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Kammer, E.

Publications and source records attributed to Kammer, E..

2 recordsLinked to original sources

Functional deficits of the inhibitory control system in children with ADHD: A task-based fMRI meta-analysis

Inhibitory control deficits have long been proposed as a central neurocognitive mechanism underlying childhood Attention Deficit/Hyperactivity Disorder (ADHD). However, neuroimaging findings remain heterogeneous, partly due to methodological variability across developmental samples and experimental paradigms. The present study aimed to characterize the neural architecture of motor response inhibition in typically developing (TD) children and identify reproducible functional abnormalities associated with pediatric ADHD using stringent, developmentally specific inclusion criteria. We conducted two coordinate-based meta-analyses using Activation Likelihood Estimation (ALE). Following a systematic literature search (up to August 2026), we identified 23 task-based fMRI studies reporting inhibitory-control-related activation in TD children (237 foci) and 17 studies comparing children with ADHD and TD peers (114 foci) during the Stop-Signal Task or Go/No-Go Task. All participants were younger than 18 years of age. Statistical significance was determined using cluster-level family-wise error (FWE) correction. In TD children, ALE revealed a robust inhibitory-control network encompassing the bilateral anterior insula (AI), inferior frontal gyrus (IFG), and the midline pre-supplementary motor area (preSMA) and anterior cingulate cortex (ACC). This spatial organization closely resembled the canonical inhibitory-control network consistently observed in adults, suggesting that the core neural architecture supporting motor inhibition is already detectably organized during development. In the between-group analysis, children with ADHD exhibited significant hypoactivation primarily within the preSMA. Notably, this region demonstrated striking spatial overlap with the preSMA cluster reliably recruited in TD children during motor inhibition. These findings provide convergent support for inhibitory-control models of ADHD and identify altered preSMA recruitment as one of the most consistent functional abnormalities associated with pediatric ADHD. While the neural infrastructure supporting inhibitory control is broadly established during childhood, children with ADHD exhibit reduced recruitment of a key cortical node within this network during motor inhibition demands.

neuroscience↗

Intestinal Stem Cells Retain an Epigenetic Memory of Prior Inflammation

Intestinal epithelial damage and impaired repair are hallmarks of ulcerative colitis (UC), even after inflammation resolves. Intestinal stem cells (ISCs) can retain stable epigenetic changes after inflammation, highlighting the potential for long-lived epithelial memory in the gut. Inflammatory injury in barrier tissues induces epigenetic memory in epithelial stem cells, and the tendency of UC to relapse at previously inflamed sites led us to hypothesize that ISCs from IBD patients acquire lasting memory of prior inflammation. To test this, we derived colonic organoids from inflamed and uninflamed regions of the same UC patients and propagated in long-term culture. Chromatin profiling revealed 2,252 accessible regions unique to prior-inflamed (PI) organoids, associated with stress response, repair, and inflammatory genes. Although these regions remained accessible, [~]95% of associated genes were not upregulated in PI organoids, indicating a primed state. Upon inflammatory or injury re-challenge, PI organoids exhibited heightened transcriptional responses and accelerated wound closure, despite reduced clonogenicity and impaired barrier function, indicating a retained inflammatory memory program. Our findings demonstrate that human ISCs retain a chromatin-based memory of inflammation that persists in the absence of immune cues and shapes future responses to injury. While this may support epithelial adaptation to secondary insults, it may predispose tissue to relapse in patients with UC.

molecular biology↗