Boys Town National Research Hospital

Neurobrain science provides the motivation for research on causal modeling. The existing causal discovery methods have shown promising results in effective connectivity network analysis, however, they often overlook the dynamics of causality, in addition to the incorporation of spatio-temporal information in data. Dynamic effective connectivity networks (dECNs) reveal the changing directed brain activity and the dynamic causal influences among brain regions, which facilitate the identification of individual differences and enhance the understanding of human brain. To learn dynamic causality, we propose a deep spatio-temporal fusion architecture, which employs a dynamic causal deep encoder to incorporate spatio-temporal information into dynamic causality modeling, and a dynamic causal deep decoder to verify the discovered causality. The effectiveness of the proposed method is first illustrated with simulated data. Then, experimental results from Philadelphia Neurodevelopmental Cohort (PNC) demonstrate the superiority of the proposed method in inferring dECNs, which reveal the dynamic evolution of directed flow between brain regions. The analysis shows the difference of dECNs between young adults and children. Specifically, the directed brain functional networks transit from fluctuating undifferentiated systems to more stable specialized networks as one grows. This observation provides further evidence on the modularization and adaptation of brain networks during development, leading to higher cognitive abilities observed in young adults.

Recent theoretical accounts suggest that differences in the processing of probabilistic events underlie the core and associated traits of autism spectrum disorder (ASD). These theories hypothesize that autistic individuals are differentially impacted by disruptions in probabilistic input relative to neurotypical peers. According to this view, autistic individuals assign disproportionate weight to prediction errors such that novel input is overweighted relative to the aggregation of prior input; this is referred to as 'hyperplasticity' of learning. Prediction among autistic individuals has primarily been examined in nonverbal, visual contexts with older children and adults. The present study examined 32 autistic and 32 cognitively-matched neurotypical (NT) children's ability to generate predictions and adjust to changes in predictive relationships in auditory stimuli using two eye gaze tasks. In both studies, children were trained and tested on an auditory-visual cue which predicted the location of a reward stimulus. In Experiment 1 the cue was non-linguistic (instrumental sound) whereas in Experiment 2 the cue was linguistically-relevant (speaker gender). In both experiments, the cue-reward contingency was switched after the first block of trials, and predictive behavior was evaluated across a second block of trials. Analyses of children's looking behavior revealed similar performance in both groups on the non-linguistic task (Exp. 1). In the linguistically-relevant task (Exp. 2), predictive looking was less disrupted by the contingency switch for autistic children than NT children. Results suggest that autistic children may demonstrate hyperplastic learning in linguistically-relevant contexts, relative to NT peers.

People with HIV (PWH) often exhibit cognitive impairments, particularly in attention and executive function domains, despite effective viral suppression. The neurophysiological and neurochemical mechanisms underlying these deficits remain poorly understood. Herein, we used proton magnetic resonance spectroscopy (¹H-MRS) at 3 T with spectral editing to quantify the inhibitory (GABA+: GABA and co-edited macromolecules) and excitatory (Glx: glutamate and glutamine) neurotransmitter pools in the calcarine cortex of 27 virally suppressed PWH and 27 age- and sex-matched controls. We also estimated several secondary metabolites commonly implicated in neuroinflammatory and energetic processes, including total N-acetylaspartate (tNAA), total choline (tCho), total creatine (tCr), and myo-inositol (mI). Following best practices, metabolite concentrations were scaled to the unsuppressed water signal and corrected for voxel tissue composition, including gray matter, white matter, and CSF percentages. Compared with controls, PWH exhibited significantly elevated GABA+, Glx, and mI levels, suggesting parallel alterations in inhibitory, excitatory, and glial pathways. Notably, higher Glx levels were associated with longer HIV disease duration and increases in Glx and mI were coupled to decreases in attentional performance, linking neurochemical alterations to both disease progression and cognitive dysfunction. In sum, these findings provide the first evidence of concurrent GABA+ and Glx alterations in virally suppressed PWH, supporting a model in which disrupted excitatory-inhibitory balance contributes to cortical instability and attentional deficits in HIV.