Int. J. Dev. Neurosci. [JOURNAL]
Sun
200 papers
Relationship Between MOXO-D-CPT Results and Volumetric Brain MR in Attention Deficit Hyperactivity Disorder.
Tarlacı S, Çolak A
Int J Dev Neurosci · 2026 Feb · PMID 41528207 · Publisher ↗
OBJECTIVE: This study aimed to examine the multidimensional relationships between MOXO-d-CPT performance and severity profiles-attention, timing, impulsivity and hyperactivity-and regional brain volumetric and cortical t...
OBJECTIVE: This study aimed to examine the multidimensional relationships between MOXO-d-CPT performance and severity profiles-attention, timing, impulsivity and hyperactivity-and regional brain volumetric and cortical thickness measures in individuals with ADHD. METHODS: Thirty-eight adults with ADHD underwent MOXO-d-CPT assessment and high-resolution structural brain MRI. MOXO-d-CPT performance and severity levels were analysed in relation to 155 regional brain volumes and 110 cortical thickness measures using group-wise statistical comparisons. RESULTS: Attention performance and severity were associated with volumetric and cortical thickness differences primarily in frontal, temporal and cerebellar regions. Timing performance was related to cerebellar and frontal volumetric measures, whereas timing severity showed limited volumetric differences without cortical involvement. Impulsivity performance demonstrated no volumetric differences but was associated with cortical thickness variations in frontal and temporal regions. Hyperactivity performance was linked to both volumetric and cortical alterations, whereas hyperactivity severity was associated exclusively with cortical thickness differences, predominantly in occipital regions (p < 0.05). CONCLUSION: These findings highlight distinct structural brain correlates underlying MOXO-d-CPT performance and symptom severity dimensions in ADHD, supporting a multidimensional neurobiological framework that extends beyond categorical diagnostic approaches.
Treadmill Exercise Modulates TNF-α and IL-1β Expression in Rodent Models of CNS Inflammation: A Systematic Review.
Kim D, Moon HY, Lee M
Int J Dev Neurosci · 2026 Feb · PMID 41510828 · Publisher ↗
Neuroinflammation contributes to the progression of central nervous system (CNS) disorders, with tumour necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) recognized as key pro-inflammatory mediators. This syst...
Neuroinflammation contributes to the progression of central nervous system (CNS) disorders, with tumour necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) recognized as key pro-inflammatory mediators. This systematic review synthesized findings from 17 preclinical studies (26 observations) examining the effects of treadmill exercise on TNF-α and IL-1β expression in the brain tissue of male rodents (rats and mice). Cytokine responses were standardized as log₂ fold change to enable cross-study comparison. Exercise intensity showed a significant association with cytokine reduction (Kruskal-Wallis p = 0.0165; ε = 0.270), with greater reductions under vigorous versus light protocols (Dunn's p_adj = 0.0137). There were no significant differences by duration (p = 0.847), marker (TNF-α vs. IL-1β; p = 0.227) or species (rats vs. mice; p = 0.501). In neurodegenerative models, a significant marker-by-intensity interaction emerged (two-way ANOVA, p = 0.0039); moderate showed the largest overall reduction (Kruskal-Wallis p = 0.016; Dunn's p_adj = 0.0158 vs. light), whereas vigorous showed no additional benefit (p_adj ≥ 0.1056). These findings suggest that treadmill exercise may modulate neuroinflammatory signalling in the rodent brain, with exercise intensity emerging as a key moderator candidate supported by consistent evidence; however, the optimal dose appears context-dependent (pooled: vigorous > light; neurodegenerative models: moderate maximal). Interpretation should be cautious because the body of evidence derives from male-only samples, heterogeneous methods and several SYRCLE domains with frequently unclear ratings (randomization, allocation concealment, blinding, housing).
A Longitudinal Study on Symptom Severity in Early Childhood of Bilingual and Monolingual Children With Autism Spectrum Disorder.
Kara T, Kuru T, Kocaman O … +3 more , Avşar PA, Çelebi F, Özşan OY
Int J Dev Neurosci · 2026 Feb · PMID 41472332 · Publisher ↗
BACKGROUND: In increasingly globalized and multilingual societies, a key question for individuals with autism spectrum disorder (ASD) is how bilingual exposure influences their linguistic, cognitive, and social developme...
BACKGROUND: In increasingly globalized and multilingual societies, a key question for individuals with autism spectrum disorder (ASD) is how bilingual exposure influences their linguistic, cognitive, and social development. This study aimed to investigate the potential impact of a bilingual home environment on the severity and progression of ASD symptoms in children. METHODS: The study was conducted with 3-year follow-up results of a total of 69 children, 34 with bilingual home situations (BHSs) and 35 with monolingual home situations (MHSs). The Childhood Autism Rating Scale (CARS) was applied to assess the severity of the participants' ASD symptoms. Neurodevelopmental evaluations were performed using the Denver Developmental Screening Test II (DDST-II). RESULTS: No significant differences were determined between the MHS and BHS groups in terms of developmental quotient total (DQt) baseline (p = 0.618), DQt follow-up (p = 0.288), or CARS baseline (p = 0.970) scores. However, CARS follow-up scores, indicative of greater symptom severity, were significantly higher in the BHS group (p = 0.030). While the MHS group showed a notable decrease in CARS scores, the BHS group's scores tended to persist, with the decrease in CARS scores being significantly lower than that observed in the MHS group (p < 0.001). CONCLUSIONS: These findings suggest that children with ASD raised in bilingual home environments may exhibit comparatively less improvement in symptom severity over time. The influence of bilingualism on ASD may involve a range of complex linguistic, cognitive, and social factors. Future research should explore these variables in larger, more detailed studies.
A Multidimensional Examination of Temperament, Problematic Media Use, Emotion Regulation, Behavioural Problems and Developmental Outcomes in Preschool Children.
Çelebi SB, Binokay H, Gürbüz AA … +2 more , Dağ C, Teke H
Int J Dev Neurosci · 2026 Feb · PMID 41469023 · Publisher ↗
INTRODUCTION: This study examined relationships between temperament, problematic media use (PMU), emotion regulation, behavioural problems and developmental outcomes in preschool children, focusing on temperament's media...
INTRODUCTION: This study examined relationships between temperament, problematic media use (PMU), emotion regulation, behavioural problems and developmental outcomes in preschool children, focusing on temperament's mediating role between PMU and emotion regulation. METHODS: A cross-sectional study was conducted with 205 children (mean age: 54.28 months; 55.6% male) from a child psychiatry outpatient clinic. Parents completed standardized measures including the Short Temperament Scale for Children, Problematic Media Use Measure (PMUM), Emotion Regulation Checklist (ERC) and Strengths and Difficulties Questionnaire (SDQ). Children's development was objectively assessed using the Denver Developmental Screening Test-II (DDST-II). Data analysis involved correlation, group comparisons and mediation analysis using the PROCESS macro. RESULTS: Problematic media use was significantly higher in children with developmental delays (p < 0.001) and strongly correlated with delays in all DDST-II domains (p < 0.001). A significant negative correlation was found between PMU and emotion regulation. Crucially, mediation analysis revealed that temperament fully mediated the relationship between PMU and emotion regulation (indirect effect: 0.018, 95% CI [0.0052, 0.030], p = 0.006), accounting for 62.7% of the total effect. Children with higher reactivity temperament traits showed stronger associations between PMU and emotional lability. CONCLUSIONS: The findings indicate that problematic media use is significantly associated with developmental delays in preschoolers. This underscores the necessity of moving beyond uniform screen time guidelines towards individualized, temperament-informed interventions to support healthy emotional development in the digital age.
Morphological Correlates of Music-Induced Plasticity in the Central Auditory System.
Meng N, Yajun Z, Xun L
Int J Dev Neurosci · 2026 Feb · PMID 41469022 · Publisher ↗
Music exposure may promote neuroplasticity that affects emotional processing pathways, auditory discrimination, and cognitive development. To determine the potential underlying mechanisms, histological and molecular meth...
Music exposure may promote neuroplasticity that affects emotional processing pathways, auditory discrimination, and cognitive development. To determine the potential underlying mechanisms, histological and molecular methodologies were employed to assess neuroanatomical adaptations in feline auditory pathways. Using Nissl staining, immunohistochemistry and western blotting, we measured and compared total neuronal density, GABAergic interneuron density, the ratio of GABAergic to total neurons and levels of GABA receptor and NMDAR1 proteins between controlled music stimulation and ambient noise. We found that the overall neuronal distribution was comparable between the two groups. However, the music-exposed group displayed a 1.38-fold increase in GABAergic interneuron density compared to controls. Stratified cortical analysis revealed layer-specific elevations in GABAergic proportions, with an increase of 1.29-fold and 1.22-fold in Layers IV and V, respectively. We further demonstrated a concurrent upregulation of inhibitory and excitatory signaling components, showing a 2.1-fold increase in GABA receptor expression and a 1.8-fold increase in NMDAR1 expression. These structural changes suggest a dual mechanism involving amplified GABA-mediated inhibition and potentiated glutamate-driven excitation in the primary auditory cortex. The rebalanced excitation-inhibition ratio may refine thalamocortical signal processing that enhances spectral-temporal resolution for complex acoustic stimuli. Our findings establish cytoarchitectural correlates for music-induced neuroadaptation, offering insights into the structural underpinnings of auditory-emotional integration in feline models.
CASPR2-Deficiency Neurodevelopmental Disorder Associated With Biallelic CNTNAP2 Gene Variants: Phenotypic and Genetic Analysis From Prenatal to Paediatric Period.
Wang S, He Y, Zhao Z … +1 more , Yang B
Int J Dev Neurosci · 2025 Dec · PMID 41416563 · Publisher ↗
Variants of the CNTNAP2 gene are closely associated with various neurological disorders, including neurodevelopmental disorders, schizophrenia and behavioural abnormalities. Biallelic CNTNAP2 gene variants may lead to mo...
Variants of the CNTNAP2 gene are closely associated with various neurological disorders, including neurodevelopmental disorders, schizophrenia and behavioural abnormalities. Biallelic CNTNAP2 gene variants may lead to more complex or severe neurodevelopmental phenotypes; however, due to a lack of sufficient reports, especially regarding prenatal manifestations, the relationship between CASPR2-deficiency neurodevelopmental disorder and genotype remains unclear. Herein, we report the case of a child with neurodevelopmental disorder who presented with a dysplastic corpus callosum on prenatal ultrasound. The proband experienced seizures, delayed growth and development and autism after birth. This prompted whole-exome sequencing of the family, which revealed that the proband had compound heterozygous variants in the CNTNAP2 gene. Variant 1 was NM_014141.6:c.551-2A > T, inherited from his father, and Variant 2 was loss1 (EXON:2-3), inherited from his mother. We constructed a plasmid for Variant 1 and performed a minigene experiment, which revealed that the variant was a frameshift variant that resulted in a truncated protein, p.Trp184TyrfsTer7. Our findings suggest that biallelic CNTNAP2 gene variants may affect brain development during the foetal period, and physicians should be vigilant for CNTNAP2 gene variants in cases of agenesis of the corpus callosum or cortical dysplasia.
Differential Functional Connectivity Between Silent Reading and Resting-State fMRI and Their Relationships With Reading Performance in Children With and Without Dyslexia.
Gengeç Benli Ş, Demirci E, İçer S … +3 more , Ak Z, Sağır GR, Karaman ZF
Int J Dev Neurosci · 2025 Dec · PMID 41413843 · Publisher ↗
The clinical diagnostic parameters of dyslexia and the alterations it creates on brain connectivity continue to be the focus of current studies. In this study, where clinical neuropsychiatric tests and neuroimaging resul...
The clinical diagnostic parameters of dyslexia and the alterations it creates on brain connectivity continue to be the focus of current studies. In this study, where clinical neuropsychiatric tests and neuroimaging results are examined together, it is aimed to examine the functional connectivity differences that occur in the brain regions related to the reading pathway in children with dyslexia in a resting state and task-based manner and to compare them with healthy controls. Correlation analyses were performed to evaluate the correlation between the resting state and the reading task of the groups with age, word reading count and WISC-4 score and mean brain activity. The findings indicate that dyslexia is linked to deficits in the phonological component and that the correlation between intelligence and reading speed is lower in the dyslexia group than in healthy controls. It has also been observed that children with dyslexia have difficulties in the development of phonological input, semantics and phonological output, independent of intelligence and that neuronal connections are affected in a similar way. These findings contribute to the functional differences detected in dyslexia by neuroimaging, and may help to understand the complex nature of dyslexia and to make educational and therapeutic methods more effective.
Adolescent Chronic Sleep Disruption Increases Blood-Brain Barrier Permeability, but in a Time-, Region- and Sex-Dependent Manner in CD-1 Mice.
Hinterberger A, Esposito P, Cappelletti L … +2 more , Wang L, Ismail N
Int J Dev Neurosci · 2025 Dec · PMID 41413780 · Full text
During puberty and adolescence, there is a natural change in the circadian rhythm, which could result in inadequate sleep and increase the likelihood of physical and mental health issues. Previously, we have developed a...
During puberty and adolescence, there is a natural change in the circadian rhythm, which could result in inadequate sleep and increase the likelihood of physical and mental health issues. Previously, we have developed a mouse model showing that adolescent chronic sleep disruption (CSD) induces depression-like behaviour in male and female CD-1 mice. However, the mechanisms underlying this effect are unknown. The current study investigates blood-brain barrier (BBB) permeability as a possible mechanism through which CSD may impact the brains of male and female CD-1 mice. At 6 weeks old, mice underwent either CSD for seven consecutive days or were left undisturbed. Mice were euthanized at either 24 h, 72 h, or 7 days following the last sleep disruption. BBB permeability was assessed in the whole brain and in specific brain regions (prefrontal cortex, hippocampus and hypothalamus). Results showed that at 72 h post-CSD, sleep-disrupted females had greater BBB permeability in the prefrontal cortex and hippocampus than non-sleep-disrupted females and sleep-disrupted males. At 7 days post-CSD, sleep-disrupted male and female mice displayed higher BBB permeability in the hypothalamus than non-sleep-disrupted mice. These findings demonstrate that CSD increases BBB permeability in a sex-, time- and brain region-dependent manner and females may be particularly vulnerable to the effects of CSD during adolescence. Understanding the factors disrupting BBB integrity will broaden our understanding of the impact of adolescent stress on brain function and behaviour.
Neuroprotective Effect of Palmatine Against Anti-Epileptic Drug Induced Autism in Wistar Rat Pups.
Singh K, Dhingra D
Int J Dev Neurosci · 2025 Dec · PMID 41408954 · Publisher ↗
BACKGROUND: Autism spectrum disorder is a developmental disorder that affects the central nervous system. It is characterized by impaired social interaction and communication, along with patterns of repetitive behaviours...
BACKGROUND: Autism spectrum disorder is a developmental disorder that affects the central nervous system. It is characterized by impaired social interaction and communication, along with patterns of repetitive behaviours. The present study was conducted to evaluate the effect of palmatine in autistic male rat pups. METHODS: In this study, sodium valproate (400 mg/kg) was injected by subcutaneous route on the 13th gestational day to Wistar female rats to induce autism-like symptoms in their pups. Palmatine (0.25, 0.5 and 1 mg/kg) was orally administered for 35 consecutive days (from postnatal day 24 to 58) to autistic male pups. The pups were subjected to various behavioural tests like the tail immersion test, actophotometer, tail suspension test, elevated zero maze, social interaction test and Morris water maze. One hour after the administration of drugs on postnatal day 58, animals were sacrificed by cervical dislocation followed by the collection of brain and blood samples which were used for estimations of biochemical parameters. Histopathological studies on the cerebellum part of the brain of pups were also carried out. RESULTS: The results demonstrated a significant decrease in body weight; a significant increase in eye opening time; and significant impairment of motor coordination (as indicated by a significant increase in negative geotaxis score) in male pups, indicating the induction of autism in them. There was a significant increase in pain threshold, hyperlocomotion, depressive and anxious behaviours, impairment of learning and memory and impairment of social interaction in autistic pups. There was a significant increase in oxidative stress (indicated by elevated malondialdehyde and nitrite levels along with a decrease in catalase activity and GSH level), acetylcholinesterase and MAO-A activities in the brain of autistic pups. There was also an increase in plasma corticosterone levels in autistic pups. Palmatine significantly reversed behavioural, biochemical and histopathological alterations in autistic male rat pups. CONCLUSION: It was concluded that palmatine produced neuroprotective activity in autistic male rat pups possibly through amelioration of brain oxidative stress, inhibition of acetylcholinesterase and MAO-A activities and decrease of plasma corticosterone concentration.
Novel KDM3B Variants in Two Chinese Patients With Global Developmental Delay and Autism.
Cao F, Xiong L, Wu H … +2 more , Chen Y, Zha J
Int J Dev Neurosci · 2025 Dec · PMID 41408900 · Publisher ↗
BACKGROUND: Haploinsufficiency of KDM3B has also been linked to developmental delay, intellectual disability, autism spectrum disorder (ASD) and immunodeficiency known as developmental delay, intellectual disability, joi...
BACKGROUND: Haploinsufficiency of KDM3B has also been linked to developmental delay, intellectual disability, autism spectrum disorder (ASD) and immunodeficiency known as developmental delay, intellectual disability, joint contractures and facial dysmorphism; immunodeficiency; and short stature (DIJOS) syndrome. However, the phenotypic spectrum is not fully defined, and genotype-phenotype associations need to be further studied. METHODS: Here we report on two unrelated patients with global developmental delay and autistic features and provide detailed clinical information of both patients, including cranial magnetic resonance imaging (MRI), electroencephalography (EEG), metabolic screening, hearing assessment and neurodevelopmental testing. Whole exome sequencing (WES) was performed for potential genetic causes, and candidate variants were verified via Sanger sequencing. Interpretation of variants was performed in accordance with ACMG guidelines. RESULTS: For Patient 1, we detected a de novo pathogenic heterozygous nonsense variant in KDM3B (c.1970C > G, p.Ser657*). The canonical splice-site variant (c.3973-1G > C) in KDM3B that we found in Patient 2 was classified as likely pathogenic. Clinically, Patient 1 had severe developmental retardation, deafness and autistic tilt, whereas Patient 2 had milder retardation and autistic behaviours with normal hearing. The splice-site variant in Patient 2 may disrupt an upstream intron and is predicted to influence splicing, which may elicit nonsense-mediated mRNA decay and contribute a more severe interference, comparatively. CONCLUSION: Our results broaden the mutational and phenotypic spectrum of KDM3B-related disorder and highlight the phenotypic heterogeneity even in patients with the same type of variant. Functional analysis underscores the importance of KDM3B in neurodevelopment, optic nerve formation and cognition. Additional studies will be required to define the differences in clinical phenotype at the molecular level.
Deficiency of the Tangier Disease Gene Abca1 Is Associated With Microglial Defects in Mice.
Celis T, Ramírez-Herrera O, Barraza M … +5 more , Calfunao S, Saavedra F, Romo-Toledo P, Busso D, Santander N
Int J Dev Neurosci · 2025 Dec · PMID 41361956 · Publisher ↗
Microglia, the resident macrophages of the central nervous system, are a diverse population that develop during embryonic and postnatal stages in the mouse. Several signalling pathways are involved in their specification...
Microglia, the resident macrophages of the central nervous system, are a diverse population that develop during embryonic and postnatal stages in the mouse. Several signalling pathways are involved in their specification and maturation, but other types of cues might be involved, including lipid metabolism. Here, we evaluated the effect of the inactivation of two main cholesterol transporters in mice, ABCA1 and SR-B1, on microglial development. Using public datasets, we showed that both transporters are expressed in microglia and are differentially regulated in neurodegeneration models. Inactivation of either transporter was associated with distinct effects on microglial density and/or morphology at different developmental stages and in different brain regions. These studies suggest that microglia require appropriate lipid transport to support their homeostatic identity and could implicate this process in neurodegenerative diseases.
Sericin Administration During Gestation Improves Reflexive Motor Behaviour and Serum Growth Hormone and IGF Levels in Mice Offspring.
Fadaei S, Hassanpour S, Eidi A … +1 more , Zendehdel M
Int J Dev Neurosci · 2025 Dec · PMID 41358574 · Publisher ↗
This study investigated the effect of sericin consumption during gestation on the neurodevelopmental reflexes, motor behaviour and biochemical profiles of mice offspring. Forty pregnant NMRI mice were randomly assigned i...
This study investigated the effect of sericin consumption during gestation on the neurodevelopmental reflexes, motor behaviour and biochemical profiles of mice offspring. Forty pregnant NMRI mice were randomly assigned into four groups: a control group and three experimental groups that received sericin (112.5, 225 and 450 mg/kg) via oral administration on Days 5, 8, 11, 14 and 17 of gestation. Then, neurodevelopmental reflex tests included ambulation, hindlimb foot angle, hindlimb suspension, surface righting, front-limb suspension, grip strength and negative geotaxis were assessed. Additionally, blood samples were collected to evaluate biochemical parameters, including serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), total antioxidant capacity (TAC), growth hormone (GH) and insulin-like growth factor (IGF) levels. The findings revealed that prenatal sericin exposure improved ambulation scores, reduced hindlimb foot angle and increased hindlimb suspension scores (p < 0.05). Sericin administration led to an increase in grip strength and front-limb suspension scores (p < 0.05). Furthermore, sericin administration decreased serum and brain MDA levels while increasing serum and brain SOD, GPx and TAC levels (p < 0.05). Sericin exposure also increased serum GH and IGF levels (p < 0.05). The results indicated that maternal sericin consumption during gestation had a positive impact on offspring's motor skills and antioxidant status.
Low Expression Levels of MAOA and TPH1 Genes May Represent Risk Factors in Boys With Autism Spectrum Disorder-A Case-Control Study.
Akalin H, Bilgic B, Avcil S … +1 more , Orenay-Boyacioglu S
Int J Dev Neurosci · 2025 Dec · PMID 41346126 · Publisher ↗
INTRODUCTION: It has been reported that disruptions in the metabolic pathways of tryptophan, the precursor of the neurotransmitter serotonin, may contribute to the development of autism spectrum disorder (ASD); however,...
INTRODUCTION: It has been reported that disruptions in the metabolic pathways of tryptophan, the precursor of the neurotransmitter serotonin, may contribute to the development of autism spectrum disorder (ASD); however, further research is needed. Therefore, this study aims to assess the gene expression levels of two key enzymes involved in tryptophan metabolism, monoamine oxidase A (MAOA) and tryptophan hydroxylase-1 (TPH1), in male children diagnosed with ASD, and to explore their relationship with autism severity. METHODS: For this purpose, 30 male children diagnosed with ASD according to the DSM-5 diagnostic criteria, who presented to the Institutional Child and Adolescent Psychiatry outpatient clinic, and 30 male children who presented to the same clinic with no psychiatric disorders detected were recruited as the control group. The subjects were administered the Childhood Autism Rating Scale. The expressions of MAOA and TPH1 genes were determined using Quantitative Real-Time PCR. RESULTS: The expression levels of MAOA and TPH1 genes were significantly reduced in the patient group compared to the control group (p = 0.017 and 0.000, respectively). No statistically significant results were obtained between autism severity and the expression levels of these genes within the patient group (p > 0.05). CONCLUSION: This study is the first to investigate and establish a correlation between the expression levels of the MAOA and TPH1 genes and ASD using human blood samples. Low MAOA and TPH1 gene expression levels, may contribute to serotonergic dysregulation potentially acting as risk factors involved in ASD.
Zebrafish: The Aquatic Pioneers of Brain Research.
Mishra M, Nayak BP
Int J Dev Neurosci · 2025 Dec · PMID 41340267 · Publisher ↗
Zebrafish (Danio rerio) have emerged as a pivotal model organism in translational neuroscience, neuropharmacology and CNS disorder research, leveraging their striking anatomical and physiological parallels to humans. Wit...
Zebrafish (Danio rerio) have emerged as a pivotal model organism in translational neuroscience, neuropharmacology and CNS disorder research, leveraging their striking anatomical and physiological parallels to humans. With a brain architecture and functional pathways that are closely similar to those of humans, zebrafish enable critical insights into brain development, neuro-circuitry and disease mechanisms. Notably, zebrafish have a number of benefits over more conventional mammalian models like mice and rats, including their rapid development, optical transparency allowing for real-time imaging and capacity to perform high-throughput genetic and pharmacological screens inexpensively. The combination of vertebrate complexity and experimental tractability that zebrafish possesses renders them uniquely placed for large-scale investigations of brain function and disease. This review synthesizes recent advancements in utilizing zebrafish to model brain disorders such as depression, anxiety, psychoses, autism spectrum disorders, cognitive impairments and drug-induced neurobehavioural alterations. By integrating findings from genetic, pharmacological and behavioural studies, we underscore zebrafish's unique advantages, including genetic tractability, cost-efficiency, high-throughput screening capacity and conserved neuroendocrine and behavioural responses. These features facilitate the exploration of complex neuropsychological processes and drug-brain interactions, bridging gaps between molecular mechanisms and behavioural outcomes. Zebrafish models have proven instrumental in unravelling the neurobiological underpinnings of human psychiatric and neurological disorders, offering a versatile platform for studying gene-environment interactions, neurodevelopmental trajectories and pharmacological interventions. Their translational relevance is further enhanced by rapid developmental cycles, optical transparency during early stages and robust behavioural assays that capture nuanced phenotypes. This review highlights the transformative role of zebrafish in accelerating drug discovery, optimizing neuropharmacological screening and advancing personalized therapeutic strategies. By consolidating evidence from diverse studies, we highlight zebrafish's capacity to address fundamental questions in neuroscience while fostering innovative approaches to diagnose, treat and prevent brain disorders, ultimately driving progress towards precision medicine in neurology and psychiatry.
Catalase Gene Variants and Oxidative Stress in Autism Spectrum Disorder: A Northern Lebanon Cohort and Aripiprazole In Vitro Toxicity.
Bacha JD, Zoebi NE, Al-Attrache H
Int J Dev Neurosci · 2025 Nov · PMID 41277029 · Publisher ↗
BACKGROUND: Autism spectrum disorder (ASD) is a multifactorial neurodevelopmental condition influenced by genetic, epigenetic and environmental factors. Oxidative stress and antioxidant enzyme polymorphisms, particularly...
BACKGROUND: Autism spectrum disorder (ASD) is a multifactorial neurodevelopmental condition influenced by genetic, epigenetic and environmental factors. Oxidative stress and antioxidant enzyme polymorphisms, particularly catalase (CAT), have been implicated in ASD, but findings remain inconsistent. In parallel, pharmacological interventions such as aripiprazole, which is widely used in ASD, have cellular toxicological profiles that remain incompletely defined. METHODS: A total of 94 participants (39 ASD patients and 55 controls) were genotyped for the CAT polymorphism rs7943316 using tetra-primer amplification refractory mutation system PCR (T-ARMS-PCR). Genotype distributions were statistically compared using χ and Fisher's exact tests. In vitro toxicological assays were performed in Saccharomyces cerevisiae wild type (BY4741) and mutant strains deficient in oxidative stress and lipid metabolism genes (CAT1, CPT2, PXA2 and FAA1). Yeast growth was quantified under increasing concentrations of aripiprazole, and IC values were determined. RESULTS: Genotype distribution of rs7943316 showed no significant difference between ASD and control groups (p = 0.866), indicating no association between this CAT polymorphism and ASD risk in this Lebanese cohort. Toxicological profiling revealed that aripiprazole caused dose-dependent growth inhibition. Mutant strains lacking CAT1, CPT2 or PXA2 exhibited significantly reduced IC values compared to wild type (p < 0.05), highlighting oxidative stress detoxification, carnitine-mediated acetyl-CoA transport and peroxisomal fatty acid import as key determinants of drug sensitivity. CONCLUSION: CAT polymorphism rs7943316 is not associated with ASD in this population. However, aripiprazole exerts dose-dependent toxicity strongly modulated by oxidative stress and metabolic pathways. These findings support the integration of genetic and toxicological approaches for understanding ASD and optimizing therapeutic safety.
FGF-21 and 8-OHdG Biomarkers in Drug-Naïve Children With Autism Spectrum Disorder.
Baraúna S, Sylvestre G, Quagliato L
Int J Dev Neurosci · 2025 Nov · PMID 41261335 · Publisher ↗
Autism spectrum disorder (ASD) is a neuropsychiatric condition characterized by significant difficulties in social communication and repetitive behaviours, with multifactorial causes that include genetic predisposition a...
Autism spectrum disorder (ASD) is a neuropsychiatric condition characterized by significant difficulties in social communication and repetitive behaviours, with multifactorial causes that include genetic predisposition and environmental factors. Recent studies have highlighted altered levels of specific biomarkers associated with DNA damage in children with ASD. These alterations become more evident due to increased oxidative stress, a common feature in individuals diagnosed with ASD. This study aimed to investigate plasma levels of FGF-21-an endogenous protein with metabolic and, primarily, neuroprotective functions-and its relationship with the biomarker 8OHdG, which is widely recognized as an indicator of oxidative stress and cellular and DNA damage. The research included 29 drug-naive children diagnosed with ASD and 31 healthy control children. The 8OHdG result showed a statistically significant difference when comparing patients diagnosed with ASD to healthy controls (t = 2.768, df = 58, p = 0.004), indicating a relevant difference in the levels of this biomarker and DNA damage between patients with ASD and controls. In contrast, the analysis of FGF-21 (p = 0.44) did not show a significant difference in both groups. These findings pave the way for future research that may lead to innovative therapeutic approaches for the treatment of children with ASD, focusing on reducing oxidative stress and DNA repair.
Could Transforming Growth Factor Beta and Target MicroRNA Dysregulation Serve as Biomarkers of Symptom Severity in Patients With Obsessive-Compulsive Disorder?
Altunoz S, Dolapoglu N, Baykan O … +3 more , Bolat H, Avcikurt AS, Karlidere T
Int J Dev Neurosci · 2025 Nov · PMID 41239944 · Publisher ↗
INTRODUCTION: This study investigated the regulation of miRNA-132-3p on TGF-β levels and its association with OCD severity. We hypothesized that miRNA-132-3p and TGF-β influence OCD aetiology and severity, with their lev...
INTRODUCTION: This study investigated the regulation of miRNA-132-3p on TGF-β levels and its association with OCD severity. We hypothesized that miRNA-132-3p and TGF-β influence OCD aetiology and severity, with their levels correlating with disease severity. METHODS: The study included 48 OCD patients diagnosed via SCID-5-CV per DSM-V and 48 matched healthy controls. Blood samples were analysed for miRNA-132-3p and TGF-β using RT-PCR and ELISA. Participants completed Y-BOCS, symptom list, HAMA, HAMD, consent and sociodemographic forms. RESULTS: OCD patients had significantly lower TGF-β levels (p = 0.008), negatively correlating with Y-BOCS scores (r = -0.220, p = 0.045) and disease duration (r= -0.473, p = 0.002). miRNA-132-3p levels were 1.92 times higher in OCD patients (p = 0.003), positively correlating with Y-BOCS scores (r = 0.208, p = 0.045). CONCLUSIONS: Altered TGF-β and miRNA-132-3p levels may contribute to OCD pathophysiology by affecting BDNF regulation, inflammatory responses (Th1/Th2, Th17/Treg balance) and synaptic plasticity-related genes.
Proteomic Findings in ADHD: A Systematic Review.
Karabulut OB, Unal D
Int J Dev Neurosci · 2025 Nov · PMID 41236087 · Publisher ↗
Attention-deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder that causes a notable burden on the patients, their families and society. Identifying and treating ADHD in the early stages is cruci...
Attention-deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder that causes a notable burden on the patients, their families and society. Identifying and treating ADHD in the early stages is crucial for minimising the long-term impact of the disorder. Despite growing evidence of differences revealed by neuroimaging, neurophysiology, and genetic studies in ADHD populations, a reliable biomarker has not been shown yet. However, the use of proteomics has the potential to identify biomarkers for clinical screening and diagnosis, as well as to monitor treatment response, which has been proven beneficial in some other brain disorders before. According to our systematic literature review, the majority of proteomic studies in the context of ADHD have been conducted using animal models. The identified proteins appear to be predominantly associated with processes such as inflammation, myelination, neurotransmission, mitochondrial metabolism, cellular structural integrity and various intracellular signalling pathways. The results of these studies are discussed and integrated from a clinician's point of view in this review.
No Elevated Genomic Damage Despite High Oxidative Stress and Homocysteine Levels Among ADHD Children.
Başay BK, Yıldırım HÇ, Ünal EB … +1 more , Başay Ö
Int J Dev Neurosci · 2025 Nov · PMID 41235991 · Publisher ↗
This study aimed to examine oxidative stress and DNA damage in medication-naïve children with attention deficit hyperactivity disorder (ADHD), focusing on total oxidant and antioxidant levels, homocysteine, vitamin B12 (...
This study aimed to examine oxidative stress and DNA damage in medication-naïve children with attention deficit hyperactivity disorder (ADHD), focusing on total oxidant and antioxidant levels, homocysteine, vitamin B12 (VB12), folic acid (FA) and vitamin D (VD). Forty-two medication-naïve children diagnosed with ADHD and 36 age- and sex-matched healthy controls participated in the study. Biochemical analyses included measurements of total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), homocysteine, VB12, FA and VD levels via ELISA. Genomic DNA damage was evaluated through the comet assay. Children with ADHD exhibited significantly higher TOS, OSI and homocysteine levels, indicating increased oxidative stress (respectively t = 2.956, p = 0.005; t = 3.218, p = 0.002; t = 2.868, p = 0.006). However, contrary to expectations, DNA damage parameters (tail intensity, tail moment and tail migration) were significantly lower in the ADHD group than in controls (respectively t = -3.830, p = 0.000; t = -3.871, p = 0.000; t = -2.340, p = 0.022). VD levels were also higher in the ADHD group (t = 2.313, p = 0.023), while no significant group differences were observed in VB12 or FA (p > 0.05). Despite increased oxidative stress, children with ADHD showed no signs of elevated genomic damage. These findings suggest the presence of compensatory mechanisms such as efficient DNA repair or enhanced antioxidant responses in this population. The unexpected pattern of elevated VD and stable genomic integrity highlights the complexity of biological processes underlying ADHD and the importance of considering adaptive cellular factors in biomarker research.
What Do Parents Know and Perceive About Child and Adolescent Psychiatry and Treatments?
Cicek AU, Bozok BK, Bozok SE … +4 more , Abanoz E, Arslan SC, Ucuz I, Sireli O
Int J Dev Neurosci · 2025 Nov · PMID 41235882 · Publisher ↗
PURPOSE: Parents' knowledge, understanding and attitudes have a strong influence on treatment outcomes in child and adolescent psychiatry (CAP). However, little is known about parents' knowledge, perceptions and awarenes...
PURPOSE: Parents' knowledge, understanding and attitudes have a strong influence on treatment outcomes in child and adolescent psychiatry (CAP). However, little is known about parents' knowledge, perceptions and awareness regarding assessment, intervention and treatment options in CAP. METHODS: We evaluated 1872 parents (1104 mothers [59.0%], 768 fathers [41.0%]) who were over 18 years of age and had at least one child between the ages of 0-18, regardless of whether their child had previously received CAP treatment, using a questionnaire containing 29 questions. RESULTS: The most common misconceptions about CAP application records were that psychiatric records would cause difficulties in getting a job (92.6%) and would be obstacles to appointment to civil service (65.8%) and to getting driver's licence (34.8%). Regarding CAP drug treatments, the most frequently reported false beliefs were that psychiatric drugs cause weight gain (80.1%), are addictive (65.1%), cause long-lasting side effects (53.5%), numb the mind and cause drowsiness (52.7%), alter children's personalities (44.4%) and increase suicide risk (42.9%). Furthermore, 1105 (59.0%) participants answered 'Psychiatric disorders cannot be treated effectively even if psychiatric medications are used.' CONCLUSIONS: Our results indicated that parents' knowledge level was inadequate, and their attitudes and beliefs were negative and limited regarding CAP and treatments; in turn, they avoided treatment and did not engage in help-seeking behaviours. This study shows an urgent need for mental health education programs to increase parents' awareness and understanding of CAP and promote appropriate access to services.
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