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Anti-epileptics and diuretics, used for unapproved purposes, have been reported to ameliorate social deficits in individuals with autism spectrum disorder. However, the underlying neural mechanisms remain unclear. Here, we explored the effects of bumetanide, clonazepam, and phenytoin, all with clinically reported properties for improving social deficits, in a prenatal valproic acid exposure male mouse model. By combining comprehensive behavioral analysis with brain-wide mapping of Arc, an immediate early gene, we found a correlation between social behaviors and Arc-positive cell counts across brain areas. Network analysis identified the medial prefrontal and sensory-related cortices as critical nodes with high centrality, playing critical roles in connecting other brain regions. These metrics are associated with both the decreased social behaviors and their recovery following drug treatment. Our findings suggest that restoring the centralities of the medial prefrontal and sensory-related cortices serve as a potential biomarker for evaluating drug efficacy in autism spectrum disorder.
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http://dx.doi.org/10.1038/s41598-025-05996-w | DOI Listing |
Sci Bull (Beijing)
August 2025
Beijing Key Laboratory of Brainnetome and Brain-Computer Interface, Institute of Automation, Chinese Academy of Sciences, Beijing 100190, China; Brainnetome Center, Institute of Automation, Chinese Academy of Sciences, Beijing 100190, China; Xiaoxiang Institute for Brain Health and Yongzhou Central
J Affect Disord
September 2025
Department of Psychiatry, Taipei Veterans General Hospital, Taipei, Taiwan; Division of Psychiatry, School of Medicine, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan; Institute of Brain Science, National Yang Ming Chiao Tung University, Taipei, Taiwan. Electronic addr
Background: In adolescents, the role of functional dysconnectivity in the default mode network (DMN), salience network (SAN), frontoparietal network (FPN), and reward network as markers of borderline personality disorder (BPD) remains uncertain.
Methods: A total of 45 adolescents with BPD comorbid with a mood disorder (bipolar disorder or major depressive disorder), 31 adolescents without BPD but with a mood disorder, and 47 healthy adolescents were enrolled in the study. All participants underwent resting-state functional connectivity magnetic resonance imaging.
Eur Arch Psychiatry Clin Neurosci
September 2025
Department of Psychiatry, University of Pittsburgh, 121 Meyran Avenue, Pittsburgh, PA, 15213, USA.
Psychotic-like experiences (PLEs) -subclinical experiences or symptoms that resemble psychosis, such as hallucinations and delusional thoughts-often emerge during adolescence and are predictive of serious psychopathology. Understanding PLEs during adolescence is crucial due to co-occurring developmental changes in neural reward systems that heighten the risk for psychotic-related and affective psychopathology, especially in those with a family history of severe mental illness (SMI). We examined associations among PLEs, clinical symptoms, and neural reward function during this critical developmental period.
View Article and Find Full Text PDFInt J Eat Disord
September 2025
Department of Physiology, Monash University, Clayton, Victoria, Australia.
Objective: Converging evidence from neuroimaging studies and genome-wide association study (GWAS) suggests the involvement of prefrontal cortex (PFC) and striatum dysfunction in the pathophysiology of anorexia nervosa (AN). However, identifying the causal role of circuit-specific genes in the development of the AN-like phenotype remains challenging and requires the combination of novel molecular tools and preclinical models.
Methods: We used the activity-based anorexia (ABA) rat model in combination with a novel viral-based translating ribosome affinity purification (TRAP) technique to identify transcriptional differences within a specific neural pathway that we have previously demonstrated to mediate pathological weight loss in ABA rats (i.
J Neurosurg
September 2025
4Carle Illinois College of Medicine, University of Illinois Urbana-Champaign, Champaign, Illinois.
Objective: Major depressive disorder is a significant cause of disability, impacting an estimated 193 million individuals worldwide. Forty percent are estimated to have little to no response to standard pharmacological therapies. Deep brain stimulation (DBS) has emerged as a favorable neuromodulation therapy for treatment-resistant depression, but it remains unclear which brain targets are optimal.
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