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Brain Sciences
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Rethinking Neurodevelopmental Disorders: Beyond One-Size-Fits-All
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Rethinking Neurodevelopmental Disorders: Beyond One-Size-Fits-All

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Developmental Neuroscience".

Deadline for manuscript submissions: 15 January 2027 | Viewed by 7611

Special Issue Editor

Dr. Salman Zubedat

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Guest Editor
Spatial Perception and Memory Lab, Department of Neuroscience, The Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 32000, Israel
Interests: neuroscience; behavior and behavior mechanism; neurobiology and brain physiology; neurodevelopmental disorders

Special Issue Information

Dear Colleagues,

Neurodevelopmental disorders are a diverse group of conditions that arise from atypical brain development and functioning, often manifesting early in life. Accumulating research in neuroimaging, genomics, and neurobiology has improved our understanding, yet many underlying mechanisms and etiology remain poorly understood. Research indicates that disruptions in neural connectivity, synaptic plasticity, and neurotransmitter systems play critical roles in the pathophysiology of these disorders. However, no single pathway accounts for all cases; rather, multiple interacting biological pathways contribute to the diverse clinical presentations observed. In this Special Issue, we invite researchers to submit relevant papers that think “outside the box” and we particularly welcome in vivo, in vitro, and mathematical models, as well as theoretical studies on new concepts and novel models that can be applied to the exploration of the homo-heterogeneity in neurodevelopmental disorders.

Dr. Salman Zubedat
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • ADHD
  • autism
  • intellectual disability
  • communication disorders

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Published Papers (3 papers)

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Research

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13 pages, 922 KB  
Article
Auditory Stimulation Rescues Cognitive Deficit in Fmr1-KO Mice
by Mohamed Ouardouz, Amanda E. Hernan, J. Matthew Mahoney and Rodney C. Scott
Brain Sci. 2026, 16(4), 380; https://doi.org/10.3390/brainsci16040380 - 30 Mar 2026
Viewed by 462
Abstract
Background/Objectives: Fragile X Syndrome (FXS) is a neurodevelopmental disorder caused by a triplet repeat expansion in the Fmr1 gene leading to the loss of Fragile X Messenger Ribonucleoprotein (Fmr1 protein). The loss of Fmr1 protein modulates many cell biological processes and leads [...] Read more.
Background/Objectives: Fragile X Syndrome (FXS) is a neurodevelopmental disorder caused by a triplet repeat expansion in the Fmr1 gene leading to the loss of Fragile X Messenger Ribonucleoprotein (Fmr1 protein). The loss of Fmr1 protein modulates many cell biological processes and leads to the emergence of intellectual disability and autism. FXS is modeled in Fmr1-KO mice that display features consistent with human FXS, including hypersensitivity, cognitive and learning deficits, hyperactivity and audiogenic seizures. Here, we investigated the effect of auditory stimulation during a range of developmental stages on recognition memory and sociability deficits in Fmr1-KO mice. Methods: Fmr1-KO mice were subjected to auditory stimulation for 2 min three times a day at one-hour intervals for 5 days at the nursing, juvenile and adult stages. The animals were tested for social interaction and novel object recognition at 2 to 3 months old. Results: During auditory stimulation, the wild running phenotype was observed in the Fmr1-KO juvenile animals and two animals at the nursing stage experienced status epilepticus and died. Fmr1-KO animals showed social deficits compared to both the control and animals exposed to auditory stimulation at the juvenile stage. In the novel object recognition task, auditory stimulation was more effective at the nursing and juvenile stages. Conclusions: These data show that auditory stimulation may be an effective way to restore cognitive and social deficits in FXS. Full article
(This article belongs to the Special Issue Rethinking Neurodevelopmental Disorders: Beyond One-Size-Fits-All)
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Review

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18 pages, 401 KB  
Review
Neuropsychiatric Phenotype and Treatment Challenges in 47,XYY Syndrome: A Narrative Review with a Case Series of Adolescents
by Maria Giulia D’Acunto, Chiara Bosetti, Deianira Rinaldi, Marika Ricci, Stefano Berloffa, Gabriele Masi and Maria Mucci
Brain Sci. 2026, 16(2), 232; https://doi.org/10.3390/brainsci16020232 - 15 Feb 2026
Viewed by 1452
Abstract
Background: 47,XYY syndrome is a relatively common sex chromosome aneuploidy that remains largely underdiagnosed. While its somatic phenotype is often mild, growing evidence indicates a substantial burden of neurodevelopmental and psychiatric morbidity. However, the characterization of the neuropsychiatric phenotype across development, particularly during [...] Read more.
Background: 47,XYY syndrome is a relatively common sex chromosome aneuploidy that remains largely underdiagnosed. While its somatic phenotype is often mild, growing evidence indicates a substantial burden of neurodevelopmental and psychiatric morbidity. However, the characterization of the neuropsychiatric phenotype across development, particularly during adolescence, and the associated treatment challenges remain incomplete. Objectives: To provide a comprehensive narrative review of the neuropsychiatric phenotype of 47,XYY syndrome and to illustrate clinical complexity and treatment response through a case series of adolescents. Methods: A narrative review of the literature was conducted focusing on genetics, neurodevelopmental and psychiatric features, neuroimaging and neurophysiology findings, clinical course, and management strategies in 47,XYY syndrome. This review is complemented by a case series of adolescents with confirmed 47,XYY karyotype, evaluated for developmental history, psychiatric comorbidity and response to pharmacological and non-pharmacological interventions. Results: The literature consistently describes increased risks of language impairment, executive dysfunction, ADHD, autism spectrum traits, and emotional and behavioral dysregulation in males with 47,XYY syndrome. Psychiatric vulnerability appears to increase during adolescence and adulthood, with elevated rates of mood, psychotic, and substance use disorders. The presented cases illustrate a convergent clinical trajectory marked by early developmental delays, progressive behavioral dysregulation in adolescence and limited or inconsistent response to multiple classes of psychotropic medications, suggesting a pattern of pharmacoresistance in a subset of patients. Conclusions: 47,XYY syndrome is associated with a distinct and heterogeneous neuropsychiatric phenotype that extends beyond early neurodevelopmental disorders. Early diagnosis alone may be insufficient to prevent severe psychiatric outcomes, highlighting the need for long-term monitoring and integrated, multidisciplinary management. Further research is required to identify early predictors of high-risk trajectories and to optimize treatment strategies for this population. Full article
(This article belongs to the Special Issue Rethinking Neurodevelopmental Disorders: Beyond One-Size-Fits-All)
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32 pages, 1782 KB  
Review
Neurobiological and Behavioral Heterogeneity in Adolescents with Autism Spectrum Disorder
by Gerry Leisman, Rahela Alfasi and Robert Melillo
Brain Sci. 2025, 15(10), 1057; https://doi.org/10.3390/brainsci15101057 - 28 Sep 2025
Cited by 3 | Viewed by 5229
Abstract
Background: Adolescents with autism spectrum disorder (ASD) display distinct neurodevelopmental trajectories marked by atypical neural activation and white matter maturation compared to neurotypical peers. Introduction: While improvements in face recognition and cognitive skills occur during childhood and adolescence, individuals with ASD often experience [...] Read more.
Background: Adolescents with autism spectrum disorder (ASD) display distinct neurodevelopmental trajectories marked by atypical neural activation and white matter maturation compared to neurotypical peers. Introduction: While improvements in face recognition and cognitive skills occur during childhood and adolescence, individuals with ASD often experience a plateau in these areas as they transition to adulthood, impacting daily living, executive function, social cognition, and emotional awareness. Results: Neuroimaging studies reveal altered white matter growth and connectivity in brain regions associated with social processing, which may underlie these functional challenges. Intellectual disability further compounds developmental difficulties by limiting foundational abilities and slowing progress. Discussion: The multifaceted and persistent service needs spanning legal, educational, vocational, health, and psychosocial domains highlight the necessity for coordinated, individualized, and family-centered approaches, particularly during the transition to adulthood. Advances in research integrating genetic, neurobiological, and behavioral data hold potential for refining diagnostic subgroups and personalizing interventions. Conclusion: Continued advocacy and innovation in service delivery are essential to address gaps in adult support systems and enhance long-term outcomes for individuals with ASD. Full article
(This article belongs to the Special Issue Rethinking Neurodevelopmental Disorders: Beyond One-Size-Fits-All)
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