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At least 19 recordsLinked to original sources
PubMed2024

Prenatal cannabis exposure is associated with alterations in offspring DNA methylation at genes involved in neurodevelopment, across the life course.

Prenatal cannabis exposure (PCE) is of increasing concern globally, due to the potential impact on offspring neurodevelopment, and its association with childhood and adolescent brain development and cognitive function. However, there is currently a lack of research addressing the molecular impact of PCE, that may help to clarify the association between PCE and neurodevelopment. To address this knowledge gap, here we present epigenome-wide association study data across multiple time points, examining the effect of PCE and co-exposure with tobacco using two longitudinal studies, the Avon Longitudinal Study of Parents and Children (ALSPAC) and the Christchurch Health and Development Study (CHDS) at birth (0 y), 7 y and 15-17 y (ALSPAC), and ~27 y (CHDS). Our findings reveal genome-wide significant DNA methylation differences in offspring at 0 y, 7 y, 15-17 y, and 27 y associated with PCE alone, and co-exposure with tobacco. Importantly, we identified significantly differentially methylated CpG sites within the genes LZTS2, NPSR1, NT5E, CRIP2, DOCK8, COQ5, and LRP5 that are shared between different time points throughout development in offspring. Notably, functional pathway analysis showed enrichment for differential DNA methylation in neurodevelopment, neurotransmission, and neuronal structure pathways, and this was consistent across all timepoints in both cohorts. Given the increasing volume of epidemiological evidence that suggests a link between PCE and adverse neurodevelopmental outcomes in exposed offspring, this work highlights the need for further investigation into PCE, particularly in larger cohorts.

DNA Methylation↗
PubMed2026

CNNM2 in schizophrenia: multilevel evidence of genetic susceptibility, magnesium homeostasis, neurodevelopment and cognitive dysfunction.

Schizophrenia (SCZ) is a common psychiatric disorder with a complex, genetically and environmentally influenced etiology, but the specific pathogenesis remains unclear. In recent years, the SCZ susceptibility gene CNNM2 (encoding cyclin M2) located at the 10q24.32-33 locus has received widespread attention. The well-validated SCZ risk interval 10q24.32-33 harbors two independent risk variants: rs11191580 in NT5C2 (significantly associated with CNNM2 mRNA and protein levels) and rs7914558 in CNNM2. Results from functional genomic analyses indicate that lower CNNM2 expression is significantly associated with SCZ. Imaging genetics studies have demonstrated that carriers of risk alleles of CNNM2 SNPs exhibit alterations in brain structure. Animal model studies have revealed that Cnnm2 downregulation in mice leads to impairments in sensorimotor gating and cognitive function. As an Mg2+ transporter, CNNM2 primarily maintains systemic Mg2+ homeostasis. According to clinical studies, a proportion of patients with SCZ exhibit reduced Mg2+ concentrations in plasma and cerebrospinal fluid. CNNM2 dysfunction may contribute to the pathology of SCZ by disrupting Mg2+ homeostasis, thereby affecting neurodevelopment and synaptic plasticity. A systematic consolidation of current evidence supporting the involvement of CNNM2 in SCZ pathogenesis provides a direction for further investigation of the pathological mechanisms underlying this disease, and for identification of novel targets for clinical intervention..

Schizophrenia↗
PubMed1992

Neurodevelopment in late infancy after prenatal exposure to benzodiazepines--a prospective study.

Growth and neurodevelopment at 6, 10 and 18 months of age have been studied prospectively and longitudinally in a series of 17 children born to mothers who used benzodiazepines (BZD) in therapeutic doses as their only psychotropic drug throughout pregnancy. The results were compared with a group of 29 children born to mothers without any known use of psychotropic drugs. The BZD-exposed children caught up their low mean birth-weight, at an early stage, whereas the slightly decreased head circumference at birth remained at the same low level. In five infants, a pattern of craniofacial anomalies was found. Deviating neurodevelopmental and clinical symptoms and signs were common. The gross motor development was retarded at 6 and 10 months, but was nearly normal at 18 months. Impaired fine motor functions were found on all follow-up occasions. At 18 months, the most prominent finding was a delayed development of pincer grasp. The BZD-exposed children showed deviations in muscle tone and pattern of movements more frequently than children in the reference group. The study suggests that the use of BZD in therapeutic doses throughout pregnancy can have negative effects on the development of children up to 18 months of age. The long-term hazards cannot be evaluated from these results. A further follow-up at early school age is needed and is in progress.

Abnormalities, Drug-Induced↗
PubMed1990

A longitudinal follow up of neurodevelopment of high risk newborns--a comparison of Amiel-Tison's method with Bayley Scales of Infant Development.

The neurodevelopment of 42 high risk babies and 7 control babies was assessed longitudinally till the age of 12 months by using two different methods. The method of neurological evaluation described by Amiel-Tison was used, and the results compared with those of a standard developmental test, the Bayley Scales of Infant Development. The Amiel-Tison method was found to be a sensitive test for picking up abnormalities till the age of 9 months, but lost its advantage over the Bayley Scales at 12 months. Besides, the test was quick, simple to learn and did not need a special kit or a trained psychologist and was hence found to be a good screening method.

Child, Preschool↗
PubMed2026

Personalized functional topography-based multisite brain age prediction modeling reveals divergent neurodevelopment in major depression.

Major depressive disorder (MDD) is associated with widespread alterations in functional brain networks across the lifespan. However, heterogeneity in atypical brain development among patients with MDD remains largely uncharacterized. Using a multisite resting-state functional MRI dataset consisting of 1,105 MDD patients and 1,065 healthy controls, we constructed a harmonized multicenter brain age prediction model based on individualized functional topography and identified two patient subgroups with positive or negative brain age gaps (BAGs). In patients with a positive BAG (BAG+), expansion of the salience network (SAL) into the dorsolateral prefrontal and ventrolateral prefrontal cortices, in addition to contraction of the sensorimotor and dorsal attention networks (DAN), contributes to accelerated brain aging. Conversely, in the negative BAG (BAG-) group, SAL expansion into the orbitofrontal cortex (OFC) and contraction of the visual and sensorimotor networks (SMN) were linked to delayed brain development. These subgroups also exhibited distinct neurodevelopmental trajectories. Clinically, BAG+ patients showed stronger associations between higher-order network topography and mood symptoms, whereas BAG- patients exhibited links between visual/default mode network topography and insomnia. At the molecular level, both groups showed enrichment of genes related to synaptic signaling but displayed distinct expression patterns and divergent expression trajectories in key neurodevelopmental gene sets. Notably, antidepressant treatment modulated the brain in ways that were specific to each subgroup. These findings reveal heterogeneous neurodevelopmental profiles in MDD with distinct biological and clinical signatures, offering insights into personalized precision medicine for this disorder.

Humans↗
PubMedDate not supplied

Lead-impaired neurodevelopment. Mechanisms and threshold values in the rodent.

Mechanisms underlying the cognitive deficits arising from chronic low level lead exposure are viewed as a consequence of impaired neurodevelopmental events. These events are exemplified within the cerebellum which is formed completely after birth and, therefore, encompasses all major epochs of development. Further, the unique pharmacokinetic distribution of juvenile blood lead levels is developmentally regulated and can be correlated to the periods of impaired structuring and threshold values indicating no-effect levels established. Here, the endpoint value is related to lead-induced dysfunctioning of a morphoregulator--the neural cell adhesion molecule (NCAM). During final synaptic structuring its normal developmental sequence is perturbed when blood lead levels exceed 20 micrograms/dl. These events are similar, and compared to, those seen in the cerebellum of the staggerer mouse mutant (sg/sg) where the selection of circuits to be preserved from those transiently overproduced during development is impaired.

Animals↗
PubMed1989

Disturbances of brain maturation and neurodevelopment during chronic renal failure in infancy.

Fifteen infants with moderate to severe congenital renal disease were prospectively studied by serial renal, neurodevelopmental, neurophysiologic, and anthropometric assessments. The observation period ranged from 3 to 25 months (mean = 10.9). Eight patients maintained a Mental Development Index (MDI) above the 16th percentile (greater than -1 SD) and comprised group 1. Of the remaining seven patients (group 2), three had an MDI less than 16th percentile when first studied and four had serial decreases of the MDI to less than 16th percentile. Although motor development was more delayed in group 2 at study entry, there were no significant changes of motor performance levels for either group during the study period. Group 2 patients had smaller length (p less than 0.05) and head circumference (p less than 0.05) standard deviation scores in comparison with group 1, and they had higher serum creatinine values (mean = 3.8 vs 1.3 mg/dl, respectively; p less than 0.01). By spectral electroencephalography, the expected progressive increase of the frequency of cerebral cortical background activity with age was demonstrated in group 1 but was not seen in group 2 (multivariate analysis of variance p less than 0.03). This increase of faster-frequency activity was primarily manifested in the left cerebral hemisphere of group 1 patients (p less than 0.01), a finding that was also absent in group 2. The frequent occurrence of neurodevelopmental abnormalities in infants with renal failure is possibly a consequence of impaired dominant hemispheric maturation in the first several years of life, which is clinically manifested as deterioration of cognitive function.

Cephalometry↗
PubMed1992

Neurodevelopment in infants and preschool children with congenital hypothyroidism: etiological and treatment factors affecting outcome.

Studied global intelligence and specific abilities of children from 1 to 5 years old, 108 with congenital hypothyroidism (CH) diagnosed by newborn screening and 71 sibling controls. Intelligence levels of the CH group were within the normal range but differed significantly from controls at age 5. CH demonstrated a language deficit at age 3, which diminished with age, as well as significantly poorer visuospatial and verbal skills at age 5. Children with absent thyroid glands or evidence of hypothyroidism in utero were outperformed by other CH children in most ability areas from 1 year on. Different components of ability were correlated with specific factors reflecting timing or duration of thyroid hormone deficiency, suggesting unique critical periods of thyroid hormone sensitivity for different specific cognitive abilities and their neural substrates. It is concluded that even though screened CH children are markedly improved by neonatal diagnosis, they are still at risk for subtle irreversible deficits, which depend on factors such as type, age at onset, and duration of disease.

Age Factors↗
PubMed1988

In utero exposure to organic solvents and human neurodevelopment.

Recent reports of growth and mental retardation in infants whose mothers abused solvent-containing substances, and of an association between central nervous system malformations and solvent exposure, have suggested that in utero exposure to organic solvents may have a profound effect on the development of the human brain. The present investigation compared the neurobehavioral development of 41 children whose mothers worked with organic solvents during pregnancy with a group of matched, unexposed children. The children were compared on a variety of measures, including the McCarthy Scales of General Abilities, growth (weight, height and head circumference) and mother's report of developmental milestones, behavior and personality. Potential confounders were controlled for in multiple regression analyses. Despite adequate power, no differences could be found between the two groups on any of the measures of neurobehavioral development or growth. This study suggests that in utero exposure to relatively low levels of organic solvent is not associated with adverse neurodevelopmental outcome.

Brain↗
PubMed1989

Cerebral blood-flow velocity during the first week of life of preterm infants and neurodevelopment at two years.

Disturbances in perinatal cerebral perfusion appear to be associated with unfavourable neurodevelopmental outcome. Using transcutaneous Doppler technique, the authors investigated cerebral blood-flow velocity patterns in the anterior cerebral artery (ACA) of an intensive care-unit population of preterm infants during the first week of life. The results were correlated with neurodevelopmental outcome at two years of age. Children with major disability at two years of age had significantly higher pulsatility index (PI) values, mainly increased peak systolic flow velocity (PSFV), compared with children with normal or more favourable outcome. End diastolic flow velocity and area under the velocity curve values of the ACA did not differ between the groups, indicating that cerebrovascular resistance and cerebral blood-flow were not different. It is thought that the higher PI and PSFV values were caused by increased compliance of the vascular bed supplied by the ACA, possibly induced by congestion and oedema of the periventricular white-matter due to ischaemic lesions, which also cause periventricular leukomalacia.

Blood Flow Velocity↗
PubMed2026

Sodium supplementation strategies in preterm infants: effects on growth, electrolyte balance, and exploratory evidence on neurodevelopment - a systematic review and meta-analysis.

This study evaluated the effects of sodium supplementation on growth, electrolyte balance, and neurodevelopmental outcomes in preterm infants. A systematic review and meta-analysis of published studies were conducted using data from PubMed, Embase, Scopus, and Google Scholar, including randomized controlled trials and observational studies involving infants born before 37 weeks of gestation. Twelve studies comprising more than 2,800 participants were analysed using random-effects models. Sodium supplementation was associated with improved weight gain and a significant reduction in the risk of hyponatremia (RR = 0.28, 95% CI: 0.08-0.96). Pooled incidence estimates indicated hypernatremia (32%) and intraventricular hemorrhage (29%) among supplemented cohorts; however, substantial heterogeneity was observed, and comparative risk estimates were limited. Only one study reported long-term neurodevelopmental follow-up, suggesting potential benefit; however, the available evidence remains limited and hypothesis-generating.These findings suggest that sodium supplementation may support growth and is associated with a lower risk of hyponatremia in preterm infants; however, hypernatremia and other morbidity estimates reported here are largely descriptive frequencies within supplemented cohorts rather than comparative treatment effects, and careful, individualized therapy with close monitoring is needed to minimize potential risks.

Growth outcomes↗
PubMed2026

When Neurodevelopment Meets Autoimmunity: Pemphigus Foliaceus in Rett Syndrome Expands the Clinical Spectrum-A Case Report.

Rett syndrome (RTT, OMIM 312750) is a complex multisystem neurodevelopmental disorder. Evidence suggests that RTT may have an autoimmune component and inflammatory activation. However, the autoimmune manifestations remain poorly described. Pemphigus foliaceus is a debilitating autoimmune blistering condition caused by IgG autoantibodies that target desmoglein-1 (Dsg1), resulting in widespread skin blistering and lesions. We report a case of pemphigus foliaceus in a 20-year-old female with RTT and discuss its clinical implications. Clinical data obtained from electronic health records were extracted and reviewed. Genetic testing was performed to identify the specific methyl-CpG-binding protein 2 (MECP2) mutation and on an expanded panel of 55 genes associated with pemphigus foliaceus and related blistering disorders. The individual had pemphigus foliaceus, which required immunosuppression, intravenous immunoglobulin (IVIg) therapy, and Rituximab. The disease trajectory was complicated by infections, aspiration pneumonia, and hypoxic cardiac arrest. There was progressive functional decline, and disease control was difficult to achieve, with frequent flares. Genetic testing confirmed a heterozygous pathogenic MECP2 variant (NM_001110792.1:c.952C>T; p.(Arg318Cys)). HLA genotyping identified alleles consistent with the HLA-DRB1*04:02-HLA-DQA1*03:01-HLA-DQB1*03:02 (DR4/DQ8) haplotype. Furthermore, genetic analysis identified a heterozygous DSG1 variant rs12967407. This study reports the first case of pemphigus foliaceus in RTT, expanding the clinical spectrum of RTT beyond its neurodevelopmental phenotype. The DR4/DQ8 haplotype, previously associated with pemphigus susceptibility, supports a background of genetic susceptibility in this individual. No causal association between RTT and pemphigus foliaceus can be inferred from this single case. Rather, this case demonstrates that a rare autoimmune disorder such as pemphigus foliaceus can co-occur with a pathogenic MECP2 mutation. The coexistence of a genetic and autoimmune disease can result in a more complex clinical presentation and treatment course. The case further emphasises the need for increased vigilance in identifying new and emerging systemic pathology alongside RTT.

Humans↗
PubMed1975

Neurodevelopment and sensory integration.

This is the report of a nine-month study of three profoundly retarded, multiply handicapped subjects less than five years of age, who received mother-administered, clinic-supervised treatment for neurodevelopmental sensory integration. The emergence of more advanced postural reactions, changes in affect, and responses to objects were recorded. Trends toward early cognitive emergence are discussed in terms of the development of interest and affect, as related to the concept of "fixation attention" of normal nine-month-old thinking infants.

Affect↗
PubMed1992

Neurodevelopment of preterm infants: neonatal neurosonographic and serum bilirubin studies.

In this study of 249 preterm infants of less than 34 weeks' gestation, the relationships between maximal serum total bilirubin concentrations during the neonatal period, neonatal cranial ultrasonographic abnormalities, and severe neurodevelopmental sequelae are described. The subjects, who were selected on the basis of serial cranial ultrasonographic findings, had repeated neurologic and developmental examinations during late infancy and early childhood that established the presence (n = 45) or absence (n = 204) of spastic forms of cerebral palsy. Of the 204 subjects without cerebral palsy, 23 scored abnormally low on standardized developmental testing during early childhood. All but seven of the subjects with cerebral palsy had grade III/IV intracranial hemorrhage or moderate to severe periventricular echogenicity or both, ultrasonographic abnormalities that probably reflect a disruption in the blood-brain barrier as well as extravasation of blood into brain tissue; however, analysis of the data did not suggest that these cranial ultrasonographic abnormalities increased either the maximum serum bilirubin concentration during the neonatal period or the susceptibility of the subjects to neurologic damage from hyperbilirubinemia. Also, there was no evidence to suggest that bilirubinemia in the range studied (2.3 to 22.5 mg/100 mL total serum bilirubin) was causally related to cerebral palsy, early developmental delay, or the development of periventricular cysts in this population of preterm infants.(ABSTRACT TRUNCATED AT 250 WORDS)

Apgar Score↗
PubMed1992

Schizophrenia and neurodevelopment.

Schizophrenia is characterised by the psychotic symptoms of hallucinations and delusions, accompanied by variable degrees of loss of insight. Whilst there is heterogeneity in the clinical profile, and presumably in the pathogenesis of what is currently called 'schizophrenia', it has become absolutely clear over the past decade that schizophrenic symptoms are consequent upon serious brain dysfunction. This new perspective has laid to rest a variety of 'crazy' theories, including the notion that mental illness was a myth, or that schizophrenia could be caused by faulty child rearing. The use of dopamine-blocking drugs has led to an improvement in symptom control, and diminished the need for prolonged hospital stays. It was hoped that the clear relationship between antipsychotic activity and dopamine blockade would help to elucidate the pathophysiology of schizophrenia, but to date no consistent abnormalities of the dopamine system have been found. Nevertheless, we have learned much about both the aetiology of schizophrenia and the origin of particular symptoms. Much of this has stemmed from increased understanding of the brain abnormalities underlying the disorder.

Adolescent↗