Errors inhibit attainment of our goals, but there are many ways to get back on track: from increased caution to heightened attention. In this report we examined EEG signatures of control and perception in 21 participants who completed a luminance-varying flanker task. Hierarchical Sequential Sample Modeling with a shrinking spotlight model was used for algorithmic decomposition of post-error adjustments. Control-related changes included a relationship between frontal midline theta power and raised decision threshold, as well as faster drift rate. Yet contrary to our hypothesis, these relationships were not significantly modulated following an error. Perceptual changes elicited by the luminance manipulation scaled with posterior alpha/beta power; both these extrinsic and intrinsic features loaded on an enhanced drift rate. Most importantly, after an error, this relationship between alpha/beta power and drift rate was enhanced. These findings support separate roles of neural systems in adaptive control: midfrontal regions were linked to generic control, whereas sensory-specific mechanisms of attentional adjustment were specifically recruited to boost evidence accumulation when control is needed.

The neural basis of recently learned stimulus-response associations involves interactions between premotor, supplementary motor, sensorimotor, and striatal regions, but the causal contribution of premotor cortex to their posttraining expression remains unclear. Thirty-five right-handed volunteers learned six stimulus-response-outcome mappings in a single experimental session. Continuous theta-burst stimulation (cTBS) was then delivered over a right dorsal premotor target or a vertex active-control site before participants completed outcome-devaluation, slips-of-action, and baseline tests. The primary behavioral analyses showed no detectable group differences in reaction time or response accuracy during the outcome-devaluation or slips-of-action tests. Baseline performance was also comparable between groups, providing no evidence that stimulation affected retention of the recently learned mappings. Under the present limited-training protocol, posttraining cTBS over the right dorsal premotor target did not produce detectable behavioral differences relative to vertex cTBS. However, given the modest between-subject sample, the variability of devaluation-based measures, and the possibility that vertex stimulation affected adjacent medial motor regions, smaller or shared stimulation effects cannot be excluded.

Flickering light sources, such as fluorescent lamps, evoke neural oscillations in the occipital cortex aligning with the flicker frequency; however, this flicker often remains outside conscious awareness. This discrepancy suggests neural mechanisms gating flicker perception. While functional magnetic resonance imaging studies have indicated the involvement of large-scale frontal and parietal networks in conscious flicker perception, their low temporal resolution limits insights into the underlying dynamic interactions. Using electroencephalography and physically identical stimuli near the critical flicker-fusion frequency, we investigated the temporal dynamics of phase synchrony and power distribution. Flicker perception was characterized by an early increase in higher beta-band (19-28 Hz) synchrony, followed by an increase in gamma-band (29-48 Hz) synchrony between fronto-parietal and parieto-occipital regions at approximately 300 ms post-stimulus. This was accompanied by a global expansion of gamma-band power from occipital to fronto-parietal areas-effects not observed during fused perception. Conversely, alpha-band (8-14 Hz) synchrony between anterior and posterior regions showed a more pronounced reduction specifically during fusion. These findings suggest that frequency-specific coordination and global information sharing across large-scale networks may underlie conscious flicker perception. The emergence of broad gamma-band synchrony at around 300 ms may reflect the integration of local sensory signals into distributed cortical networks. Early beta-band synchrony may facilitate the initiation of this process through top-down modulation, whereas attenuated alpha-band synchrony during fusion may reflect insufficient engagement of these networks. Such dynamic interplay within distributed networks is suggested to be involved in shaping the temporal resolution of visual awareness.

The article presents the results of investigation of the cerebral wall layer cytoarchitecture, overall cell density, and expression of neuronal markers N200 and MAP2 in human fetuses (n = 20) at early gestational stages (8-11 completed weeks). At 8 week of embryogenesis, the telencephalic wall consisted of the ventricular, intermediate, and marginal zones. By week 10, the subventricular zone, subplate, and cortical plate had formed; however, no distinct cortical layering was observed at this stage. The developing neural tissue demonstrated wave-like changes in cell density. Active proliferation, reflected by the highest density of DAPI-positive nuclei, was recorded at week 8, followed by regression with a decline in cell numbers by week 9 and a partial recovery of the cell pool by weeks 10-11. A similar trend was observed for the relative proportion of N200-positive cells, a marker of developing corticofugal neurons. The proportion of N200-positive cells was highest at 8 weeks of gestation, decreased significantly by week 10, and increased again by week 11. In contrast, no changes in the dynamics of synaptogenesis were revealed, as assessed by the area occupied by MAP2-positive structures, which remained stable at all studied time points, with no significant intergroup differences. The distribution of this marker in the intermediate zone and its absence in the ventricular and marginal zones from week 8 indicated an early onset of dendritic differentiation of neuroblasts during radial migration, before their final positioning in the cortical plate.

Problematic smartphone use (PSU) is an important behavioral health concern, but its longitudinal psychological, neural, and molecular correlates remain unclear. In a two-wave longitudinal study, 50 university students completed questionnaire and structural MRI assessments. Annualized changes in hypomanic excitement, fear of missing out (FoMO), PSU severity, gray matter volume (GMV), and morphometric similarity (MS) gradients were examined. Excitement change was positively associated with PSU change, whereas the association between FoMO change and PSU change did not survive multiple-comparison correction. Whole-brain analysis identified a left frontal pole (FP) cluster in which GMV change was negatively associated with PSU change. Exploratory mediation analysis identified an adjusted indirect association between excitement change and PSU change through FP GMV change. PSU change was also associated with local, but not global, prefrontal MS-gradient changes. A highly exploratory serial mediation analysis further identified an unadjusted indirect association linking excitement change to PSU change through FP GMV change and local second-gradient reorganization in the FP. Imaging transcriptomic analysis linked the PSU-related GMV pattern to spatial gene-expression profiles associated with energy metabolism, myelin- and axon-related processes, transcriptional regulation, and neurodevelopment. These findings associate hypomanic excitement change with longitudinal PSU change and localized prefrontal structural reorganization, while providing an indirect molecular annotation of the associated GMV pattern.

Historically regarded as a hub for autonomic control, the brainstem is now increasingly recognized for its role in cognition. However, little information is available regarding its specific contribution to cognitive function, particularly in midlife, when modifiable cardiovascular risks begin to shape brain health trajectories. Because the brainstem houses key nuclei that regulate cardiovascular dynamics and cerebral perfusion, we focused on carotid-femoral pulse wave velocity (cfPWV), a well-established index of central arterial stiffness that directly reflects cerebral hemodynamic load. This study investigated whether brainstem volume is associated with cognitive performance in healthy midlife adults and whether this relation is moderated by cfPWV. A total of 198 adults aged 40-65 years underwent neuropsychological testing, fasting cardiovascular and metabolic assessments, and structural MRI. Linear regression models examined brainstem volume as a predictor of attention, executive function, and memory, adjusting for age, sex, education, and total intracranial volume. Additional models tested the interaction between cfPWV and brainstem volume, controlling for cardiometabolic covariates. Greater brainstem volume was significantly associated with better memory performance (p = .010, FDR q = 0.030), but not attention or executive function. Greater brainstem volume was also associated with lower systolic and pulse pressure. Notably, cfPWV moderated the relationship between brainstem volume and memory, such that the positive association was strongest among individuals with higher arterial stiffness (p = .001, FDR q = 0.002). These findings suggest that the brainstem may serve as a structural hub linking peripheral vascular health and cognitive function in midlife, particularly under conditions of elevated arterial stiffness.

Neuropathic pain (NP), arising from lesions or dysfunction of the somatosensory system, remains a major clinical challenge due to its subjective and multidimensional nature. Traditional pain assessments rely on self‑report scales, which lack objectivity and reproducibility. Electroencephalography (EEG), with its high temporal resolution and accessibility, provides a promising avenue for identifying candidate neurophysiological biomarkers of pain. The current narrative review integrates mechanistic insights and electrophysiological evidence to delineate EEG alterations in NP. Resting‑state θ increases and dominant‑frequency slowing are relatively recurrent in chronic NP, whereas α‑, β‑ and γ‑band findings remain heterogeneous. Network analyses further reveal aberrant prefrontal‑limbic and sensorimotor connectivity, as well as altered cross‑frequency coupling, but the direction and topology of these findings remain dependent on the patient population, recording configuration and analytical metric. Advances in computational EEG analysis, graph theory and machine learning are facilitating exploration of objective, individualized pain assessment frameworks. Emerging portable EEG and multimodal approaches may provide opportunities for future clinical translation. Overall, EEG offers a feasible and dynamic method to bridge subjective pain perception with measurable neurophysiological signatures, paving the way toward precision diagnostics and neuromodulation in NP.

The brain's ability to consolidate a wide range of memories while maintaining their distinctiveness across experiences remains poorly understood. Sharp-wave ripples, neural oscillations that occur predominantly within CA1 of the hippocampus during immobility and sleep, have been shown to play a critical role in the consolidation process. More recently, evidence has uncovered functional heterogeneity of pyramidal neurons within distinct sublayers of CA1 that display unique properties during ripples, potentially contributing to memory specificity. Despite this, it remains unclear exactly how ripples shift the activity of CA1 neuronal populations to accommodate the consolidation of specific memories and how sublayer differences manifest. Here, we studied interactions between the anterior cingulate cortex (ACC) and CA1 neurons during ripples and discovered a reorganization of their communication following learning. Specifically, using a generalized linear model decoder, we demonstrated the pre-existence of ACC-to-CA1 communication, which is weakened during post-training sleep following learning, suggesting that ACC activity reallocates the contribution of CA1 neurons during memory formation. Interestingly, the reorganization appeared unique for a subset of CA1 superficial (CA1sup) neurons that were task inactive, whereas communication between the ACC and CA1deep neurons remained largely stable across pre- and post-training sleep. Consistent with this sublayer-selective reorganization, we found that optogenetic stimulations of the ACC preferentially suppressed CA1sup neurons while activating a unique subset of CA1 interneurons. Overall, these findings highlight an important role of the ACC in rebalancing CA1 neuronal populations' contribution in learning and memory consolidation.

In this registered report, we introduce a new discordant sibling random-intercept cross-lagged panel model and apply it to investigate within-person/family and between-family bidirectional associations of parental monitoring-related phenotypes and youth externalizing behaviors. We used data from 1,956 twin/sibling pairs (Mage at first assessment = 10 years; 51% male, 59% White; 14% Black; 15% Hispanic; <1% Asian; 11% Other race/ethnicity) contributing up to six annual waves of data collection from the adolescent brain and cognitive development study, a nationally representative data collection effort including 11,875 children enrolled and assessed across 21 sites across the United States. DS latent curve models with structured residuals models were needed to account for change over time, converged, and fit the data well. We found few within-person/family effects consistent with hypotheses, concentrated from age 13-15 that were likely environmentally mediated. Potentially causal effects within-person/family effects included more youth-reported child disclosure at age 13 predicting lower parent-reported externalizing at age 14, and more youth externalizing problems at age 13 with less monitoring at age 14; other within-person/family associations were driven by familial confounding. Unexpected positive between-family lagged effects in the same developmental window reflect novel family-level processes that may be driven by evocative gene-environment correlations.