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PubMed1997

Position paper of the American Council on Science and Health: public health concerns about environmental polychlorinated biphenyls (PCBs).

Polychlorinated biphenyls, or PCBs, were widely used in various industrial applications for their insulating and fire retardant properties. In the 1960s, PCBs were found in soil and water, and research confirmed that some PCB congeners degrade very slowly in the environment and can build up in the food chain. Two widespread poisoning episodes in Japan and Taiwan were initially attributed to the consumption of rice bran oil contaminated with PCBs. Although subsequent analysis suggested that toxic thermal degradation products of PCBs in the oil, rather than the PCBs, were responsible for the observed health effects, commercial production of PCBs in the United States was discontinued in 1979. Several regulatory and advisory agencies have categorized PCBs as animal carcinogens; however, studies of workers exposed to high doses of PCBs over long periods of time have not demonstrated an increased cancer risk. In fact, the only health effects that could be attributed to PCBs were skin and eye irritation. Recent studies of the possible effects of prenatal exposure to PCBs on neurodevelopment in infants and children have been criticized for methodological deficiencies. There is no conclusive evidence that PCB levels in the general population are causing intellectual deterioration in children exposed in utero. Some investigators have also suggested that PCBs and other chemicals in the environment can interfere with the body's endocrine system, leading to infertility, certain types of cancer, and other hormone-related disorders. Evidence for estrogenic effects of environmental PCBs remains weak and circumstantial. The following actions are recommended: development of innovative, cost-effective remediation techniques, particularly for sites that are difficult to remediate (e.g., river sediments); and scientifically based improvements to risk assessment, to reduce the considerable uncertainty associated with PCB exposure to health effects in humans.

Animals↗

PubMed2002

Metals and women's health.

There is a lack of information concerning whether environmental-related health effects are more or less prevalent or manifested differently in women compared to men. Previously, most research in the area of toxicology and environmental and occupational health involved male subjects. The present work aims at reviewing exposure and health effects of cadmium, nickel, lead, mercury, and arsenic manifested differently in women than in men. The gender difference in exposure to nickel results in a much higher prevalence of nickel allergy and hand eczema in women than in men. The internal cadmium dose is generally higher in women than in men, due to a higher gastro-intestinal absorption at low iron stores. This was probably one major reason why Itai-itai disease was mainly a woman's disease. Yet, data are sparse regarding the risk for women relative to men to develop cadmium-induced kidney damage in populations exposed to low levels of cadmium. Lead is accumulated mainly in bone and increased endogenous lead exposure has been demonstrated in women during periods of increased bone turnover, e.g., menopause. Both lead and mercury exposure in pregnant women has to be kept low in order to prevent neurodevelopment effects in the developing fetus and child. Limited data indicate that women are more affected than men following exposure to methylmercury at adult age, while males seem to be more sensitive to exposure during early development. Regarding arsenic, some data indicate gender differences in the biotransformation by methylation, possibly also in susceptibility to certain arsenic-related cancers. Obviously, gender-related differences in exposure and health effects caused by metals are highly neglected research areas, which need considerable focus in the future.

Arsenic↗

PubMed2002

Methionine homozygosity at codon 129 in the prion protein is associated with white matter reduction and enlargement of CSF compartments in healthy volunteers and schizophrenic patients.

Twin studies point toward a substantial heritability in individual variations in the size of the human brain. However, the etiology is largely unknown. The prion protein (gene name: PRNP) aids cellular resistance to oxidative stress and neurodegeneration and is involved in neurodevelopment. This study examines the influence of a polymorphism in the PRNP gene on brain morphology in 47 healthy males and 43 male schizophrenic patients. All subjects underwent identical MRI scanning sessions followed by segmentation in cerebrospinal fluid (CSF), gray and white matter tissue, and genotyping for a biallelic polymorphism in PRNP (Met129Val). Genotype and allele frequencies did not differ between schizophrenic patients and controls but the polymorphism was associated with white matter tissue reduction (P = 0.024) and enlargement of CSF compartments (P = 0.039). These findings suggest that homozygosity for methionine at codon 129 is associated with decreased white matter tissue and larger CSF volume in right-handed male healthy volunteers and schizophrenic patients. This, however, being a novel finding, should warrant further investigation.

Adolescent↗

PubMed2001

Acute exposure of cerebellar granule neurons to ethanol suppresses stress-activated protein kinase-1 and concomitantly induces AP-1.

The current studies were designed to examine the mechanisms of acute effects of ethanol on cerebellar granule neurons (CGNs) during neurodevelopment, with specific reference to activator protein-1 (AP-1). CGNs, isolated from 3-day-old Sprague-Dawley rats and cultured for 3 days, were exposed to 0, 22.5, and 100 mM ethanol for 1 h. Gel shift assays performed on the nuclear protein extracts showed increased AP-1 and heat shock factor-1 (HSF-1) transcriptional activation in response to ethanol. Western blots and RT-PCR showed increased c-JUN and phosphorylated c-JUN (serine 73) protein, as well as c-jun mRNA. Ethanol paradoxically decreased the activity of stress-activated protein kinase-1 (SAPK-1) while increasing p44 and p42 mitogen-activated protein kinase (MAPK) activity. The protein synthesis-inhibiting and SAPK-1 activity-inducing antibiotic, anisomycin (30 and 500 microM) decreased AP-1 transcriptional activation to 47 and 23% of control values, respectively. The anisomycin effect was enhanced in the presence of 100 mM ethanol. Similarly, cycloheximide decreased ethanol-induced AP-1 transcriptional activation. Pretreatment with the MAPK kinase (MEK) pathway inhibitor PD98059 resulted in decreases in both ethanol-induced and control AP-1 DNA binding. Thus this acute ethanol-induced increased AP-1 transcriptional activation requires protein synthesis and involves MEK-independent increased MAPK phosphorylation, on the one hand, and decreased SAPK-1 activity on the other. The ethanol effect is thus ascribed to the activities of alternate kinase pathways and/or the inhibition of (a) protein phosphatase(s). Exposure of CGNs to ethanol for 24 h resulted in decreased AP-1 DNA binding, an observation that could have consequences for overall neuronal function under chronic exposure conditions.

Animals↗

PubMed1991

Surgical treatment and long-term neurodevelopmental outcome for infants with idiopathic aqueductal stenosis.

Evaluation of in utero shunting for fetal ventriculomegaly requires an analysis of the ex utero treatment of a comparison population of infants with idiopathic aqueductal stenosis (IAS). In this study, 14 neonates with IAS were followed with detailed developmental assessment profiles for 18 months or longer. Using magnetic resonance imaging, the preoperative and postoperative frontal cortical mantle widths (FCMW) were determined for each patient. Four of 14 children demonstrated normal outcomes while 5 of 14 children showed abnormal outcomes. The remaining 5 children demonstrated minimally impaired outcomes. No child with a postoperative FCMW below 30 mm showed normal development on any scale, while all children with abnormal development demonstrated a postoperative FCMW of 21 mm or less. In conclusion, the prognosis for normal long-term neurodevelopment in infants with IAS, despite prompt ex utero treatment, is guarded; the majority of such children will show developmental delays of varying degrees. The FCMW serves as a reasonable prognostic indicator in this patient population.

Cerebral Aqueduct↗

PubMed1994

Teratogenic effects in a case of maternal treatment for acute myelocytic leukaemia--neonatal and infantile course.

Experience with the use of cytotoxic drugs in the first trimester of pregnancy is limited. We report on the clinical phenotype and infantile development of a girl born to a 36-year-old mother. Before recognition of pregnancy, the latter had been treated for acute myelocytic leukaemia receiving cytarabine, daunorubicin and doxorubicin at conception and cytarabine and thioguanine at about 35-37 days post conception. At delivery, there were severe brachycephaly, hypoplasia of the anterior cranial base and the midface as well as synostoses of both coronal and metopic sutures. Further findings included bilateral four-finger hands with hypoplastic thumbs and absent radii. This phenotype is reminiscent of the Baller-Gerold syndrome. The child, at present 15 months old, has had to undergo two operations for fronto-orbital advancement because of insufficient growth of the mid-face, nasal airway hypoplasia and increased intracranial pressure. Motor milestones are slightly retarded--neurodevelopment is otherwise normal. These findings are discussed in the context of the few previous reports and are particularly important for future genetic counselling.

Abnormalities, Drug-Induced↗

PubMed2003

Renal transplantation.

Renal transplantation offers the best renal replacement therapy for most children with end stage renal disease improving their potential for growth and nutrition, neurodevelopment and quality of life. Advances in organ retrieval and preservation, improved surgical techniques, newer immunosuppressive drugs and prevention and treatment of infections have significantly improved patient and graft survival. The absolute requirements for a transplant are compatible blood group and a negative cytotoxic crossmatch. The immunosuppressive drugs most often used are cyclosporin A (or tacrolimus), azathioprine (or mycophenolate mofetil) and prednisone. Complications following transplantation include episodes of acute rejection, serious bacterial and viral infections, hypertension and recurrence of primary disease in the allograft. Each centre must have standard protocols for pre-transplant evaluation, management of immunosuppression and prevention of infections. Socio-economic factors should be carefully evaluated before offering transplantation to children in developing countries. Preemptive transplantation from a living donor may be a more viable option for these children.

Child↗

PubMed1993

Neuropeptides as growth and differentiation factors in general and VIP in particular.

During the course of neurodevelopment a large population of neurons die normally (Berg, 1982; Oppenheim et al., 1989). Are neuropeptides involved in the regulation of neuronal survival, maturation, and maintenance? The peptides are an ever growing family of neuroactive agents and this review shall emphasize VIP (vasoactive intestinal peptide [Said and Mutt, 1970; Gozes and Brenneman, 1989]), which has been shown to be involved in maturation, growth, and maintenance of neurons (Brenneman et al., 1985a, 1987, 1988, 1990, 1990b; Brenneman and Eiden, 1986; Brenneman and Nelson, 1986). Comparative actions of other neuropeptides will also be discussed.

Animals↗

PubMed2004

Zinc in child health and disease.

Zinc deficiency is common in children from developing countries due to lack of intake of animal foods, high dietary phytate content, inadequate food intake and increased fecal losses during diarrhea. Zinc has a fundamental role in cellular metabolism, with profound effects on the immune system and the intestinal mucosa. Zinc supplementation has shown significant benefits in prevention and treatment of diarrhea and pneumonia. Routine zinc supplementation given to low birth weight babies for a year has resulted in substantial reduction in mortality. Zinc deficiency may have adverse effects on physical growth and neurodevelopment. WHO Task Force, 2001, and the National task Force of IAP has recommended use of zinc in the treatment of diarrhea. It is also recommended as part of standard case management in persistent diarrhea and in those with severe malnutrition. Further evidence is required for qualifying its use in treatment of other infective diseases like pneumonia and malaria. Improved dietary quality & intake, food fortification and cultivation of zinc dense plants are some ways of mitigating zinc deficiency.

Child↗

PubMed2004

Gene-environment interplay in schizopsychotic disorders.

Genetic studies have sought to identify subtypes or endophenotypes of schizophrenia in an effort to improve the reliability of findings. A number of chromosomal regions or genes have now been shown to have had replicated linkage to schizophrenia susceptibility. Molecules involved in neurodevelopment or neurotransmitter function are coded by many of the genes that have been implicated in schizophrenia. Studies of neurotransmitter function have identified, among others, a possible role for GABA, glutamate and dopamine in animal models of schizophrenia. GABA neurons that co-express the calcium binding protein parvalbumin have been implicated as have glutamatergic metabotropic receptors and dopamine D3 receptors. Stress influences glutamate and dopamine providing another environmental factor that may interact with the influence of genes on neurotransmitter function. Neurotransmitter interactions include influences on signaling molecules and these too have been implicated in forms of learning thought to be affected in schizophrenia. Results continue to unravel the interplay of genes and environment in the etiology of schizophrenia and other psychotic disorders.

Animals↗

PubMed2003

Brain sites of movement disorder: genetic and environmental agents in neurodevelopmental perturbations.

In assessing and assimilating the neurodevelopmental basis of the so-called movement disorders it is probably useful to establish certain concepts that will modulate both the variation and selection of affliction, mechanisms-processes and diversity of disease states. Both genetic, developmental and degenerative aberrations are to be encompassed within such an approach, as well as all deviations from the necessary components of behaviour that are generally understood to incorporate "normal" functioning. In the present treatise, both conditions of hyperactivity/hypoactivity, akinesia and bradykinesia together with a constellation of other symptoms and syndromes are considered in conjunction with the neuropharmacological and brain morphological alterations that may or may not accompany them, e.g. following neonatal denervation. As a case in point, the neuroanatomical and neurochemical points of interaction in Attention Deficit and Hyperactivity disorder (ADHD) are examined with reference to both the perinatal metallic and organic environment and genetic backgrounds. The role of apoptosis, as opposed to necrosis, in cell death during brain development necessitates careful considerations of the current explosion of evidence for brain nerve growth factors, neurotrophins and cytokines, and the processes regulating their appearance, release and fate. Some of these processes may possess putative inherited characteristics, like alpha-synuclein, others may to greater or lesser extents be endogenous or semi-endogenous (in food), like the tetrahydroisoquinolines, others exogenous until inhaled or injested through environmental accident, like heavy metals, e.g. mercury. Another central concept of neurodevelopment is cellular plasticity, thereby underlining the essential involvement of glutamate systems and N-methyl-D-aspartate receptor configurations. Finally, an essential assimilation of brain development in disease must delineate the relative merits of inherited as opposed to environmental risks not only for the commonly-regarded movement disorders, like Parkinson's disease, Huntington's disease and epilepsy, but also for afflictions bearing strong elements of psychosocial tragedy, like ADHD, autism and Savantism.

Ataxia↗

PubMed2003

Neurotoxicity of organomercurial compounds.

Mercury is a ubiquitous contaminant, and a range of chemical species is generated by human activity and natural environmental change. Elemental mercury and its inorganic and organic compounds have different toxic properties, but all them are considered hazardous in human exposure. In an equimolecular exposure basis, organomercurials with a short aliphatic chain are the most harmful compounds and they may cause irreversible damage to the nervous system. Methylmercury (CH(3)Hg(+)) is the most studied following the neurotoxic outbreaks identified as Minamata disease and the Iraq poisoning. The first description of the CNS pathology dates from 1954. Since then, the clinical neurology, the neuropathology and the mechanisms of neurotoxicity of organomercurials have been widely studied. The high thiol reactivity of CH(3)Hg(+), as well as all mercury compounds, has been suggested to be the basis of their harmful biological effects. However, there is clear selectivity of CH(3)Hg(+) for specific cell types and brain structures, which is not yet fully understood. The main mechanisms involved are inhibition of protein synthesis, microtubule disruption, increase of intracellular Ca(2+) with disturbance of neurotransmitter function, oxidative stress and triggering of excitotoxicity mechanisms. The effects are more damaging during CNS development, leading to alterations of the structure and functionality of the nervous system. The major source of CH(3)Hg(+) exposure is the consumption of fish and, therefore, its intake is practically unavoidable. The present concern is on the study of the effects of low level exposure to CH(3)Hg(+) on human neurodevelopment, with a view to establishing a safe daily intake. Recommendations are 0.4 micro g/kg body weight/day by the WHO and US FDA and, recently, 0.1 micro g/kg body weight/day by the US EPA. Unfortunately, these levels are easily attained with few meals of fish per week, depending on the source of the fish and its position in the food chain.

Animals↗

PubMed2001

Genetic predisposition and environmental causes in periodic and systematic catatonia.

The nosological heterogeneity of catatonic schizophrenia was the focus of a family study involving 139 catatonic patients. The clinical dichotomization of catatonia into periodic catatonia and systematic catatonia revealed good inter-rater reliability and stability of the diagnoses at follow-up. Analysis of the cumulative morbidity risk among first-degree relatives gave an excessive familial aggregation of homogenous psychoses in periodic catatonia with a risk of 26.9%. The mode of inheritance was consistent with an autosomal dominant model. In contrast, first-degree relatives of probands with systematic catatonia had a morbidity risk of 4.6%. Subsequent investigations pointed to a potential association of systematic catatonia to exposure to midgestational infections in the index cases and linked these sporadic disorders to disturbances of fetal neurodevelopment. The periodic catatonia, an unequivocally genetically transmitted illness, is at present under investigation in a genome-wide linkage analysis.

Catatonia↗

PubMed2002

Elevated methyl-CpG-binding protein 2 expression is acquired during postnatal human brain development and is correlated with alternative polyadenylation.

Rett syndrome is caused by mutations in MECP2 and characterized by arrested postnatal neurodevelopment. MECP2 is ubiquitously expressed, but its protein product, methyl-CpG-binding protein 2 (MeCP2), is highly expressed in a subpopulation of cells in the adult brain. Automated quantitation of MeCP2 expression on a human developmental tissue microarray was performed by laser scanning cytometry. A significant correlation between age and MeCP2 level, population heterogeneity, and percentage of MeCP2 high-expressing cells was specifically observed in cerebral but not renal samples. In contrast, an inverse correlation between use of the long 3' UTR of MECP2 and age was observed, suggesting that an acquired switch in polyadenylation is responsible for the elevated MeCP2. Acquired elevated MeCP2 expression in neurons beginning in infancy and progressing through childhood may explain the delayed onset and developmental arrest of Rett syndrome

Adolescent↗

PubMed2006

Di-(2-ethylhexyl)-phthalate affects lipid profiling in fetal rat brain upon maternal exposure.

Lipids, especially essential fatty acids (EFAs), play critical roles in guiding proper fetal development. Exposure to xenobiotics that may alter the fetal supply of EFAs/lipids could potentially lead to fetotoxicity. In this study, we investigated the effects of the peroxisome proliferator chemical, di-(2-ethylhexyl)-phthalate (DEHP), on the lipid metabolomic profile of the rat fetal brain upon maternal exposure during gestation. Female Sprague-Dawley rats were orally gavaged with a control vehicle or DEHP (1,500 mg/kg) from gestational day (GD) 0 to GD 19 and fetal brain tissue was isolated at GD 20. The concentrations of 11 lipid classes [free fatty acid, free cholesterol (FC), cholesterol ester (CE), diacylglycerol (DAG), triacylglyceride, phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine (PS), lysophosphatidylcholine (LYPC), cardiolipin, and sphingomyelin (SM)] were determined, as well as the differences in the composition of individual fatty acids. The total lipid concentration decreased with DEHP exposure, particularly for FC and SM, by 33 and 54%, respectively. The same trend was observed in the fatty acid compositions, particularly the unsaturated fatty acids, where a greater decrease was observed with longer fatty acid chain length. The compositions of docosahexaenoic acid decreased significantly in five lipid classes (P < 0.05), including CE (43%), DAG (60%), PS (33%), LYPC (35%), and SM (40%). In contrast, the most remarkable reduction of arachidonic acid presented in two lipid classes, CE and LYPC, with a decrease of up to 33%. These results suggest that in utero exposure to DEHP alters the lipid metabolome in the fetal brain, which may lead to aberrant neurodevelopment.

Analysis of Variance↗

PubMed2004

The hippocampus in schizophrenia: a review of the neuropathological evidence and its pathophysiological implications.

This paper puts the case for the hippocampus as being central to the neuropathology and pathophysiology of schizophrenia. The evidence comes from a range of approaches, both in vivo (neuropsychology, structural and functional imaging) and post mortem (histology, morphometry, gene expression, and neurochemistry). Neuropathologically, the main positive findings concern neuronal morphology, organisation, and presynaptic and dendritic parameters. The results are together suggestive of an altered synaptic circuitry or "wiring" within the hippocampus and its extrinsic connections, especially with the prefrontal cortex. These changes plausibly represent the anatomical component of the aberrant functional connectivity that underlies schizophrenia. Glutamatergic pathways are prominently but not exclusively affected. Changes appear somewhat greater in the left hippocampus than the right, and CA1 is relatively uninvolved compared to other subfields. Hippocampal pathology in schizophrenia may be due to genetic factors, aberrant neurodevelopment, and/or abnormal neural plasticity; it is not due to any recognised neurodegenerative process. Hippocampal involvement is likely to be associated with the neuropsychological impairments of schizophrenia rather than with its psychotic symptoms.

Animals↗

PubMed2006

Neonatal treatment with a competitive NMDA antagonist results in response-specific disruption of conditioned fear in preweanling rats.

RATIONALE: The N-methyl-D-aspartate (NMDA) receptor has been implicated in processes of neurodevelopment, including cell proliferation, synaptogenesis, and apoptosis. Several studies have reported that administration of NMDA antagonists early in development can cause long-lasting changes in behavior. For example, Gould and Cameron [Behav Neurosci 111:49-56 (1997a)] have shown that a single injection of the competitive NMDA antagonist CGP 43487 on postnatal day (PD) 5 affected behavioral immobility in young rats exposed to the odor of a natural predator. OBJECTIVES: This experiment was undertaken to determine whether the behavioral effects previously reported would also be seen with conditioned cues. Both stimulus-elicited behavioral immobility (freezing) and changes in heart rate were recorded to examine impairments in responding across multiple measures. METHODS: Animals were given a single injection of 0, 2.5, or 5.0 mg/kg CGP 43487 on PD 5. On PD 20 subjects were given paired or unpaired presentations of either an olfactory or auditory conditioned stimulus (CS) with a 110-dB-white-noise unconditioned stimulus. CS-elicited freezing and changes in heart rate were measured. RESULTS: Pups treated with CGP exhibited impairments in conditioned freezing, but were unaffected in their expression of conditioned changes in heart rate, to both olfactory and auditory stimuli. CONCLUSIONS: These results indicate that neonatal treatment with an NMDA antagonist affects the expression of fear in a response-specific manner. The data suggest that antagonist-induced alterations in neural systems involved in the expression of freezing are affected by NMDA receptor blockade early in life.

2-Amino-5-phosphonovalerate↗

PubMed1999

Late neurosonographic screening is important to the diagnosis of periventricular leukomalacia and ventricular enlargement in preterm infants.

BACKGROUND: Recent cost-containment strategies suggest limiting screening neurosonograms to the second week of life in premature infants with lower gestational ages (< 30 weeks), birth weights (< 1250 g), or more complicated clinical courses. OBJECTIVE: To determine if such strategies reduce detection of cystic periventricular leukomalacia (cPVL) and persistent ventricular enlargement (pVE)--late sonographic abnormalities highly predictive of adverse neurodevelopment in preterm infants. METHODS: Timing, findings, and number of neurosonograms were reviewed for all survivors born at < or = 32 weeks' gestation at University Hospital, Denver, Colo., between January 1992 and June 1995. RESULTS: Of 236 surviving infants, 61 (26%) were never scanned, and 175 (74%) had a total of 432 scans. Only 106 infants (45%) had a neurosonogram on or after 28 days (timed to detect all cPVL/pVE). Eleven infants (4.7%) had cPVL, and 19 (8%) had pVE. Severity of clinical course did not predict development of cPVL, but was a better predictor of pVE. Initial neurosonograms were normal in 6/11 (55%) with cPVL and 5/19 (26%) with pVE. Screening declined from 86% of infants in 1992 (average 2.54 neurosonograms each), to 64% by 1994-1995 (average of 2.22 neurosonograms each). Infants > 30 weeks' gestation comprised 55 of 61 patients without any neurosonograms (90%), 4 of 11 patients with cPVL (36%), and 4 of 19 patients with pVE (21%). CONCLUSION: Screening neurosonography has declined from 1992 to 1995, particularly in larger premature infants (30-32 weeks' gestation) who remain at risk for cPVL and pVE. Clinical course or results of initial studies do not always predict the development of these late abnormalities. We recommend that one neurosonogram be done at > or = 4 weeks of age in all premature infants < or = 32 weeks' gestation, regardless of birth weight, clinical course, or results of prior studies. An earlier neurosonogram should be obtained for infants < 30 weeks' gestation in the second week of life to detect complications of intracranial hemorrhage.

Birth Weight↗