Poisoning young minds? Methyl parathion may be linked to neurodevelopment problems.
Explore the source record for details and available documents.
Attention↗
SEARCH · PubMed Health
Results for “Neurodevelopment”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
New thinking on neurodevelopment.
Explore the source record for details and available documents.
Biomedical Research↗
Neurodevelopment and endocrine disruption.
In this article I explore the possibility that contaminants contribute to the increasing prevalence of attention deficit hyperactivity disorder, autism, and associated neurodevelopmental and behavioral problems in developed countries. I discuss the exquisite sensitivity of the embryo and fetus to thyroid disturbance and provide evidence of human in utero exposure to contaminants that can interfere with the thyroid. Because it may never be possible to link prenatal exposure to a specific chemical with neurodevelopmental damage in humans, I also present alternate models where associations have been made between exposure to specific chemicals or chemical classes and developmental difficulties in laboratory animals, wildlife, and humans.
Adult↗
A case for revisiting the safety of pesticides: a closer look at neurodevelopment.
The quality and quantity of the data about the risk posed to humans by individual pesticides vary considerably. Unlike obvious birth defects, most developmental effects cannot be seen at birth or even later in life. Instead, brain and nervous system disturbances are expressed in terms of how an individual behaves and functions, which can vary considerably from birth through adulthood. In this article I challenge the protective value of current pesticide risk assessment strategies in light of the vast numbers of pesticides on the market and the vast number of possible target tissues and end points that often differ depending upon timing of exposure. Using the insecticide chlorpyrifos as a model, I reinforce the need for a new approach to determine the safety of all pesticide classes. Because of the uncertainty that will continue to exist about the safety of pesticides, it is apparent that a new regulatory approach to protect human health is needed.
Environmental Exposure↗
Effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 years of life among inner-city children.
Our prospective cohort study of nonsmoking African-American and Dominican mothers and children in New York City is evaluating the role of prenatal exposure to urban pollutants, including polycyclic aromatic hydrocarbons (PAHs) , environmental tobacco smoke (ETS) , and pesticides, in the pathogenesis of neurobehavioral disorders. We used the Bayley Scales of Infant Development to evaluate the effects on child mental and psychomotor development of prenatal exposure to airborne PAHs monitored during pregnancy by personal air sampling. Behavioral development was assessed by the Child Behavior Checklist. We adjusted for potential confounders including sociodemographic factors and prenatal exposure to ETS and chlorpyrifos. Prenatal exposure to PAHs was not associated with psychomotor development index or behavioral problems. However, high prenatal exposure to PAHs (upper quartile) was associated with lower mental development index at age 3 [beta=-5.69; 95% confidence interval (CI), -9.05 to -2.33; p<0.01]. The odds of cognitive developmental delay were also significantly greater for children with high prenatal exposure (odds ratio=2.89; 95% CI, 1.33 to 6.25; p=0.01). General estimated equation analysis showed a significant age times PAH effect on mental development (p=0.01), confirming the age-specific regression findings. Further adjustment for lead did not alter the relationships. There were no differences in effect sizes by ethnicity. The results require confirmation but suggest that environmental PAHs at levels recently encountered in New York City air may adversely affect children's cognitive development at 3 years of age, with implications for school performance.
Adult↗
New data about embryonic and fetal neurodevelopment and behavior obtained by 3D and 4D sonography.
The development of the human central nervous system (CNS) begins in the early embryonic period and proceeds through a sequence of very complicated processes long after delivery. Although the neurodevelopmental processes are genetically determined, their complexity and intensity implicates the vulnerability of the CNS to number of environmental factors. There is substantial evidence to show that many neurological problems, from minor cerebral dysfunction to the cerebral palsy, originate form the prenatal, rather than perinatal or postnatal periods of life. A variety of neurological and neuropsychiatric diseases is nowadays considered to originate, at least partly, from the prenatal incidents. In most of these conditions, there is no reliable parameter for detection or prediction of cerebral lesions and there is an urgent need to develop strategies that would enable the early detection of cerebral lesions or indications that such lesions might occur. The new, advanced, imaging techniques such as 3-dimensional and 4-dimensional sonography, opened a new perspective for the investigation of structural and functional development of fetal CNS. The application of these techniques might improve our understanding of the prenatal neurodevelopmental events and possibly facilitate the development of diagnostic strategies for early detection or prevention of brain dysfunctions and damage.
Behavior↗
[Investigation of neurodevelopment delay etiology: resources and challenges].
To verify the reach of development delay investigation, we brought the experience in the pediatrics, infantile neurology and clinical genetics diagnoses, with resources of a tertiary health care, in 73 children, from 1 to 47 months age, between 1999 and 2001, attending a Stimulation Program of the Association of Parents and Friends of Exceptional Children of Batatais-SP. With a transversal and prospective method, six groups were identified: motor disturbances, dysmorphisms, malnutrition, macrocephaly, microcephaly and motor delay. In the analysis of the contribution of the antecedents, physical or laboratory exams to the diagnosis, it stands out the brain image in the groups "motor disturbances" and "macrocephaly"; and for the remaining groups, the physical examination and maternal data. The causes were detected in 48 (66%), being 38.4% of environmental and 24.6% genetics origin. It is emphasized the specialist evaluation, and the need of appropriate flow of information in the net of health.
Child, Preschool↗
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↗
Effects of methylmercury exposure on neurodevelopment.
Explore the source record for details and available documents.
Central Nervous System Diseases↗
Effects of methylmercury exposure on neurodevelopment.
Explore the source record for details and available documents.
Animals↗
Neurotransmitters and neurodevelopment. Role of dopamine in neurite outgrowth, target selection and specific synapse formation.
Neurotransmitters and their receptors appear early during nervous system development and are thought to play important roles in neurite outgrowth, growth cone motility, target cell selection and synaptogenesis. In vivo studies in both vertebrates and invertebrates have shown that the perturbations of embryonic transmitter expression result in abnormal morphological and synaptic development. In vitro studies have further revealed that transmitters are capable of affecting neurite outgrowth and growth cone behaviour. The precise cellular mechanisms by which neurotransmitters affect these developmental steps are, however, poorly defined. In vitro, a presynaptic neuron from the mollusc Lymnaea stagnalis releases dopamine, which induces both growth cone attraction and growth cone collapse of target and non-target cell growth cones, respectively. We propose that the ability of dopamine to differentially affect growth cone motility of two cell types results from a divergence of the dopamine receptor-activated second messenger pathways at the G-protein level. Such transmitter-receptor interactions between growth cones of specific neurons may not only induce changes in the growth cone motility, but may subsequently play an important role in target cell selection and specificity of synaptogenesis.
Animals↗
Complexity of transcriptional control in neuropeptide gene expression; enkephalin gene regulation during neurodevelopment.
The gene for enkephalin is expressed only in specific subsets of neurons in the mammalian central nervous system (CNS), whereas the large majority of neurons do not express the gene. This restricted expression is the result of a developmental process during which some of the multipotent neural progenitors express the gene for enkephalin and thereby become enkephalinergic neurons. The regulation of this process is not well understood. We have used a novel approach to identify DNA-protein interactions that regulate the developmental expression of the gene for enkephalin. We have identified four novel DNA regulatory sites and their binding proteins that are expressed in the developing mammalian CNS. These protein-DNA interactions regulate DNA and nuclear structures through DNA bending, DNA sliding, chromatin remodelling and far-distant DNA interactions. The concerted and co-ordinated interactions of these four DNA elements and their binding proteins contribute to the guiding of multipotent neural progenitors into enkephalinergic neurons. The provided examples suggest an important role for architectural transcriptional regulation during CNS development.
Animals↗
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↗
p35 and p39 are essential for cyclin-dependent kinase 5 function during neurodevelopment.
Cyclin-dependent kinase 5 (Cdk5) plays a pivotal role in brain development and neuronal migration. Cdk5 is abundant in postmitotic, terminally differentiated neurons. The ability of Cdk5 to phosphorylate substrates is dependent on activation by its neuronal-specific activators p35 and p39. There exist striking differences in the phenotypic severity of Cdk5-deficient mice and p35-deficient mice. Cdk5-null mutants show a more severe disruption of lamination in the cerebral cortex, hippocampus, and cerebellum. In addition, Cdk5-null mice display perinatal lethality, whereas p35-null mice are viable. These discrepancies have been attributed to the function of other Cdk5 activators, such as p39. To understand the roles of p39 and p35, we created p39-null mice and p35/p39 compound-mutant mice. Interestingly, p39-null mice show no obvious detectable abnormalities, whereas p35(-/-)p39(-/-) double-null mutants are perinatal lethal. We show here that the p35(-/-)p39(-/-) mutants exhibit phenotypes identical to those of the Cdk5-null mutant mice. Other compound-mutant mice with intermediate phenotypes allow us to determine the distinct and redundant functions between p35 and p39. Our data strongly suggest that p35 and p39 are essential for Cdk5 activity during the development of the nervous system. Thus, p35 and p39 are likely to be the principal, if not the only, activators of Cdk5.
Animals↗
The role of thyroid hormone in fetal neurodevelopment.
Thyroid hormones are necessary for normal brain development during fetal and postnatal life. The stage at which the central nervous system becomes thyroid hormone sensitive, however, has not been clearly defined. There is increasing evidence from epidemiological studies and patient reports that these hormones are already needed for orderly development during the first trimester, when the fetus is entirely dependent on the maternal transfer of thyroxine, the main substrate for intracellular generation of the more active 3,5,3'-triiodothyronine for binding to the nuclear hormone receptors. A decrease in maternal circulating thyroxine during the first trimester, whether or not accompanied by increased circulating thyroid-stimulating hormone, may well result in irreversible mental and psychomotor impairments. The very frequent cause of this is an iodine intake insufficient to meet the requirements of the pregnant woman. It appears urgent to ensure the use of iodine supplements from before or very early in pregnancy, and to screen all women for hypothyroxinemia as early as possible. Maternal thyroxine continues to be important for the exposure of fetal tissues to adequate amounts of this hormone during the second and, possibly, the third trimesters. Premature birth, which interrupts this transfer, results in neonatal hypothyroxinemia. This is more severe the earlier it occurs during development, and is an important cause of the poorer mental and neuromotor development of many preterm infants. The possibility of supplying them with thyroxine during the neonatal period is being seriously tested.
Animals↗
[Neurodevelopment and schizophrenia].
The evidence of neuroleptics' antipsychotic action due to their antagonism of dopamine receptors led to the hyperdopaminergic theory of schizophrenia. But the functional disturbance of the dopamine neurons should explain the increase and the reduction of some symptoms at the same time through the D2 receptors blockade. The prodromical manifestations of schizophrenia include abnormal movements which precede and predict the beginning of the disease. They also suggest a dopamine deficit. An injury in the mesocortical dopamine projection during the neural development could result in a functional impairment of the prefrontal cortex which causes the cognitive deficit symptoms. It would result also in an excessive compensatory subcortical dopamine activity which would cause the psychotic symptoms. The evidence in behalf of this physiopathology is complex. The mechanism of the subcortical compensation of the prefrontal dopamine deficit remains unknown. It is necessary to find out which is the exact mechanism of the injury that causes the mesocortical projection loss in the schizophrenia. We have suggested that the injury would depend on the excitotoxicity induced by the perinatal hypoxia which would provoke the selective death of a dopamine neurons subset which are very sensitive during the critical period of the mesencephalic development.
Adult↗
Schizophrenia and bipolar disorder: similarities in pathogenic mechanisms but differences in neurodevelopment.
Over the past 100 years, the Kraepelinian classification of psychoses has dominated our approach to schizophrenia and bipolar disorder. However, controversy as to the nature of the illnesses--whether they can be viewed as completely distinct, essentially the same, or occupying different points along a psychosis spectrum--has intensified in recent years. This paper reviews the evidence for these differing opinions, examining both the commonalities between the two diseases and the distinctions. A genetic propensity towards psychotic disorders is widely acknowledged; more recent studies suggest a considerable overlap in genetic susceptibility to schizophrenia and bipolar disorder. The influence of early environmental effects, such as obstetric complications, on schizophrenia is also established but little such evidence exists for bipolar disorder. Structural abnormalities of the brain of developmental origin as well as neuropsychological deficits have been clearly identified in schizophrenia but less evidence has been found in bipolar disorder. The most plausible explanation is that one or more susceptible genes are shared between schizophrenia and bipolar illness, and can be thought of as predisposing individuals to psychosis, perhaps by producing a dysregulation of the dopaminergic response to stress. Other genes and environmental factors are likely to have more specific effects and contribute to producing the patterns that psychiatrists recognize as 'classical' schizophrenia and mania. In particular, genes involved in early cortical development and early neurodevelopmental insults causing developmental impairment may put individuals on a trajectory towards schizophrenia rather than bipolar illness.
Adult↗
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↗