During childhood, schools are a crucial environment for social interactions, making them ideal forevaluating the inclusion of children with special educational needs (SEN). Children with AutismSpectrum Disorder (ASD) often face challenges in peer relationships, yet how this condition impactsspecific social dynamics and school coexistence is not well understood. To address this issue, weexamined social relationships and dynamics within elementary schools. We hypothesized that,compared to their peers without ASD, children with ASD: (i) occupy more peripheral positions withinsocial networks, reflecting a low degree of centrality, and (ii) engage less in reciprocal relationships,indicating diminished social reciprocity. To test these hypotheses, we introduced a novel ecologicalapproach, using game theory to quantify social integration and reciprocity among children with ASDin elementary schools. Social networks were constructed for each classroom based on the children'speer selections during a distributive game in which they had to send tokens to their peers. Afteranalyzing centrality and reciprocity network measures, we found that children with ASD weresignificantly less central and less involved in reciprocal peer relationships compared to their peerswithout ASD or with other SEN conditions. These results highlight the relevance of interventionsthat promote social inclusion and open new avenues for future research to explore the intersectionof neurodevelopmental conditions and social dynamics. This exploration has the potential to informpolicies and practices contributing to how educational systems accommodate diverse learningneeds.

Multiple sclerosis (MS) is a prevalent neurological disorder marked by inflammation and demyelination, with fatigue being one of the most reported and debilitating symptoms. While fatigue occurs across various neurological conditions and even in healthy individuals, the specific mechanisms contributing to fatigue in each context remain unclear. In this study, we conducted a cross-sectional analysis involving 33 people with relapsing MS (PwRMS) and 29 healthy controls who also reported fatigue. Participants underwent MRI scans, including T1-weighted and diffusion-weighted imaging, to evaluate brain structure. Additionally, the Modified Fatigue Impact Scale was utilized. To investigate the hypothesis that fatigue correlates differently with brain structures in PwRMS, we employed Bayesian LASSO and Spike-and-Slab LASSO regression models. Our findings indicated that lower white matter volume and compromised microstructural integrity in specific brain regions—such as the caudate part of cingulate gyrus, inferior frontal gyrus, and the banks of the superior temporal sulcus—were significantly associated with fatigue scores in PwRMS. These results suggest that alterations in specific brain regions may play a critical role in the clinical manifestation of fatigue in MS. Understanding these insights could help differentiate general mechanisms of fatigue from those affecting people with relapsing MS, which may guide future therapeutic strategies.

Patients recovering from COVID-19 commonly exhibit cognitive and brain alterations, yet the specific neuropathological mechanisms and risk factors underlying these alterations remain elusive. Given the significant global incidence of COVID-19, identifying factors that can distinguish individuals at risk of developing brain alterations is crucial for prioritizing follow-up care. Here, we report findings from a sample of patients consisting of 73 adults with a mild to moderate SARS-CoV-2 infection without signs of respiratory failure and 27 with infections attributed to other agents and no history of COVID-19. The participants underwent cognitive screening, a decision-making task, and MRI evaluations. We assessed for the presence of anosmia and the requirement for hospitalization. Groups did not differ in age or cognitive performance. Patients who presented with anosmia exhibited more impulsive alternative changes after a shift in probabilities (r = − 0.26, p = 0.001), while patients who required hospitalization showed more perseverative choices (r = 0.25, p = 0.003). Anosmia correlated with brain measures, including decreased functional activity during the decision-making task, thinning of cortical thickness in parietal regions, and loss of white matter integrity. Hence, anosmia could be a factor to be considered when identifying at-risk populations for follow-up.

Adapting our behavior to environmental demands relies on our capacity to perceive and manage potential conflicts within our surroundings. While evidence implicates the involvement of the lateral prefrontal cortex and theta oscillations in detecting conflict stimuli, their roles in conflict expectation remain elusive. Consequently, the exact computations and neural mechanisms underlying these cognitive processes still need to be determined. To address this gap, we employed an integrative approach involving cognitive computational modeling, fMRI, TMS, and EEG. Our results revealed a computational process underlying conflict expectation, which correlated with activity in the superior frontal gyrus (SFG). Furthermore, rhythmic TMS in the theta range applied over the SFG, but not over the inferior frontal junction, induced endogenous theta activity, enhancing computations associated with conflict expectation. These findings provide compelling evidence for the causal involvement of SFG theta activity in learning and allocating cognitive resources to address forthcoming conflict stimuli. Significant Statement Alterations in the processing of expectations of conflict events have been associated with several neuropsychiatric disorders that significantly affect the quality of life for many individuals. This article describes a cognitive computation underlying the conflict expectation and its causal neural mechanism involving theta brain activity in the superior frontal gyrus (SFG). Thus, unraveling this mechanism holds promise for developing interventions to address cognitive alterations related to anticipation of conflict events in neuropsychiatric disorders, improving overall cognitive function and quality of life.

Background The ageing population has increased the prevalence of disabling and high-cost diseases, such as dementia and mild cognitive impairment (MCI). The latter can be considered a prodromal phase of some dementias and a critical stage for interventions to postpone the impairment of functionality. Working memory (WM) is a pivotal cognitive function, representing the fundamental element of executive functions. This project proposes an intervention protocol to enhance WM in these users, combining cognitive training with transcranial electrical stimulation of alternating current (tACS). This technique has been suggested to enhance the neuronal plasticity needed for cognitive processes involving oscillatory patterns. WM stands to benefit significantly from this approach, given its well-defined electrophysiological oscillations. Therefore, tACS could potentially boost WM in patients with neurodegenerative diseases. Methods This study is a phase IIb randomised, double-blind clinical trial with a 3-month follow-up period. The study participants will be 62 participants diagnosed with MCI, aged over 60, from Valparaíso, Chile. Participants will receive an intervention combining twelve cognitive training sessions with tACS. Participants will receive either tACS or placebo stimulation in eight out of twelve training sessions. Sessions will occur twice weekly over 6 weeks. The primary outcomes will be electroencephalographic measurements through the prefrontal theta oscillatory activity, while the secondary effects will be cognitive assessments of WM. The participants will be evaluated before, immediately after, and 3 months after the end of the intervention. Discussion The outcomes of this trial will add empirical evidence about the benefits and feasibility of an intervention that combines cognitive training with non-invasive brain stimulation. The objective is to contribute tools for optimal cognitive treatment in patients with MCI. To enhance WM capacity, postpone the impairment of functionality, and obtain a better quality of life. Trial registration ClinicalTrials.gov NCT05291208. Registered on 28 February 2022. ISRCTN87597719 retrospectively registered on 15 September 2023.