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Neurodevelopment
Kinds of Neurodevelopment Selected AbstractsNEURODEVELOPMENT AND PRENATAL ALCOHOL CONSUMPTIONADDICTION, Issue 8 2009RON GRAY No abstract is available for this article. [source] Neurodevelopment of infants with end-stage renal disease: Is it improving?PEDIATRIC TRANSPLANTATION, Issue 1 2002Bradley A. Warady MD No abstract is available for this article. [source] Poster session 1: Neurodevelopment and movement disorders (P39,P70)ANNALS OF NEUROLOGY, Issue S11 2007Article first published online: 29 AUG 200 First page of article [source] Poster session 2: Nursing (P136); Neuromuscular (P137,P140); Neurodevelopment (P141,P142)ANNALS OF NEUROLOGY, Issue S11 2007Article first published online: 29 AUG 200 No abstract is available for this article. [source] Impact of chorioamnionitis and preeclampsia on neurodevelopmental outcome in preterm infants below 32 weeks gestational ageACTA PAEDIATRICA, Issue 10 2010Luregn J Schlapbach Abstract Aim:, Intrauterine conditions may interfere with foetal brain development. We compared the neurodevelopmental outcome between infants <32 weeks gestational age after maternal preeclampsia or chorioamnionitis and controls. Methods:, Case-control study on infants with maternal preeclampsia, chorioamnionitis and controls (each n = 33) matched for gestational age. Neurodevelopment at 2 years was assessed with the Bayley Scales of Infant Development II. Results:, A total of 99 infants were included with a median gestational age of 29 weeks (range 25,32). Median mental developmental index (MDI) was 96 in the control, 90 in the chorioamnionitis and 86 in the preeclampsia group. Preeclampsia infants had a lower MDI compared with the control group (univariate p = 0.021, multivariate p = 0.183) and with the chorioamnionitis group (univariate p = 0.242; multivariate p = 0.027). Median psychomotor index was 80.5 in the control, 80 in the preeclampsia and 85 in the chorioamnionitis group and was not different between these three groups (p > 0.05). Chorioamnionitis or preeclampsia exposure was not associated with major neurodevelopmental impairments (cerebral palsy, MDI<70, PDI<70). Conclusion:, The results of this preliminary study suggest that preeclampsia and chorioamnionitis play a relatively minor role among risk factors for adverse neurodevelopment outcome. Postnatal factors such as ventilation and bronchopulmonary dysplasia may have a greater impact on neurodevelopmental outcome. [source] Neurodevelopment of children born very preterm and free of severe disabilities: the Nord-Pas de Calais Epipage cohort studyACTA PAEDIATRICA, Issue 5 2010ML Charkaluk Abstract Aim:, To describe the development of very preterm children free of cerebral palsy or severe sensory impairment in the domains of gross and fine motor functions, language and sociability at a corrected age of 2 years; to identify factors associated with performances in each domain. Methods:, A total of 347 children born in 1997 before 33 weeks of gestation, part of the EPIPAGE population-based cohort study, had their psychomotor development assessed with the Brunet-Lezine scale. Results:, The study population had a mean gestational age of 30.1 ± 2.0 weeks. Lower developmental quotients (DQ) were observed in the study group compared to the reference sample (96 ± 13 vs 104 ± 8, p < 0.01). Fine motor function, language and sociability were all affected with a p value <0.01. Multivariate analysis showed that duration of intubation and parents' educational and occupational levels were the only variables significantly related to each developmental domain (p < 0.01). Conclusions:, Children very preterm and free of severe disabilities had mild delays in multiple areas of development. The mechanisms by which neonatal factors played a role need further investigation. However socioeconomic status had a great impact on development and our results underline the need for improved support of socioeconomically disadvantaged parents after a preterm birth. [source] Orexins/hypocretins and orexin receptors in apoptosis: a mini-reviewACTA PHYSIOLOGICA, Issue 3 2010M. Laburthe Abstract An unexpected and fascinating aspect of the neuropeptides orexins has recently emerged when it was shown that orexins acting at orexin receptors OX1R or OX2R induce dramatic apoptosis resulting in massive reduction in cell growth in various cancer cell lines. This mini-review will provide the reader with recent findings related to the proapoptotic actions of orexins and the entirely novel mechanism whereby the seven membrane-spanning G-protein-coupled receptor (GPCR) OX1R triggers apoptosis. Recent data show that orexins induce tyrosine phosphorylation of the tyrosine-based motifs , immunoreceptor tyrosine-based inhibitory motif and immunoreceptor tyrosine-based switch motif , in OX1R. These phosphorylations result in the recruitment and activation of the phosphotyrosine phosphatase SHP-2 and subsequent cytochrome c -mediated mitochondrial apoptosis. Finally, this mini-review will also speculate on: (1) the potential importance of tyrosine-based motifs in the large family of GPCRs; (2) the interest of orexin receptors as therapeutic targets in cancer therapy; (3) the possible role of orexin receptor-mediated apoptosis in physiology and pathophysiology in the brain (neurodevelopment, neurodegenerative diseases) and in the periphery. [source] A novel ARX phenotype: rapid neurodegeneration with Ohtahara syndrome and a dyskinetic movement disorderDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 3 2010MICHAEL ABSOUD ARX mutations are associated with variable clinical phenotypes. We report a new neurodegenerative phenotype associated with a known ARX mutation and causing early abnormal neurodevelopment, a complex movement disorder, and early infantile epileptic encephalopathy with a suppression-burst pattern (Ohtahara syndrome). A male infant presented at age 5 months with a dyskinetic movement disorder, which was initially diagnosed as infantile spasms. Clinical deterioration was accompanied by progressive cortical atrophy with a reduction in white matter volume and resulting in death in the first year of life; such a rapidly progressive and severe phenotype has not previously been described. ARX mutation testing should be undertaken in children aged less than 1 year with Ohtahara syndrome and a movement disorder, and in infants with unexplained neurodegeneration, progressive white matter loss, and cortical atrophy. [source] Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturationDEVELOPMENTAL PSYCHOBIOLOGY, Issue 3 2008Lauren M. Ellman Abstract The purpose of the study was to determine the specific periods during pregnancy in which human fetal exposure to stress hormones affects newborn physical and neuromuscular maturation. Blood was collected from 158 women at 15, 19, 25, and 31 weeks' gestation. Levels of placental corticotropin-releasing hormone (CRH) and maternal cortisol were determined from plasma. Newborns were evaluated with the New Ballard Maturation Score. Results indicated that increases in maternal cortisol at 15, 19, and 25 weeks and increases in placental CRH at 31 weeks were significantly associated with decreases in infant maturation among males (even after controlling for length of gestation). Results also suggested that increases in maternal cortisol at 31 weeks were associated with increases in infant maturation among females, although these results were not significant after controlling for length of gestation. Findings suggest that stress hormones have effects on human fetal neurodevelopment that are independent of birth outcome. © 2008 Wiley Periodicals, Inc. Dev Psychobiol 50: 232,241, 2008. [source] Neuroprotection in emerging psychotic disordersEARLY INTERVENTION IN PSYCHIATRY, Issue 2 2007Gregor Berger Abstract Aim:, The emerging phase of psychotic disorders is pleomorphic and fluctuates in presentation. Hence, from a clinical perspective, treatment modalities are often unclear. This paper investigates the rational and potential use of neuroprotective agents in emerging psychotic disorders. Methods:, Medline databases were searched from 1966 to 2006 followed by the cross-checking of references using following keywords: neuroprotection, apoptosis, natural cell death, neurodevelopment, plasticity, neurogenesis, combined with brain and schizophrenia. Results:, Agents such as atypical antipsychotics, antidepressants, omega-3 fatty acids, modulators of glutamateric neurotransmission (e.g. ampakines, glycine, memantine), erythropoietin, N -acetylcysteine, COX-2 inhibitors or antioxidants have neuroprotective (anti-apoptotic) properties and may therefore be able to protect brain maturational processes disturbed in emerging psychotic disorders. Clinical trials suggest that atypical antipsychotics, antidepressants, omega-3 fatty acids and low-dose lithium as sole treatments were able to improve symptoms and functioning, and delay or in some cases even prevent the onset of frank psychosis. Initially these substances have been chosen because they have been used either as sole or augmentation treatments in established psychotic disorders. However, chronicity and already effective treatments may overshadow their potential clinical use in emerging (prodromal) psychosis. Conclusion:, Neuroprotection as a new treatment paradigm for at-risk mental states seems to be promising and pilot data are suggestive that more benign interventions may already be sufficient to delay or even prevent the onset of frank psychosis. A coordinated research effort will be necessary to address the question which agents should be used under which circumstances. [source] Alcohol consumption during pregnancy and its effects on neurodevelopment: what is known and what remains uncertainADDICTION, Issue 8 2009Ron Gray ABSTRACT It has been claimed that mothers' drinking during pregnancy may affect the neurodevelopment of around 1% of all children. If this is true, then prenatal alcohol exposure represents an important risk factor for neurodevelopmental problems, giving rise to a large burden of disability which could be potentially preventable. Evidence to support this idea has come from animal experiments and human observational studies. However, such findings need to be supported by more robust research designs. Because randomized controlled trials in this area are neither feasible nor ethical, suggestions are made for further research making more use of natural experiments. [source] IMAGING STUDY: Prefrontal cortex morphometry in abstinent adolescent marijuana users: subtle gender effectsADDICTION BIOLOGY, Issue 4 2009Krista Lisdahl Medina ABSTRACT Adult human studies suggest frontal dysfunction associated with chronic marijuana (MJ) use, but due to continued neuromaturation, adult studies may not generalize to adolescents. This study characterized prefrontal cortex (PFC) morphometry in chronic MJ-using adolescents following 1 month of monitored abstinence. Data were collected from MJ users (n = 16) and controls (n = 16) aged 16,18. Extensive exclusionary criteria included co-morbid psychiatric and neurologic disorders. Substance use and anatomical measures were collected after 28 days of monitored abstinence. PFC volumes were ascertained from manual tracing by reliable raters on high-resolution magnetic resonance images. After controlling for lifetime alcohol use, gender and intracranial volume, MJ users did not differ from controls in PFC volume. However, marginal group-by-gender interactions were observed (P < 0.09): female MJ users demonstrated comparatively larger PFC volumes while male MJ users had smaller volumes compared with same-gender controls. Further, group status and total PFC volume interacted in predicting executive functioning (P < 0.05). Among MJ users, smaller PFC total volume was associated with better executive functioning while the opposite pattern was seen among the controls. These preliminary results indicate that gender may moderate the relationship between MJ use and PFC morphometry. Given the relationship between larger PFC total volumes and poorer executive functioning among MJ users, female MJ users may be at increased risk for neurocognitive consequences. Future research will measure PFC gray and white matter separately and follow boys and girls over adolescence to examine the influence of MJ use on neurodevelopment. [source] PRECLINICAL STUDY: Different effects of chronic phencyclidine on brain-derived neurotrophic factor in neonatal and adult rat brainsADDICTION BIOLOGY, Issue 2 2006Jun'ichi Semba ABSTRACT The N-methyl-D-aspartate (NMDA) receptor and brain-derived neurotrophic factor (BDNF) are both known to play major roles in the normal development of the brain. We have hypothesized that the chronic blockade of NMDA with phencyclidine (PCP) may have a different effect on BDNF synthesis at different stages of development. In an acute experiment, rat pups and adult rats were injected with PCP (2.5, 5 or 10 mg/kg) at postnatal day (PD) 15 or 49, respectively. In a chronic experiment, rat pups were injected daily from PD 5 to PD 14 with PCP (2.5, 5 or 10 mg/kg), while adult rats were injected daily with the same dose from PD 39 to PD 48. BDNF levels in the hippocampus, striatum and frontal cortex were determined by ELISA assay 24 hours after the last injection. Chronic PCP treatment of neonatal rats induced a dose-dependent decrease in BDNF in the hippocampus but not in the frontal cortex and striatum. Single injection of PCP to rat pups showed a slight reduction of BDNF in the hippocampus but only at higher doses. In contrast to neonatal brain, neither acute nor chronic injection of PCP influenced BDNF in adult brain. These findings suggest that chronic blockade of NMDA receptor in the early neonatal period has an inhibitory effect on BDNF synthesis in the hippocampus and may impair normal neurodevelopment in rat pups. [source] A role for Connexin43 during neurodevelopmentGLIA, Issue 7 2007Amy E. Wiencken-Barger Abstract Connexin43 (Cx43) is the predominant gap junction protein expressed in premitotic radial glial cells and mature astrocytes. It is thought to play a role in many aspects of brain development and physiology, including intercellular communication, the release of neuroactive substances, and neural and glial proliferation and migration. To investigate the role of Cx43 in brain physiology, we generated a conditional knockout (cKO) mouse expressing Cre recombinase driven by the human GFAP promoter and a floxed Cx43 gene. The removal of Cx43 from GFAP-expressing cells affects the behavior of the mice and the development of several brain structures; however, the severity of the phenotype varies depending on the mouse background. One mouse subline, hereafter termed Shuffler, exhibits cellular disorganization of the cortex, hippocampus, and cerebellum, accompanied by ataxia and motor deficits. The Shuffler cerebellum is most affected and displays altered distribution and lamination of glia and neurons suggestive of cell migration defects. In all Shuffler mice by postnatal day two (P2), the hippocampus, cortex, and cerebellum are smaller. Disorganization of the ventricular and subventricular zone of the cortex is also evident. Given that these are sites of early progenitor cell proliferation, we suspect production and migration of neural progenitors may be altered. In conclusion, neurodevelopment of Shuffler/Cx43 cKO mice is abnormal, and the observed cellular phenotype may explain behavioral disturbances seen in these animals as well as in humans carrying Cx43 mutations. © 2007 Wiley-Liss, Inc. [source] Healthy babies for mothers with serious mental illness: A case management framework for mental health cliniciansINTERNATIONAL JOURNAL OF MENTAL HEALTH NURSING, Issue 6 2008Yvonne Hauck ABSTRACT Women with a serious mental illness (SMI), notably schizophrenia, bipolar disorder, and personality disorders are considered high risk for adverse pregnancy and birth outcomes, which in turn, are associated with poor neurodevelopment in the child. Failure to access antenatal care, poor adherence with folate supplementation, an unhealthy lifestyle, and inappropriate health decisions can contribute to poor outcomes. Many women with SMI continue contact with mental health services while pregnant. This primary prevention project aimed to develop a framework for community mental health clinicians to improve the reproductive health outcomes for women with SMI. The consultation process involved discussions with key stakeholders, an environmental scan to determine current service delivery issues, a literature review, and individual and group interviews with community mental health clinicians, consumers, general practitioners, and midwives. Three key elements underpin the framework: early detection and monitoring of pregnancy, providing reproductive choices, and implementing a ,small known team approach' in the management of the pregnant client. Specific modules within the framework focus upon establishing a professional support network, assessing the risk of pregnancy, the early detection of pregnancy, monitoring during pregnancy, preparing for birth, and planning for the postnatal period. Implementation of the framework has the potential to significantly improve obstetric and neonatal outcomes for this high-risk group. [source] The transcription factor ATF5: role in neurodevelopment and neural tumorsJOURNAL OF NEUROCHEMISTRY, Issue 1 2009Lloyd A. Greene Abstract We review recent findings regarding the properties of ATF5 and the major roles that this transcription factor plays in development of the nervous system and in survival of neural tumors. ATF5 is a widely expressed basic leucine zipper protein that has been subject to limited characterization. It is highly expressed in zones of neuroprogenitor cell proliferation. In vitro and in vivo studies indicate that it functions there to promote neuroprogenitor cell expansion and to suppress their differentiation into neurons or glia. ATF5 expression is down-regulated by trophic factors and this is required for their capacity to promote neuroprogenitor cell cycle exit and differentiation into either neurons, oligodendroglia or astrocytes. ATF5 is also highly expressed in a number of tumor types, including neural tumors such as neuroblastomas, medulloblastomas and glioblastomas. Examination of the role of ATF5 in glioblastoma cells indicates that interference with its expression or activity causes them to undergo apoptotic death. In contrast, normal astrocytes and neurons do not appear to require ATF5 for survival, indicating that it may be a selective target for treatment of glioblastomas and other neural neoplasias. Further studies are needed to identify the transcriptional targets of ATF5 and the mechanisms by which its expression is regulated in neuroprogenitors and tumors. [source] Is the modulation of retinoid and retinoid-associated signaling a future therapeutic strategy in neurological trauma and neurodegeneration?JOURNAL OF NEUROCHEMISTRY, Issue 3 2008Andrea Malaspina Abstract The complex molecular pathways that mediate the effects of vitamin A and its derivatives, are increasingly recognized as a component of the repair capacity that could be activated to induce protection and regeneration in the mature nervous tissue. Retinoid and retinoid-associated signaling plays an essential role in normal neurodevelopment and appears to remain active in the adult CNS. In this paper, we review evidence which supports the hypothesis of an activation of retinoid-associated signaling molecular pathways in the mature nervous tissue and its significance in the context of neurodegenerative, trauma-induced and psychiatric disorders, at spinal and supra-spinal levels. Finally, we summarize the potential therapeutic avenues based on the modulation of retinoid targets undergoing reactivation under conditions of acute injury and chronic degeneration in the central nervous system, and discuss some of the unresolved issues linked to this treatment strategy. [source] Epigenetic modifications of SOX2 enhancers, SRR1 and SRR2, correlate with in vitro neural differentiation,JOURNAL OF NEUROSCIENCE RESEARCH, Issue 8 2008Marianna Sikorska Abstract SOX2 is a key neurodevelopmental gene involved in maintaining the pluripotency of stem cells and proliferation of neural progenitors and astroglia. Two evolutionally conserved enhancers, SRR1 and SRR2, are involved in controlling SOX2 expression during neurodevelopment; however, the molecular mechanisms regulating their activity are not known. We have examined DNA methylation and histone H3 acetylation at both enhancers in NT2-D1 progenitors, neurons and astrocytes, to establish the role of epigenetic mechanisms in cell-type-specific SOX2 expression. This study showed that 1) unmethylated DNA and acetylated histones at both enhancers correlated with a high level of SOX2 expression in proliferating neural progenitors and 2) reversible modifications of the SRR1 element were observed during gene reexpression in astrocytes, whereas permanent epigenetic marks on the SRR2 enhancer were seen in neurons where the gene was silenced. Taken together, these results are clear illustrations of cell-type-specific epigenomes and suggest mechanisms by which they may be created and maintained. © 2008 Wiley-Liss, Inc. [source] Exposure to lead elevates induction of zif268 and Arc mRNA in rats after electroconvulsive shock: The involvement of protein kinase CJOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2002Kyung-Ah Kim Abstract Exposure to lead is well known to impair cognitive function in young children. Because of the importance of gene regulation for neurodevelopment, we examined the effect of lead on the induction of the mRNA of the immediate early genes zif268 and Arc. The time course for the induction of zif268 mRNA and Arc mRNA by electroconvulsant shock (ECS) was altered in the area of the dentate gyrus of the hippocampus in rats exposed to lead from postnatal days (PND) 1 to 28. Other areas of the hippocampus were not affected by lead. The effects on the induction of zif268 mRNA were observed at blood lead levels as low as 12 ,g/dl. No change in the induction of zif268 mRNA was observed in the hippocampus of rats exposed to lead from PND 28 to PND 56. Because of the possible involvement of protein kinase C (PKC) in the effect of lead, activation of different isoforms of PKC was investigated. An increase in the amount of PKC, and PKC, was observed at 60 min after ECS in the membrane fraction from hippocampus, indicating activation of these isoforms. The amount of PKC, in membranes was higher in rats exposed to lead than in rats not exposed to lead after ECS. Taken together, the data suggest that lead may disturb regulation of specific immediate early genes by activating PKC,. © 2002 Wiley-Liss, Inc. [source] Neurodevelopmental outcomes and surgery in neonatesJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 12 2006Karen Walker Abstract: A neonate requiring major surgery in 2006 has a greater prospect of survival than ever before. Increasingly, however, there is awareness that critical illness may affect later neurodevelopment. Pre-existing conditions in addition to the physiologic stresses associated with cardiac and general surgery are implicated but remain unavoidable in the case of significant structural abnormalities such as transposition of the great arteries or congenital diaphragmatic hernia. For those affected by neurodevelopmental impairment, there is a significant cost to the child, family and society. Current research focuses on the preventable causes of brain injury, before, during and after the intervention, and the rate of impairment in apparently uncomplicated procedures. In contrast to the quantity of neurodevelopmental outcome data following cardiac surgery, there remain few outcome studies dealing with non-cardiac surgery despite such intervention being two to three times more common. There appear to be compelling clinical and economic arguments for the instigation of formalised population-based developmental assessments for all infants undergoing major surgery. [source] Alcohol, Psychological Dysregulation, and Adolescent Brain DevelopmentALCOHOLISM, Issue 3 2008Duncan B. Clark While adolescent alcohol consumption has been asserted to adversely alter brain development, research in human adolescents has not yet provided us with sufficient evidence to support or refute this position. Brain constituents actively developing during adolescence include the prefrontal cortex, limbic system areas, and white matter myelin. These areas serving cognitive, behavioral, and emotional regulation may be particularly vulnerable to adverse alcohol effects. Alternatively, deficits or developmental delays in these structures and their functions may underlie liability to accelerated alcohol use trajectories in adolescence. This review will describe a conceptual framework for considering these relationships and summarize the available studies on the relationships among risk characteristics, alcohol involvement and brain development during this period. The cross-sectional designs and small samples characterizing available studies hamper definitive conclusions. This article will describe some of the opportunities contemporary neuroimaging techniques offer for advancing understanding of adolescent neurodevelopment and alcohol involvement. [source] Neuropsychologic status at the age 4 years and atopy in a population-based birth cohortALLERGY, Issue 9 2009J. Julvez Background:, Mental health has been reported to be associated with allergy, but only a few cohort studies have assessed if neurodevelopment predicts atopy. Objective:, To investigate if neurobehavioral status of healthy 4-year-old children was associated with specific immunoglobulin E (IgE) at the same age and skin prick test results 2 years later. Methods:, A population-based birth cohort enrolled 482 children, 422 of them (87%) provided neurobehavioral data, 341 (71%) had specific IgE measured at the age of 4 years; and 395 (82%) had skin prick tests completed at the age of 6 years. Atopy was defined as IgE levels higher than 0.35 kU/l to any of the three tested allergens at the age of 4 or as a positive skin prick test to any of the six tested allergens at the age of 6. McCarthy Scales of Child Abilities and California Preschool Social Competence Scale were the psychometric instruments used. Results:, Twelve percent of children at the age of 4 and 17% at the age of 6 were atopic. Neurobehavioral scores were negatively associated with 6-year-old atopy after adjustment for socio-demographic and allergic factors, A relative risk of 3.06 (95% CI: 1.30,7.24) was associated with the lowest tertile (scorings ,90 points) of the general cognitive scale. Similar results were found for verbal abilities, executive functions, and social competence. Asthma, wheezing, rhinitis, and eczema at the age of 6, but not at the age of 4, were associated with neurodevelopment at the age of 4. Conclusions:, Neuropsychologic functioning and later atopy are negatively associated in preschool age children. [source] Effect of vitamin B12 deficiency on neurodevelopment in infants: current knowledge and possible mechanismsNUTRITION REVIEWS, Issue 5 2008Daphna K Dror Severe vitamin B12 deficiency produces a cluster of neurological symptoms in infants, including irritability, failure to thrive, apathy, anorexia, and developmental regression, which respond remarkably rapidly to supplementation. The underlying mechanisms may involve delayed myelination or demyelination of nerves; alteration in the S-adenosylmethionine:S-adenosylhomocysteine ratio; imbalance of neurotrophic and neurotoxic cytokines; and/or accumulation of lactate in brain cells. This review summarizes the current knowledge concerning infantile vitamin B12 deficiency, including a pooled analysis of case studies of infants born to mothers with untreated pernicious anemia or a strict vegetarian lifestyle and a discussion of the mechanisms that may underlie the manifestations of deficiency. [source] Maternal use of folic acid supplements during pregnancy and four-year-old neurodevelopment in a population-based birth cohortPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 3 2009Jordi Julvez Summary The use of folic acid supplements during very early pregnancy is recommended in order to reduce the incidence of neural tube defects. Little is known about the possible benefits of folic acid on child neurodevelopment. A total of 420 children (87% of those eligible) from a birth cohort had complete data for final analyses at age 4 years. Information about folic acid and other over-the-counter dietary supplements was obtained prospectively using interviewer-administered questionnaires at the end of the first trimester of pregnancy. Psychological outcomes were assessed by two psychologists and teachers 4 years later. Low maternal socio-economic status, smoking, high parity and short duration of breast feeding were associated with lower prevalence of folic acid supplement use. Verbal (b = 3.98, SE = 1.69), motor (b = 4.54, SE = 1.66) and verbal-executive function (b = 3.97, SE = 1.68) scores, social competence (b = 3.97, SE = 1.61) and inattention symptom [OR = 0.46; 95% CI 0.22, 0.95] scores were associated with reported folic acid use. Reported folic acid supplement use during pregnancy was associated with improved neurodevelopment in children after adjusting for a number of sociodemographic and behavioural factors. [source] Prediction for developmental delay on Neonatal Oral Motor Assessment Scale in preterm infants without brain lesionPEDIATRICS INTERNATIONAL, Issue 1 2010Sen-Wei Tsai Abstract Background:, Preterm infants often have difficulty in achieving a coordinated sucking pattern. To analyze the correlation between preterm infants with disorganized sucking and future development, weekly studies were performed of 27 preterm infants from initiation of bottle feeding until a normal sucking pattern was recognized. Methods:, A total of 27 preterm infants without brain lesion participated in the present study. Neonatal Oral Motor Assessment Scale (NOMAS) was utilized to evaluate the sucking pattern. Infants who were initially assessed as having disorganized sucking on NOMAS and regained a normal sucking pattern by 37 weeks old were assigned to group I; infants with a persistent disorganized sucking pattern after 37 weeks were assigned to group II. The mental (MDI) and psychomotor (PDI) developmental indices of Bayley Scales of Infant Development, second edition were used for follow-up tests to demonstrate neurodevelopment at 6 months and 12 months of corrected age. Results:, At 6 months follow up, subjects in group I had a significantly higher PDI score than group II infants (P= 0.04). At 12 months follow up, group I subjects had a significantly higher score on MDI (P= 0.03) and PDI (P= 0.04). There was also a higher rate for development delay in group II at 6 months (P= 0.05). Conclusion:, NOMAS-based assessment for neonatal feeding performance could be a helpful tool to predict neurodevelopmental outcome at 6 and 12 months. Close follow up and early intervention may be necessary for infants who present with a disorganized sucking pattern after 37 weeks post-conceptional age. [source] Neuroscientific approaches and applications within anthropologyAMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY, Issue S47 2008James K. Rilling Abstract Many of the most distinctive attributes of our species are a product of our brains. To understand the function, development, variability, and evolution of the human brain, we must engage with the field of neuroscience. Neuroscientific methods can be used to investigate research topics that are of special interest to anthropologists, such as the neural bases of primate behavioral diversity, human brain evolution, and human brain development. Traditional neuroscience methods had to rely on investigation of postmortem brains, as well as invasive studies in living nonhuman primates. However, recent neuroimaging methods have made it possible to compare living human and nonhuman primate brains using noninvasive techniques such as structural and functional magnetic resonance imaging, positron emission tomography, and diffusion tensor imaging. These methods are providing an integrated picture of brain structure and function that was not previously available. With a combination of these traditional and modern neuroscience methods, we are beginning to explore and understand the neural bases of some of the most distinctive cognitive and behavioral attributes of the human species, including language, tool use, altruism, and mental self-projection, and we can now begin to propose plausible scenarios by which the neural substrates supporting these human specializations evolved from pre-existing neural circuitry serving related functions in common ancestors we shared with the living nonhuman primates. Consideration of the process of neurodevelopment suggests plausible mechanisms by which the highly encephalized human brain might have evolved. Neurodevelopmental studies also demonstrate that experience can shape both brain structure and function, providing a mechanism by which people of different cultures learn to act and think differently. Finally, not only can anthropologists benefit from neuroscience, neuroscience can benefit from the more sophisticated concept of evolution that anthropology offers, including an appreciation of evolutionary diversity as well as consideration of the process by which the human brain was formed during evolution. Yrbk Phys Anthropol 51:2,32, 2008. © 2008 Wiley-Liss, Inc. [source] Neurodevelopmental sequelae of postnatal maternal care in rodents: clinical and research implications of molecular insightsTHE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 3-4 2007Arie Kaffman Parental care plays an important role in the emotional and cognitive development of the offspring. Children who have been exposed to abuse or neglect are more likely to develop numerous psychopathologies, while good parent,infant bonding is associated with improved resiliency to stress. Similar observations have also been reported in non-human primates and rodents, suggesting that at least some neurodevelopmental aspects of parent,offspring interactions are conserved among mammals and could therefore be studied in animals. We present data to suggest that frequency of licking and grooming provided by the dam during a critical period in development plays an important role in modifying neurodevelopment. These findings are examined in the broader context in which exposure to other sensory modalities such as vision or hearing during a specific period in development shapes brain development with functional consequences that persist into adulthood. We also discuss recent rodent work showing that increased frequency of licking and grooming provided by the dam during the first week of life is associated with changes in DNA methylation of promoter elements that control expression of these genes and behavior. The stability of DNA methylation in postmitotic cells provides a possible molecular scaffold by which changes in gene expression and behavioral traits induced by postnatal maternal care are maintained throughout life. Finally, the relevance of findings reported in rodents to those noted in non-human primates and humans are assessed and the research and clinical implications of these observations for future work are explored. [source] Antenatal maternal stress and long-term effects on child neurodevelopment: how and why?THE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 3-4 2007Nicole M. Talge We review a significant body of evidence from independent prospective studies that if a mother is stressed while pregnant, her child is substantially more likely to have emotional or cognitive problems, including an increased risk of attentional deficit/hyperactivity, anxiety, and language delay. These findings are independent of effects due to maternal postnatal depression and anxiety. We still do not know what forms of anxiety or stress are most detrimental, but research suggests that the relationship with the partner can be important in this respect. The magnitude of these effects is clinically significant, as the attributable load of emotional/behavioral problems due to antenatal stress and/or anxiety is approximately 15%. Animal models suggest that activity of the stress-responsive hypothalamic-pituitary-adrenal (HPA) axis and its hormonal end-product cortisol are involved in these effects in both mother and offspring. The fetal environment can be altered if stress in the mother changes her hormonal profile, and in humans, there is a strong correlation between maternal and fetal cortisol levels. However, many problems remain in understanding the mechanisms involved in this interaction. For example, maternal cortisol responses to stress decline over the course of pregnancy, and earlier in pregnancy, the link between maternal and fetal cortisol is less robust. It is possible that the effects of maternal anxiety and stress on the developing fetus and child are moderated by other factors such as a maternal diet (e.g., protein load). It is suggested that extra vigilance or anxiety, readily distracted attention, or a hyper-responsive HPA axis may have been adaptive in a stressful environment during evolution, but exists today at the cost of vulnerability to neurodevelopmental disorders. [source] Altered inflammatory responses in preterm children with cerebral palsyANNALS OF NEUROLOGY, Issue 2 2010Chang-Yi Lin BS Objective Perinatal inflammatory responses contribute to periventricular leukomalacia (PVL) and cerebral palsy (CP) in preterm infants. Here, we examined whether preterm children with CP had altered inflammatory responses when school-aged. Methods Thirty-two preterm children with PVL-induced CP (mean [±standard deviation] age, 7.2 ± 3.6 years) and 32 control preterm children with normal neurodevelopment (6.2 ± 2.2 years) and matched for gestational age were recruited. We measured tumor necrosis factor (TNF)-, levels in the plasma and the supernatants of peripheral blood mononuclear cells (PBMCs) before and after lipopolysaccharide (LPS) stimulation, and proinflammatory gene expression in the PBMCs. Results TNF-, expression was significantly higher in the plasma (p < 0.001) and supernatants of LPS-stimulated PBMCs (p = 0.003) in the CP group than in the control group. After LPS stimulation, the intracellular TNF-, level in the PBMCs was significantly lower in the control group (p = 0.016) and significantly higher in the CP group (p = 0.01). The CP group also had, in their nonstimulated PBMCs, significantly higher mRNA levels of inflammatory molecules: toll-like receptor 4 (TLR-4) (p = 0.0023), TNF-, (p = 0.0016), transforming growth factor-,,activated kinase 1 (p = 0.038), I,B kinase-, (p = 0.029), and c-Jun N-terminal kinase (p = 0.045). The TLR-4 mRNA levels in the PBMCs were highly correlated with TNF-, levels in LPS-stimulated PBMCs (Spearman rank correlation = 0.38, p = 0.03). Interpretation The finding that preterm children with PVL-induced CP have altered inflammatory responses indicates the possibility of programming effect of PVL or inflammation-related events during early life. ANN NEUROL 2010;68:204,212 [source] Leptin leads hypothalamic feeding circuits in a new directionBIOESSAYS, Issue 10 2004Joanne A. Harrold A decade ago, leptin (from the greek lepto meaning ,thin') was identified as the product of the ob gene.1 This adipocyte-derived hormone was found to suppress feeding and stimulate thermogenesis, and was thus proposed as a mediator in a negative feedback loop that controls body adiposity. This discovery led to a rapid revolution in the understanding of neurobiological mechanisms regulating obesity. However, while leptin's first life was as an adipostat, it is now known to have a wide range of additional neuroendocrine, metabolic and behavioural functions in the CNS and periphery. Remarkably, the pleiotropic nature of the hormone continues to be extended with the recent publication of two papers that expand on leptin's neurobiological actions in the CNS.2,3 They indicate novel regulatory roles for the hormone in both synaptic plasticity and axon guidance. Crucially, in light of the rising incidence of obesity in modern society, both of the studies reveal leptin-mediated links between nutrition and neurodevelopment, findings that have further implications for leptin's role in the regulation of energy homeostasis. BioEssays 26:1043,1045, 2004. © 2004 Wiley Periodicals, Inc. [source] |