alike? Brain-body-environment interactions in ASD.

Autism Spectrum Disorder (ASD) is characterized by rigidity of routines and restricted interests, and atypical social communication and interaction. Recent evidence for altered synchronization of neuro-oscillatory brain activity with regularities in the environment and of altered peripheral nervous system function in ASD present promising novel directions for studying pathophysiology and its relationship to ASD clinical phenotype. Human cognition and action are significantly influenced by physiological rhythmic processes that are generated by both the central nervous system (CNS) and the autonomic nervous system (ANS).

Oscillatory entrainment mechanisms and anticipatory predictive processes in children with autism spectrum disorder.

Anticipating near-future events is fundamental to adaptive behavior, whereby neural processing of predictable stimuli is significantly facilitated relative to nonpredictable events. Neural oscillations appear to be a key anticipatory mechanism by which processing of upcoming stimuli is modified, and they often entrain to rhythmic environmental sequences. Clinical and anecdotal observations have led to the hypothesis that people with autism spectrum disorder (ASD) may have deficits in generating predictions, and as such, a candidate neural mechanism may be failure to adequately entrain neural activity to repetitive environmental patterns, to facilitate temporal predictions.

Looking for consistency in an uncertain world: test-retest reliability of neurophysiological and behavioral readouts in autism.

Background: Autism spectrum disorders (ASD) are associated with altered sensory processing and perception. Scalp recordings of electrical brain activity time-locked to sensory events (event-related potentials; ERPs) provide precise information on the time-course of related altered neural activity, and can be used to model the cortical loci of the underlying neural networks. Establishing the test-retest reliability of these sensory brain responses in ASD is critical to their use as biomarkers of neural dysfunction in this population.

Ripe for solution: Delayed development of multisensory processing in autism and its remediation.

Difficulty integrating inputs from different sensory sources is commonly reported in individuals with Autism Spectrum Disorder (ASD). Accumulating evidence consistently points to altered patterns of behavioral reactions and neural activity when individuals with ASD observe or act upon information arriving through multiple sensory systems. For example, impairments in the integration of seen and heard speech appear to be particularly acute, with obvious implications for interpersonal communication.

Learning to classify neural activity from a mouse model of Alzheimer's disease amyloidosis versus controls.

The mechanisms underlying Alzheimer's disease (AD) onset and progression are not yet elucidated. The extent to which alterations in the activity of individual neurons of an AD model are significant, and the phase at which they can be captured, point to the intensity of the pathology and imply the stage at which it can be detected. Using a machine-learning algorithm, we present a successful cell-by-cell classification of intracellularly recorded neurons from the B6C3 APPswe/PS1dE9 AD model, versus wildtypes controls, at both a late stage and at an early stage, when the plaque pathology and behavioral deficits are absent or rare.

Amyloid-β disrupts ongoing spontaneous activity in sensory cortex.

Unlabelled: The effect of Alzheimer's disease pathology on activity of individual neocortical neurons in the intact neural network remains obscure. Ongoing spontaneous activity, which constitutes most of neocortical activity, is the background template on which further evoked-activity is superimposed. We compared in vivo intracellular recordings and local field potentials (LFP) of ongoing activity in the barrel cortex of APP/PS1 transgenic mice and age-matched littermate CONTROLS, following significant amyloid-β (Aβ) accumulation and aggregation.

Amyloid-β alters ongoing neuronal activity and excitability in the frontal cortex.

The effects of amyloid-β on the activity and excitability of individual neurons in the early and advanced stages of the pathological progression of Alzheimer's disease remain unknown. We used in vivo intracellular recordings to measure the ongoing and evoked activity of pyramidal neurons in the frontal cortex of APPswe/PS1dE9 transgenic mice and age-matched nontransgenic littermate controls. Evoked excitability was altered in both transgenic groups: neurons in young transgenic mice displayed hypoexcitability, whereas those in older transgenic mice displayed hyperexcitability, suggesting changes in intrinsic electrical properties of the neurons.

Interaction between amyloid-β pathology and cortical functional columnar organization.

Amyloid-β plaques are one of the major neuropathological features in Alzheimer's disease (AD). Plaques are found in the extracellular space of telencephalic structures, and have been shown to disrupt neuronal connectivity. Since the disruption of connectivity may underlie a number of the symptoms of AD, understanding the distribution of plaques in the neuropil in relation to the connectivity pattern of the neuronal network is crucial.