POU3F2, a member of the Pit-Oct-Unc (POU) domain transcription factor family, is widely expressed in the central nervous system and essential for the development and maturation of brain. POU3F2 deletion results in impaired hypothalamus and neocortex development, and most mice die between postnatal days 0 and 10. Recently, emerging evidences have demonstrated that POU3F2 is involved in neuropsychiatric disorders, including Alzheimer's disease, Parkinson's disease, Huntington's disease, bipolar disorder, schizophrenia, and autism spectrum disorder, albeit still with some limitations in current studies. Besides, POU3F2 also plays a vital role in the reprogramming of somatic cells into neuronal lineages, which provides new ideas and directions for the treatment of neuropsychiatric disorders. This review aims to systematically summarize and analyze the diverse roles of POU3F2 in brain development, neuropsychiatric disorders, and neuronal reprogramming. Furthermore, the potential of POU3F2-targeted therapies for neuropsychiatric disorders and proposed key questions for future research are also emphasized. POU3F2 plays a pivotal role in brain development, the pathogenesis of neurological and psychiatric disorders, and the reprogramming of neural cells. A more comprehensive and systematic understanding of its molecular mechanism might provide novel therapeutic approaches for neuropsychiatric disorders.

Neurocognitive functions play a fundamental role in children's learning and academic success. Among these functions, memorization-based on associative cognitive processes-is essential for knowledge acquisition. In Morocco, educational disparities between rural and urban environments and differences between public and private schools may influence cognitive development and learning outcomes among schoolchildren. This study aimed to analyze the memorization process among Moroccan school-aged children and to identify demographic and contextual factors associated with learning performance. A cross-sectional study was conducted among 441 children aged 8-15 years recruited from six public and private schools in the Marrakech-Safi region of Morocco between November 2022 and March 2023. Memorization and learning abilities were assessed using the adapted Moroccan version of the Rey-Taylor auditory-verbal learning test (AVLT). Key indicators included the total number of recalled words across 10 trials, the learning index, and retroactive interference. Associations between cognitive performance and contextual variables (age, gender, school type, and residence) were analyzed using Spearman correlation tests. The results show that the learning index is relatively higher among girls (M=4.8, standard deviation [SD]=2.70), children over 12 years old (M=5.0, SD=2.39), children from rural areas (M=5.0, SD=2.62), and those enrolled in the public sector (M=5.0, SD=2.59), compared with other categories. These variables were the least affected by retroactive interference except for the rural environment, which experienced an RI=68.8, SD=0.21. However, the data indicate a performance among private-sector and younger students in at least one learning assessment stage. The Spearman test showed a positive correlation between the learning index and the age variable (r=0.095; p=0.046), and between retroactive interference and the living environment (r=0.105; p=0.028) and the type of school (r=0.126; p=0.0008). Overall, improving memory and academic performance requires targeted pedagogy, extracurricular activities, equal school opportunities, and research on factors, such as motivation, social dynamics, and teaching methods. Similarly, longitudinal studies will help deepen the understanding of memory and guide educational policies.

Cytokines and immune imbalance in generalized anxiety disorder (GAD) have attracted greater interest of all researchers. Studies indicate the involvement of pro-inflammatory cytokines in the pathogenesis of GAD. Therefore, the present study investigated the serum concentrations of interleukin (IL)-12 and carbon-reactive protein (CRP) in GAD patients to explore their role in the pathophysiology of diseases. This study included 52 GAD patients and 30 healthy controls (HCs) matched by age and sex. A psychiatrist diagnosed GAD patients and evaluated HCs according to the DSM-5 criteria. The severity of GAD cases was assessed using a standardized and validated clinical rating scale (GAD-7). ELISA kits were utilized to measure the serum concentrations of IL-12 and CRP in blood. GAD patients revealed significantly elevated concentrations of IL-12 (7.60 ± 1.53 pg/mL) than HCs (3.73±0.42pg/mL). These increased levels were positively correlated with GAD-7 scores (r=0.377, p=0.006). This IL-12 also demonstrated strong predictive ability in the receiver operating characteristic (ROC) investigation, with an area under the curve (AUC) of 0.828 (p<0.001), indicating 81.6% sensitivity and 77.8% specificity at a threshold of 3.56pg/mL. In contrast, the level of CRP was not changed between the groups (2.59±0.13 vs. 2.55±0.16mg/L); furthermore, no association was detected between CRP levels and GAD-7 scores (r=0.021, p=0.881). Our investigation indicates that IL-12 in blood levels, but not CRP, may be associated with the pathophysiology and development of GAD. The altered serum IL-12 levels in GAD patients might be the result of disease pathogenesis. However, we recommend more advanced investigation with greater sample sizes to verify the probable diagnostic utility of IL-12.

The capacity for enhanced experience, modeled as environmental enrichment (EE) in laboratory animals, to drive positive changes in brain circuitry presents a promising avenue in the development of therapies for neurodevelopmental conditions. Less understood are the underlying mechanisms, or potential interactions of EE with other therapeutic approaches. We have previously shown that early exposure to EE can drive the partial repair of miswired uncrossed retinal projections, and the concomitant rescue of a visual behavior, in the Ten-m3 knockout (KO) mouse. This was associated with a highly spatiotemporally localized upregulation of microglial reactivity in the region where the correction was occurring which peaked around postnatal day (P)25. Aiming to confirm a causal role for microglial-mediated engulfment in this process, we assessed the effect of daily injections of minocycline or vehicle saline from P18 to P24 (inclusive) on measures of microglial reactivity and anatomical corrective pruning in P25 Ten-m3 KO mice. While an effect of EE was confirmed at this timepoint, intriguingly, we found that both the vehicle- and minocycline-treated mice had a similar lack of microglial reactivity and showed a marked absence of corrective pruning of their miswired retinal projections. This suggests that the injection procedure itself disrupted the experience-induced microglial-mediated circuit repair. These results underscore the highly sensitive nature of EE-driven corrective pruning actions of microglia and the critical importance of considering and controlling for all aspects of experience.

ABSTRACTThe retinotectal projection in Xenopus laevis is topographically organized. During the early development of the Xenopus visual system, the optic tectum increases considerably in volume, and retinotectal axons and dendrites undergo extensive activity‐dependent remodeling. We have previously observed marked changes in the three‐dimensional layout of the tectal retinotopic functional map over the course of a few days. This raised the question of whether such functional reorganization might be attributable to the migration and structural remodeling of tectal neurons as the brain grows. To examine changes in map topography in the context of individual tectal neuron morphology and location, we performed calcium imaging in the optic tecta of GCaMP6s‐expressing tadpoles in parallel with structural imaging of tectal cells that were sparsely labeled with Alexa 594‐dextran dye. We performed functional and structural imaging of the optic tectum at two developmental time points, recording the morphology of the dextran‐labeled cells and quantifying the changes in their positions and the spanning volume of their dendritic fields. Comparing anatomical growth to changes in the functional retinotopic map at these early stages, we found that dendritic arbor growth kept pace with the overall growth of the optic tectum and that individual neurons continued to receive widespread visual field input, even as the tectal retinotopic map evolved markedly over time. This suggests a period of initial growth during which inputs to individual tectal neurons maintain diffuse connectivity and broad topographic integration.

Establishing a proper balance between neuronal excitation (E) and inhibition (I) is essential for healthy brain development, with alterations in this dynamic linked to neurodevelopmental disorders. Animal models suggest that hippocampal activity rapidly increases in the early postnatal period, believed to support the development and stabilization of E/I neural circuitry. This process has not yet been examined in humans, however. Utilizing longitudinal data from the Developing Human Connectome Project, the present study evaluated the impact of early hippocampal activity and gestational age at birth on later outcomes in a cohort of preterm infants (N=58). Hippocampal activity was assessed using the amplitude of low-frequency fluctuations (ALFF) derived from resting-state functional magnetic resonance imaging collected at two timepoints in the early postnatal period (prior to 20 weeks following birth). Increases in hippocampal activity during this early postnatal period predicted better cognitive and motor function at 18 months of age. Greater gestational age was associated with greater hippocampal activity increase between timepoints. Interestingly, no significant relationships were found between baseline hippocampal activity and 18-month outcomes, suggesting that dynamic changes rather than static measures may be especially sensitive to preterm birth and subsequent alterations in neurodevelopmental processes. These findings underscore the importance of changes in early hippocampal function and gestational age as key risk factors for future neurodevelopmental concerns.

Honeybee (Apis mellifera) workers exhibit remarkable behavioral plasticity throughout adult life. In spring and summer, they transition through diverse tasks over a short lifespan of 4-6 weeks. This involves dramatic changes in sensory environment and cognitive demands associated with pronounced structural neuronal plasticity in the mushroom bodies (MBs), high-order brain centers for sensory integration, learning, and memory. This plasticity manifests as age- and experience-related volume increase in sensory input regions of the MB calyces, accompanied by pruning of projection neuron (PN) boutons in synaptic microcircuits within visual and olfactory compartments. As winter approaches, honeybees suspend brood rearing and foraging activities to survive the cold months by forming a tight, thermoregulated cluster. Unique physiological adaptations enable winter bees to live up to 8 months until a new generation emerges in spring. This extended lifespan occurs during a period of reduced sensory input and high metabolic costs raising the question of how such conditions affect structural neuronal plasticity. Using synapsin immunolabeling and 3D confocal-microscopy image analyses of MB synaptic neuropils in whole-mount brains of age-controlled worker bees, we found that winter bees retain a high degree of neuronal plasticity throughout their lifespan. MB calyces exhibit an initial volume increase followed by a period of stagnation to then undergo another expansion at the onset of spring foraging. While olfactory PN boutons exhibit continuous pruning, visual bouton numbers remain stable during winter. We conclude that winter bees retain comparable neuronal capacities to summer bees, despite strong differences in lifespan, physiological, and environmental conditions.

In this study, we present an efficient epileptic seizure detection framework driven by a graph convolutional neural network (GCNN). Unlike conventional methods that primarily rely on local features or complex feature engineering, our GCNN-based approach explicitly encodes the spatial dependencies among electroencephalogram (EEG) electrodes, thereby capturing more comprehensive spatiotemporal features. A minimal preprocessing pipeline, consisting only of bandpass filtering and segmenting, reduces system complexity and computational overhead. On the CHB-MIT scalp EEG database, our method achieved an average accuracy of 98.64%, sensitivity of 99.49%, and specificity of 98.64% at the segment-based level and sensitivity of 96.81% with FDR of 0.27/h at the event-based level. On the SH-SDU database we collected, the method yielded segment-based accuracy of 95.23%, sensitivity of 92.42%, and specificity of 95.25%, along with event-based sensitivity of 94.11%. The average testing time for 1 h of multi-channel EEG signals is 3.89 s. These excellent results and low-computation design make the framework especially suited for clinical applications, advancing EEG-based epilepsy diagnostics and improving patient outcomes.