Relevant bibliographies by topics / Neurodevelopmental

Academic literature on the topic 'Neurodevelopmental'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Neurodevelopmental"

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Given, Joanne, Rebecca L. Bromley, Florence Coste, Sandra Lopez-Leon, and Maria Loane. "An inventory of European data sources to support pharmacoepidemiologic research on neurodevelopmental outcomes in children following medication exposure in pregnancy: A contribution from the ConcePTION project." PLOS ONE 17, no. 10 (October 14, 2022): e0275979. http://dx.doi.org/10.1371/journal.pone.0275979.

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Background Studies on medication safety in pregnancy are increasingly focusing on child neurodevelopmental outcomes. Establishing neurodevelopmental safety is complex due to the range of neurodevelopmental outcomes and the length of follow-up needed for accurate assessment. The aim of this study was to provide an inventory of European data sources for use in pharmacoepidemiologic studies investigating neurodevelopment following maternal medication exposure. Method The EUROmediSAFE inventory of data sources in Europe for evaluating perinatal and long-term childhood risks associated with in-utero exposure to medication was updated by contacting colleagues across 31 European countries, literature review and internet searches. Included data sources must record at least one neurodevelopmental outcome and maternal medication use in pregnancy must be available, either in the data source itself or through linkage with another data source. Information on the domain of neurodevelopment, measure/scale used and the approach to measurement were recorded for each data source. Results Ninety data sources were identified across 14 countries. The majority (63.3%) were created for health surveillance and research with the remaining serving administrative purposes (21.1% healthcare databases,15.6% other administrative databases). Five domains of neurodevelopment were identified—infant development (36 data sources,13 countries), child behaviour (27 data sources, 10 countries), cognition (29 data sources, 12 countries), educational achievement (20 data sources, 7 countries), and diagnostic codes for neurodevelopmental disorders (42 data sources, 11 countries). Thirty-nine data sources, in 12 countries, had information on more than one domain of neurodevelopment. Conclusion This inventory is invaluable to future studies planning to investigate the neurodevelopmental impact of medication exposures during pregnancy. Caution must be used when combining varied approaches to neurodevelopment outcome measurement, the age of children in the data source, and the sensitivity and specificity of the outcome measure selected should be borne in mind.
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Sood, Erica, Jeffrey P. Jacobs, and Bradley S. Marino. "Optimising neurodevelopmental and psychosocial outcomes for survivors with CHD: a research agenda for the next decade." Cardiology in the Young 31, no. 6 (June 2021): 873–75. http://dx.doi.org/10.1017/s1047951121002171.

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AbstractNeurodevelopmental and psychosocial impairments negatively impact health-related quality of life for survivors with CHD and complicate the transition to independent adulthood. Risk for neurodevelopmental and psychosocial impairments is influenced by a complex interplay among genetic, foetal, surgical, perioperative, family, and social factors, requiring a multi-pronged approach to neuroprotection and intervention. To ensure future research can ultimately reduce the burden of CHD for individuals, families, and society, the most pressing issues in cardiac neurodevelopment requiring scientific investigation must be identified.Through funding from an R13 Grant from the National Heart, Lung, and Blood Institute of the National Institutes of Health of the United States of America, the Cardiac Neurodevelopmental Outcome Collaborative convened a two-day meeting of international experts in cardiac neurodevelopmental and psychosocial research, clinical care, and health disparities, including patient and family stakeholders, to define the cardiac neurodevelopmental and psychosocial outcomes research agenda for the next decade. Seven multidisciplinary working groups were formed to address key domains crucial to the advancement of cardiac neurodevelopmental and psychosocial outcomes research: 1) Foetal Brain Development and Neuroprotection, 2) Surgical/Perioperative Neuroprotection and Neurodevelopment, 3) Characterization of Neurodevelopmental and Psychological Outcomes, 4) Neurodevelopmental and Psychosocial Intervention, 5) Parent Mental Health and Family Functioning, 6) Neurodevelopmental Education, Outreach and Advocacy, and 7) Health Disparities and Neurodevelopmental Outcomes. Working groups identified significant gaps in knowledge and critical questions that must be answered to further knowledge, policy, care, and outcomes. The development of a research agenda in cardiac neurodevelopmental and psychosocial outcomes is critical for informing collaborative initiatives and allocation of funding for research to scientific inquiries of highest value to key stakeholders.
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Chebet, Martin, Milton W. Musaba, David Mukunya, Brian Makoko, Agnes Napyo, Ritah Nantale, Proscovia Auma, et al. "High Burden of Neurodevelopmental Delay among Children Born to Women with Obstructed Labour in Eastern Uganda: A Cohort Study." International Journal of Environmental Research and Public Health 20, no. 4 (February 16, 2023): 3470. http://dx.doi.org/10.3390/ijerph20043470.

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Over 250 million infants in low and middle-income countries do not fulfill their neurodevelopment potential. In this study, we assessed the incidence and risk factors for neurodevelopmental delay (NDD) among children born following obstructed labor in Eastern Uganda. Between October 2021 and April 2022, we conducted a cohort study of 155 children (aged 25 to 44 months), born at term and assessed their neurodevelopment using the Malawi Developmental Assessment Tool. We assessed the gross motor, fine motor, language and social domains of neurodevelopment. The incidence of neurodevelopmental delay by 25 to 44 months was 67.7% (105/155) (95% CI: 59.8–75.0). Children belonging to the poorest wealth quintile had 83% higher risk of NDD compared to children belonging to the richest quintile (ARR (Adjusted Risk Ratio): 1.83; 95% CI (Confidence Interval): [1.13, 2.94]). Children fed the recommended meal diversity had 25% lower risk of neurodevelopmental delay compared to children who did not (ARR: 0.75; 95% CI: [0.60, 0.94]). Children who were exclusively breastfed for the first 6 months had 27% lower risk of neurodevelopmental delay compared to children who were not (ARR: 0.73; 95% CI: [0.56, 0.96]). We recommend that infants born following obstructed labor undergo neurodevelopmental delay screening.
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Miller, Thomas A., Anjali Sadhwani, Jacqueline Sanz, Erica Sood, Dawn Ilardi, Jane W. Newburger, Caren S. Goldberg, David Wypij, J. William Gaynor, and Bradley S. Marino. "Variations in practice in cardiac neurodevelopmental follow-up programs." Cardiology in the Young 30, no. 11 (October 23, 2020): 1603–8. http://dx.doi.org/10.1017/s1047951120003522.

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AbstractOver the last two decades, heart centres have developed strategies to meet the neurodevelopmental needs of children with congenital heart disease. Since the publication of guidelines in 2012, cardiac neurodevelopmental follow-up programmes have become more widespread. Local neurodevelopmental programmes, however, have been developed independently in widely varying environments. We sought to characterise variation in structure and personnel in cardiac neurodevelopmental programmes. A 31-item survey was sent to all member institutions of the Cardiac Neurodevelopmental Outcome Collaborative. Multidisciplinary teams at each centre completed the survey. Responses were compiled in a descriptive fashion. Of the 29 invited centres, 23 responded to the survey (79%). Centres reported more anticipated neurodevelopment visits between birth and 5 years of age (median 5, range 2–8) than 5–18 years (median 2, range 0–10) with 53% of centres lacking any standard for routine neurodevelopment evaluations after 5 years of age. Estimated annual neurodevelopment clinic volume ranged from 85 to 428 visits with a median of 16% of visits involving children >5 years of age. Among responding centres, the Bayley Scales of Infant and Toddler Development and Wechsler Preschool and Primary Scale of Intelligence were the most routinely used tests. Neonatal clinical assessment was more common (64%) than routine neonatal brain imaging (23%) during hospitalisation. In response to clinical need and published guidelines, centres have established formal cardiac neurodevelopment follow-up programmes. Centres vary considerably in their approaches to routine screening and objective testing, with many centres currently focussing their resources on evaluating younger patients.
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Hopkins, Stephen, Jeremy Turk, Adeniyi Daramola, and Marinos Kyriakopoulos. "Autism spectrum mixed neurodevelopmental disorder associated with 6q27 deletion and multiple copies within 20q11.23: a case study." Advances in Mental Health and Intellectual Disabilities 8, no. 3 (April 29, 2014): 210–15. http://dx.doi.org/10.1108/amhid-07-2013-0050.

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Purpose – Copy Number Variations (CNVs) are not infrequently observed in aberrant neurodevelopment. CNVs can alter gene expression and have been linked to a wide range of neuropsychiatric disorders. The purpose of this case study is to report the association of CNVs with a mixed neurodevelopmental disorder. Design/methodology/approach – Array-Comparative Genomic Hybridisation analysis was carried out in a case of an eight-year-old boy presenting with a mixed neurodevelopmental disorder including autism spectrum disorder, intellectual disability, tic disorder, anxiety and severe aggression. The child's parents also underwent the same investigation. Findings – A 6q27 deletion and multiple copies within 20q11.23 were identified. The boy's father shared the 6q27 deletion and his mother also had multiple copies within 20q11.23. Originality/value – This is the first report linking the combination of 6p27 and 20q11 CNVs with a mixed neurodevelopmental presentation. Identifying CNVs that may underlie aberrant neurodevelopment is likely to assist in unravelling the aetiology of neurodevelopmental and psychiatric disorders and lead to more effective strategies for their characterisation and management.
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Malin, Ashley J., Stefanie A. Busgang, Alejandra J. Cantoral, Katherine Svensson, Manuela A. Orjuela, Ivan Pantic, Lourdes Schnaas, et al. "Quality of Prenatal and Childhood Diet Predicts Neurodevelopmental Outcomes among Children in Mexico City." Nutrients 10, no. 8 (August 15, 2018): 1093. http://dx.doi.org/10.3390/nu10081093.

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Adequate nutrition is important for neurodevelopment. Although nutrients are ingested in combination, the impact of specific nutrients within the context of a nutrient mixture has not been studied with respect to health, such as neurodevelopment. Therefore, we examined the impact of prenatal and childhood nutrient mixtures on neurodevelopmental outcomes. Participants included mother–child pairs in the Programming Research in Obesity, Growth, Environment, and Social Stress (PROGRESS) prospective birth cohort in Mexico City. We assessed prenatal and child micro- and macronutrient profiles among 65 and 329 children, respectively, via food frequency questionnaires. Neurodevelopmental outcomes of 4–6-year-old children were measured using the McCarthy Scales of Children’s Abilities (MSCA). We conducted weighted quantile sum (WQS) regression analyses to calculate indices reflecting “good” and “poor” prenatal and childhood nutrition. After adjusting for maternal education, socioeconomic status, the Home Observation for Measurement of the Environment (HOME) score, and total caloric intake, the good prenatal and childhood nutrition indices predicted more favorable neurodevelopment, while both poor nutrition indices predicted poorer neurodevelopment. These associations were stronger in prenatal than childhood models. Monounsaturated fats predicted various neurodevelopmental abilities relatively strongly in both models. Prenatal and childhood consumption of combinations of beneficial nutrients may contribute to more favorable neurodevelopment.
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Guardiola-Ripoll, Maria, and Mar Fatjó-Vilas. "A Systematic Review of the Human Accelerated Regions in Schizophrenia and Related Disorders: Where the Evolutionary and Neurodevelopmental Hypotheses Converge." International Journal of Molecular Sciences 24, no. 4 (February 10, 2023): 3597. http://dx.doi.org/10.3390/ijms24043597.

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Schizophrenia is a psychiatric disorder that results from genetic and environmental factors interacting and disrupting neurodevelopmental trajectories. Human Accelerated Regions (HARs) are evolutionarily conserved genomic regions that have accumulated human-specific sequence changes. Thus, studies on the impact of HARs in the context of neurodevelopment, as well as with respect to adult brain phenotypes, have increased considerably in the last few years. Through a systematic approach, we aim to offer a comprehensive review of HARs’ role in terms of human brain development, configuration, and cognitive abilities, as well as whether HARs modulate the susceptibility to neurodevelopmental psychiatric disorders such as schizophrenia. First, the evidence in this review highlights HARs’ molecular functions in the context of the neurodevelopmental regulatory genetic machinery. Second, brain phenotypic analyses indicate that HAR genes’ expression spatially correlates with the regions that suffered human-specific cortical expansion, as well as with the regional interactions for synergistic information processing. Lastly, studies based on candidate HAR genes and the global “HARome” variability describe the involvement of these regions in the genetic background of schizophrenia, but also in other neurodevelopmental psychiatric disorders. Overall, the data considered in this review emphasise the crucial role of HARs in human-specific neurodevelopment processes and encourage future research on this evolutionary marker for a better understanding of the genetic basis of schizophrenia and other neurodevelopmental-related psychiatric disorders. Accordingly, HARs emerge as interesting genomic regions that require further study in order to bridge the neurodevelopmental and evolutionary hypotheses in schizophrenia and other related disorders and phenotypes.
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Cormack, Barbara E., Jane E. Harding, Steven P. Miller, and Frank H. Bloomfield. "The Influence of Early Nutrition on Brain Growth and Neurodevelopment in Extremely Preterm Babies: A Narrative Review." Nutrients 11, no. 9 (August 30, 2019): 2029. http://dx.doi.org/10.3390/nu11092029.

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Extremely preterm babies are at increased risk of less than optimal neurodevelopment compared with their term-born counterparts. Optimising nutrition is a promising avenue to mitigate the adverse neurodevelopmental consequences of preterm birth. In this narrative review, we summarize current knowledge on how nutrition, and in particular, protein intake, affects neurodevelopment in extremely preterm babies. Observational studies consistently report that higher intravenous and enteral protein intakes are associated with improved growth and possibly neurodevelopment, but differences in methodologies and combinations of intravenous and enteral nutrition strategies make it difficult to determine the effects of each intervention. Unfortunately, there are few randomized controlled trials of nutrition in this population conducted to determine neurodevelopmental outcomes. Substantial variation in reporting of trials, both of nutritional intakes and of outcomes, limits conclusions from meta-analyses. Future studies to determine the effects of nutritional intakes in extremely preterm babies need to be adequately powered to assess neurodevelopmental outcomes separately in boys and girls, and designed to address the many potential confounders which may have clouded research findings to date. The development of minimal reporting sets and core outcome sets for nutrition research will aid future meta-analyses.
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Dack, Kyle, Matthew Fell, Caroline M. Taylor, Alexandra Havdahl, and Sarah J. Lewis. "Prenatal Mercury Exposure and Neurodevelopment up to the Age of 5 Years: A Systematic Review." International Journal of Environmental Research and Public Health 19, no. 4 (February 10, 2022): 1976. http://dx.doi.org/10.3390/ijerph19041976.

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Neurodevelopmental delays can interfere with children’s engagement with the world and further development, and may have negative consequences into adulthood. Mercury is highly toxic and may negatively influence neurodevelopment because it can freely cross the placenta and accumulate in the fetal brain. We searched four publication databases (Embase, PsycINFO, PubMed/MEDLINE, Scopus) for studies examining the relationship between early life mercury exposure and scores on neurodevelopmental performance measures in children aged 0 to 5 years old. Study quality was assessed using the National Institutes of Health (NIH) Quality Assessment Tool. Thirty-two prospective studies were included in the review. Neurodevelopmental performance was measured using 23 different scales, most commonly the Bayley Scales of Infant and Toddler Development (BSID). In most cases, the evidence for an association between mercury and neurodevelopment was weak. There did not appear to be exceptions for particular childhood ages, outcome scales, or mercury levels. The small number of results to the contrary were more likely to be studies which did not meet our high-quality criteria, and could be a consequence of multiple testing, selection bias, or incomplete confounder adjustment. Based on current evidence, dietary mercury exposure during pregnancy is unlikely to be a risk factor for low neurodevelopmental functioning in early childhood.
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Tran, Nguyen Quoc Vuong, and Kunio Miyake. "Neurodevelopmental Disorders and Environmental Toxicants: Epigenetics as an Underlying Mechanism." International Journal of Genomics 2017 (2017): 1–23. http://dx.doi.org/10.1155/2017/7526592.

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The increasing prevalence of neurodevelopmental disorders, especially autism spectrum disorders (ASD) and attention deficit hyperactivity disorder (ADHD), calls for more research into the identification of etiologic and risk factors. The Developmental Origin of Health and Disease (DOHaD) hypothesizes that the environment during fetal and childhood development affects the risk for many chronic diseases in later stages of life, including neurodevelopmental disorders. Epigenetics, a term describing mechanisms that cause changes in the chromosome state without affecting DNA sequences, is suggested to be the underlying mechanism, according to the DOHaD hypothesis. Moreover, many neurodevelopmental disorders are also related to epigenetic abnormalities. Experimental and epidemiological studies suggest that exposure to prenatal environmental toxicants is associated with neurodevelopmental disorders. In addition, there is also evidence that environmental toxicants can result in epigenetic alterations, notably DNA methylation. In this review, we first focus on the relationship between neurodevelopmental disorders and environmental toxicants, in particular maternal smoking, plastic-derived chemicals (bisphenol A and phthalates), persistent organic pollutants, and heavy metals. We then review studies showing the epigenetic effects of those environmental factors in humans that may affect normal neurodevelopment.
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Dissertations / Theses on the topic "Neurodevelopmental"

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Cantor-Graae, Elizabeth. "Neurodevelopmental aspects of schizophrenia." Lund : Dept. of Psychology, Lund University, 1995. http://catalog.hathitrust.org/api/volumes/oclc/39749040.html.

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Nalty, Theresa. "Neurodevelopmental theory of autism /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/7583.

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Wood, Graham. "Neurodevelopmental models of Schizophrenia." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18659.

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Despite the obvious problems of modeling a disorder that is characterized by deficits in higher cognitive functions in lower animals, animal models of schizophrenia have aided in the advancement of the developmental hypothesis of schizophrenia. In fact, using three different animal models of schizophrenia, two of which we developed in our laboratory, we have been able to add support to the hypothesis. First, using NCAM knockout mice, which completely lack the neurodevelopmental molecule PSA-NCAM, we established the first genetic model of schizophrenia that not only presents with sensorimotor gating deficits but ventricular enlargement, both of which have been repeatedly demonstrated in schizophrenics. Next, we used neonatal Endo-N injections to enzymatically remove PSA from NCAM to demonstrate that only a brief disruption of neurodevelopment if sufficient to cause dopaminergic hyper-responsiveness. Finally, while trying to establish a genetic marker for the strain specific vulnerability to neonatal ventral hippocampal lesions (nVH) in Fisher and Lewis rat, we in fact discovered that the vulnerability is solely due to environmental factors, namely, the frequency of arched back nursing (ABN). Then making use of the variation in ABN in Sprague Dawley rats we established a new model in which nVH lesioned rats are separated into groups raised by dams with a High or Low frequency of ABN. Using this model, we demonstrated that the early environment is leading to disruption of the medial prefrontal cortex (MPFC), as characterized by working memory deficits, lack of MPFC control of locomotion and decreased anxiety, only in nVH lesioned rats raised by High ABN dams. Furthermore, we established that the early environment is not leading to sparing of function of the VH since nVH lesioned rats raised by both High and Low ABN dams have deficits on reference memory. Therefore, we have confirmed that genetic factors can lead to deficits in neurodevelopment that cause deficits pa
Malgré les difficultés apparentes liées à la modélisation d'un trouble mental caractérisé par une déficience au niveau des fonctions cognitives supérieures chez les espèces inférieures, la modélisation animale de la schizophrénie a permis des avancements quant aux hypothèses proposées sur le développement de la schizophrénie. En effet, en faisant appel à trois différents modèles animaux de schizophrénie, lesquels furent conçus dans nos laboratoires, nous avons su renforcer ces hypothèses. D'abord, en utilisant des souris mutantes N-CAM, lesquelles présentaient une absence totale de molécules neurodéveloppementales PSA-N-CAM, nous avons mis au point le premier modèle de schizophrénie présentant non seulement des déficiences de filtrage sensoriel, mais aussi une hypertrophie ventriculaire, deux éléments fréquemment observés chez les schizophrènes. Ensuite, nous avons fait appel à des injections Endo-N afin de scinder enzymatiquement l'isoforme PSA de la N-CAM, dans le but de démontrer qu'une simple perturbation même très brève du développement neurologique est suffisante pour engendrer une hyperréactivité dopaminergique. Enfin, en tentant d'établir un marqueur génétique pour la souche déterminée de vulnérabilité aux lésions néonatales de l'hippocampe ventral (nVH) chez les rat Fisher et Lewis, nous avons en fait constaté que la vulnérabilité était dû strictement à des facteurs environnementaux, à savoir, la fréquence d'allaitement avec le dos arqué (ABN). En faisant appel à la variation au niveau du ABN chez des rat Sprague Dawley, nous avons pu établir un nouveau modèle dans lequel des souris furent divisées en groupes de mères faisant souvent usage ou non de l'allaitement avec le dos arqué. Par le biais de ce modèle, nous avons pu démontrer que le premier environnement peut mener à une perturbation du cortex médial préfrontal (CMPF), caractérisée par la perte de mémoire opérationnel
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Bell, Rachel Ann. "The neurodevelopmental hypothesis of schizophrenia." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312764.

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Andrew, Morag Jane. "Neurodevelopmental and visual outcomes of infants at risk of neurodevelopmental disability following dietary supplementation in infancy." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:2c4a24e3-4924-4085-bad0-fb054622cb7f.

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Background: Docosahexaenoic acid (DHA), choline and uridine-5-monophosphate (UMP) are important brain nutrients which form phosphatidylcholine, the most abundant brain membrane phospholipid. DHA, choline and UMP supplementation increases rodent brain phospholipids, synaptic components, functional brain connectivity and cognitive performance. This novel pilot study supplemented infants at risk of neurological impairment (ARNI) with a nutrient combination containing these neurotrophic compounds. Aims: 1) In a double blind randomised control trial (RCT), investigate if intake of a specific nutrient combination improves neurodevelopmental and visual outcome in infants ARNI. 2) Using novel measures of cortical visual function, investigate the effect of perinatal brain injury severity, gestational age at birth and sex upon visuocognitive development in infants at risk of neurodevelopmental impairment. Method: Recruitment was from UK neonatal units. Eligibility: ≤ 31 weeks, weight < 9th percentile; < 31 weeks with ≥ Grade II intraventricular haemorrhage (IVH) or preterm white matter injury (PWMI); 31-40 weeks with ≥ Grade II IVH or PWMI, ≥ Sarnat Grade II HIE or defined brain MRI abnormalities. Stratification was by sex, gestation and brain injury severity. Randomised infants received neurotrophic supplementation or placebo, for 2 years. Primary outcome was Bayley Scales of Infant Development III (BSID III) composite cognitive score (CCS) after 2 years. Secondary outcomes included BSID III composite language score (CLS) and BSID III composite motor score (CMS). Cortical visual measures were pattern reversal visual event related potential (PR-VERP) latency (transient and calculated), orientation reversal visual event related potentials (OR-VERP), and the Fixation Shift test (FS). Functional behavioural vision was assessed using the Atkinson Battery of Child Development for Examining Functional Vision (ABCDEFV). Local Ethics Committee approval was granted. Results: 62 neonates were recruited. After 2 years, mean CCS in the intervention group was 87.7 (SD 20.4) and 81.6 (SD 18.5) in the placebo group (mean difference = 2.28, p=0.13; -0.2, 18.2). Mean CLS in the intervention group was 91.5 (SD 20.1) and 83.2 (SD 19.6) in the placebo group (mean difference = 2.74, p=0.1; -2.4, 18.3). CMS was similar in both groups. In relation to trial visual outcome measures, more infants in the placebo group gave a statistically significant OR-VERP response than in the intervention group (p=0.03). There were no statistically significant differences between the placebo and intervention on any other trial visual outcome measure. Cohort analyses indicate that transient PR-VERP latency is prolonged in children at risk of neurodevelopmental disability compared to typically developing infants (mean difference = -23.3, p=0.015, 95% CI -42.10 - -4.54). Calculated PR-VERP latency is prolonged to an even greater extent in children at risk of neurodevelopmental disability compared to typically developing infants (mean difference -148.6, p=0.000, 95% CI -179.7- -117.43), and remains prolonged across the age range tested. Conclusions: 1) The difference in CCS and CLS between intervention and placebo groups represents a clinically significant effect size. Use of neurotrophic micronutrient supplementation in infants ARNI warrants exploration in a large multicentre RCT. 2) Calculated PR-VERP latency may be a more appropriate outcome measure of cortical visual function than transient PR-VERP latency in infants at risk of neurodevelopmental disability.
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Golbano, Rodríguez Arantxa. "Neurodevelopmental alterations in X-linked adrenoleukodystrophy." Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/669358.

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La adrenoleucodistrofia ligada al cromosoma X (X-ALD, de sus siglas en inglés) es una enfermedad rara causada por mutaciones en el transportador peroxisomal ABCD1, presentando dos formas de manifestación clínica de neurodegeneración: demielinización aguda y letal en el cerebro de niños con la forma cerebral de X-ALD (CCALD), y degeneración crónica de los tractos de la médula espinal y neuropatía periférica en adultos con adrenomielopatía (AMN). Las alteraciones psiquiátricas son un signo temprano de CCALD y coexisten con la neurodegeneración periférica de la médula espinal en AMN, poniendo de manifiesto la patología cerebral. Teniendo en cuenta que la X-ALD es una condición genética quisimos determinar si las alteraciones psiquiátricas observadas pueden ser debidas, al menos en parte, a la formación aberrante de circuitos cerebrales durante el desarrollo y no a la neurodegeneración. Con este objetivo, usamos una aproximación de arriba hacia abajo, partiendo de datos de transcriptomas de pacientes, donde hemos buscado vías de neurodesarrollo desreguladas, hasta modelos murinos de X-ALD in vitro basados en el silenciamiento de los genes Abcd1 y Abcd2 para diseccionar la compartimentalización entre neuronas y astrocitos. Se presentan cuatro resultados principales. Primero, existen vías de neurodesarrollo desreguladas en CCALD, AMN y en los cultivos neuronales deficientes en ABCD, asociado con alteración en los procesos de neuritogénesis, espinogénesis, y axonogénesis. Segundo, un crecimiento aberrante de las espinas sinápticas es en parte debido a alteraciones en la vía canoníca de señalización Wnt puesto que la espinogénesis se recupera parcialmente mediante la activación de la vía de señalización Wnt tras la inhibición farmacológica de GSK-3. Tercero, la síntesis de colesterol y la localización del mismo se encuentran cambiadas en los astrocitos deficientes en ABCD. Cuarto, el silenciamiento de los transportadores ABCD causa alteraciones metabólicas en astrocitos incluyendo disminución de la oxidación de ácidos grasos, incremento del ratio NAD+/NADH, depleción de ATP, y disminución de la cantidad total de glutatión sugiriendo el deterioro conjunto de la defensa antioxidante y la bioenergética. Quinto, los astrocitos X-ALD presentan una señalización de calcio mediada por agonistas alterada y estrés del retículo endoplamático. Concluimos que i) la X-ALD presenta un componente de neurodesarrollo que puede explicar los síntomas psiquiátricos, y quizá contribuir a la progresión de la forma CCALD, y a la conversión de la AMN en una forma cerebral de la enfermedad, y ii) la deregulacion metabólica y de la excitabilidad en astrocitos apoya la disfunción global de los astrocitos que puede poner en peligro el papel computacional y homeostático de los astrocitos en los circuitos cerebrales.
X-linked adrenoleukodystrophy (X-ALD) is a rare disease caused by mutations in the peroxisomal ABCD1 transporter, with two major clinical manifestations of neurodegeneration: acute and lethal brain demyelination in the child cerebral X-ALD (CCALD), and chronic degeneration of spinal-cord tracts and peripheral neuropathy in the adult adrenomyeloneuropathy (AMN). Psychiatric alterations are an early sign of CCALD and coexist with spinal-cord and peripheral neurodegeneration in AMN, revealing concomitant brain pathology. Since X-ALD is a genetic condition, we sought to determine whether psychiatric alterations could be due, at least in part, to abnormal formation of brain circuits during brain development and not to neurodegeneration. To this end, we used a top-down approach, moving from patient transcriptome data, where we searched for dysregulated neurodevelopmental pathways, to in vitro murine models of X-ALD based on Abcd1/Abcd2 silencing to dissect out astrocyte versus neurons compartmentalization. There are four major findings. First, developmental pathways are dysregulated in CCALD, CAMN and in ABCD-null neuronal cultures, associated with altered neuritogenesis, spinogenesis, and axonogenesis. Second, aberrant spine growth is in part due to alterations in canonical Wnt signalling alteration since the spinogenesis is partially rescued by activation of WNT pathways by pharmacological GSK-3 inhibition. Third, cholesterol synthesis and localization is changed in ABCD-null astrocytes. Four, silencing of ABCD transporters causes metabolic alterations in astrocytes including fatty acid oxidation impairment, increase of the ratio NAD+/NADH, ATP depletion, decreases in total glutathione, suggesting joint impairment of antioxidant defense and bioenergetics. Fifth, X-ALD astrocytes present altered agonist-induced calcium signaling and ER stress. We conclude that i) X-ALD has a neurodevelopmental component that may account for psychiatric symptoms, and perhaps contribute to the progression of CCALD, and to the conversion of AMN into a cerebral condition, and ii) metabolic and excitability dysregulation in astrocytes support global astrocytic dysfunction that may jeopardize computational and homeostatic role of astrocytes in neural circuits.
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Suades, González Elisabet 1981. "Socio-environmental exposures and neurodevelopmental disorders." Doctoral thesis, Universitat Pompeu Fabra, 2018. http://hdl.handle.net/10803/664809.

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Introduction The influence of the environment, and its interplay with genetics, can account for up to half of the variance of neurodevelopmental disorders. In this thesis we reviewed previous literature on air pollution and neuropsychological development. We studied the trajectories of attention development in children. Finally, we explored any association between socio-environmental factors and warning signs of dyslexia and ADHD (attention deficit hyperactivity disorder) symptoms. Methods This thesis is part of the BREATHE (BRain dEvelopment and Air polluTion ultrafine particles in scHool childrEn) and the INMA (INfancia y Medio Ambiente) projects. Results (1) We encountered sufficient evidence for an association between outdoor air pollution and a negative impact on the neuropsychological development of children. (2) We detected an ongoing development of some attention processes in primary school children, differentiating patterns by gender and ADHD symptoms. (3) Daily levels of traffic-related ambient air pollution were associated with daily variations in attention processes in primary school children. (4) Prenatal, and at some extent postnatal, exposure to NO2 at the residence address increased the risk of presenting signs of dyslexia in primary school children. (5) Within a total of 23 socio-environmental factors, only male gender, younger relative age, psychosocial adversity, smoking and prenatal exposure to alcohol associated with ADHD symptoms at preschool age using a novel method for handling correlated data. x Conclusions Traffic-related air pollution, smoking, alcohol, gender, relative age and psychosocial adversity were identified as important determinants of neurodevelopmental disorders.
Introducció La influència del medi ambient, i la seva interacció amb la genètica, pot explicar fins a la meitat de la variància dels trastorns del neurodesenvolupament. En aquesta tesi s’ha fet una revisió sobre la contaminació atmosfèrica i el desenvolupament neuropsicològic. S’han estudiat les trajectòries del desenvolupament de l'atenció en nens/es. Finalment, s’ha explorat l’associació entre factors socioambientals i indicadors d’alt risc de dislèxia i símptomes de TDAH (trastorn per dèficit d’atenció i hiperactivitat). Mètodes Aquesta tesi forma part dels projectes BREATHE (BRain dEvelopment and Air polluTion ultrafine particles in scHool childrEn) i INMA (INfància i Medi Ambient). Resultats (1) Hem trobat suficient evidència d’una associació entre la contaminació atmosfèrica i un impacte negatiu en el desenvolupament neuropsicològic dels nens/es. (2) Hem detectat trajectòries del desenvolupament de l’atenció en nens/es de primària, diferenciant patrons per gènere i símptomes de TDAH. (3) Els nivells diaris de contaminació atmosfèrica relacionada amb el trànsit es van associar amb variacions diàries en els processos atencionals en nens/es de primària. (4) L'exposició prenatal, i en certa mesura la postnatal, a la contaminació atmosfèrica relacionada amb el trànsit va augmentar el risc de presentar indicadors de dislèxia en els nens/es d'educació primària. (5) D’entre un total de 23 factors socio ambientals, només el gènere masculí, menys edat relativa (els nens/es més petits de la classe), l'adversitat psicosocial, el tabaquisme i l'exposició prenatal a l’alcohol es van associar amb símptomes de TDAH a l'edat preescolar utilitzant un mètode novedós per analitzar dades correlacionades. xii Conclusions La contaminació atmosfèrica relacionada amb el trànsit, el tabaquisme, l'alcohol, el gènere, l’edat relativa i l'adversitat psicosocial es van identificar com a determinants importants dels trastorns del neurodesenvolupament.
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Feron, Franciscus Joseph Maria. "Studies on neurodevelopmental issues in children." [Maastricht : Maastricht : Universiteit Maastricht ] ; University Library, Universiteit Maastricht [host], 2007. http://arno.unimaas.nl/show.cgi?fid=8301.

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Yu, Ka-ki Kevin, and 余嘉棋. "Neuroimaging meta-analysis in neurodevelopmental disorders." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47753171.

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 Background and Objectives: ‘Neurodevelopmental disorders’ is often synonymously used with childhood developmental disorders such as autism spectrum disorder (ASD), however, increasingly new lines of evidence from genetics and epidemiology suggests having schizophrenia and bipolar disorder to be included as well. For example, there is a strong tendency for schizophrenia and bipolar disorder to occur in people with ASD and shared aetiological factors such as prenatal infection and maternal vitamin D deficiency during pregnancy have all been linked with increased risks in all three conditions. To investigate into this, I have turned to brain imaging, a technique which has opened up a new horizon for neurobiologists. Typically, neuroimaging studies focus on one disorder, matching patients with healthy volunteers and compare their brain structures volumetric differences. On the other hand, such studies are limited by various factors including small ample size, low power, no psychiatric control group, and sample or design heterogeneity. Methods: To summarize all the data into a more meaningful biological representation, Anatomical Likelihood Estimation (ALE), a cutting edge meta-analytic approach was applied. The rationale behind ALE is that it identifies brain differences most consistently reported across studies, while filtering away differences that are least documented. In this thesis, a novel application of ALE known as “dual disorder ALE” is introduced, which serves to estimate the extent of brain regional differences implicated in either disorder – in other words, a method to quantify which areas of the brain are more likely to be affected by ASD, schizophrenia or bipolar disorder. Findings: The analysis is separated into two parts. First, dual disorder ALE technique was applied to investigate the relationship between ASD and first-episode schizophrenia. Data from 25 MRI studies was extracted comprising 660 participants (308 ASD, 352 schizophrenia) and 801 healthy controls. In ASD and FE schizophrenia, there were similar brain differences near the limbic-striato-thalamic circuitry, and distinctive brain differences including amygdala, caudate, frontal and medial gyrus for schizophrenia and putamen for ASD. In the second part comparing bipolar disorder and schizophrenia, data from 651 schizophrenic patients, 540 bipolar patients, and 1438 healthy controls was used, and matched one-to-one by pairing up bipolar disorder studies with corresponding schizophrenia studies to minimize confounders. The ALE result indicated that there are substantial overlaps across the two disorders, with schizophrenia having more extensive brain differences than bipolar disorder. Conclusions: Both parts of the analysis suggest that there are similar aetiological pressures affecting neurodevelopmental disorders including ASD, schizophrenia and bipolar disorder.
published_or_final_version
Psychiatry
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Master of Philosophy
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McConnell, B. A. "Neurodevelopmental outcome and prenatal Doppler performance." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390885.

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Books on the topic "Neurodevelopmental"

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Patel, Dilip R., Donald E. Greydanus, Hatim A. Omar, and Joav Merrick, eds. Neurodevelopmental Disabilities. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0627-9.

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Fleischhacker, W. W., and D. J. Brooks, eds. Neurodevelopmental Disorders. Vienna: Springer-Verlag, 2005. http://dx.doi.org/10.1007/3-211-31222-6.

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DiCicco-Bloom, Emanuel, and James H. Millonig, eds. Neurodevelopmental Disorders. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45493-7.

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Thomas, Michael, and Annette Karmiloff-Smith. Neurodevelopmental Disorders. 1 Oliver's Yard, 55 City Road, London EC1Y 1SP United Kingdom: SAGE Publications Ltd, 2014. http://dx.doi.org/10.4135/9781473915428.

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Eisenstat, David D., Dan Goldowitz, Tim F. Oberlander, and Jerome Y. Yager, eds. Neurodevelopmental Pediatrics. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-20792-1.

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Flynn, John T. Strabismus A Neurodevelopmental Approach. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4612-3058-8.

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Dante, Cicchetti, and Walker Elaine F, eds. Neurodevelopmental mechanisms in psychopathology. Cambridge, UK: Cambridge University Press, 2003.

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Qoronfleh, M. Walid, Musthafa Mohamed Essa, and Chidambaram Saravana Babu, eds. Proteins Associated with Neurodevelopmental Disorders. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-15-9781-7.

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Nosarti, Chiara, Robin M. Murray, and Maureen Hack, eds. Neurodevelopmental Outcomes of Preterm Birth. Cambridge: Cambridge University Press, 2009. http://dx.doi.org/10.1017/cbo9780511712166.

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Mitchell, Kevin J., ed. The Genetics of Neurodevelopmental Disorders. Hoboken, NJ, USA: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118524947.

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Book chapters on the topic "Neurodevelopmental"

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Thapar, Anita, and Michael Rutter. "Neurodevelopmental disorders." In Rutter's Child and Adolescent Psychiatry, 31–40. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118381953.ch3.

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Fawke, Joe, and Rebecca Lancaster. "Neurodevelopmental Problems." In Emerging Topics and Controversies in Neonatology, 323–49. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-28829-7_19.

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Fawer, C. L., and A. Calame. "Neurodevelopmental Outcome." In Perinatal Asphyxia, 255–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77896-4_19.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Neurodevelopmental Hypothesis." In Encyclopedia of Psychopharmacology, 842. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1409.

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Numis, Adam L., and Raman Sankar. "Neurodevelopmental disorders." In International Neurology, 641–44. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118777329.ch162.

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Abel, Ernest L. "Neurodevelopmental Abnormalities." In Fetal Alcohol Abuse Syndrome, 101–10. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4757-5217-5_10.

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Abel, Ernest L. "Neurodevelopmental Abnormalities." In Fetal Alcohol Abuse Syndrome, 111–38. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4757-5217-5_11.

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Shelton, Lyn. "Neurodevelopmental disorder." In Case Studies in Forensic Psychology, 70–88. Milton Park, Abingdon, Oxon; New York, NY: Routledge, 2019.: Routledge, 2019. http://dx.doi.org/10.4324/9780429505720-5.

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Walder, Deborah J., Janet Cohen Sherman, and Margaret B. Pulsifer. "Neurodevelopmental Assessment." In Evidence-Based Practice in Infant and Early Childhood Psychology, 167–205. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118269602.ch6.

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Lord, Katherine, and Diva D. De León-Crutchlow. "Neurodevelopmental Outcomes." In Congenital Hyperinsulinism, 155–60. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-02961-6_14.

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Conference papers on the topic "Neurodevelopmental"

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Brothwell, S., N. Subbaraya, G. Cropp, and P. Surana. "G475(P) Measuring neurodevelopmental outcomes of prematurity- before and after a neurodevelopmental follow-up service." In Royal College of Paediatrics and Child Health, Abstracts of the Annual Conference, 24–26 May 2017, ICC, Birmingham. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313087.467.

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de-la-Iglesia, Myriam, José-Sixto Olivar, and Ruth Pinedo. "SPECIAL EDUCATION: COMMUNICATION IN NEURODEVELOPMENTAL DISORDERS." In International Conference on Education and New Learning Technologies. IATED, 2016. http://dx.doi.org/10.21125/edulearn.2016.0455.

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Kaur, Gurjot, and Deepti Kakkar. "Fuzzy Based Integrated Diagnostic System for Neurodevelopmental Disorders." In 2019 6th International Conference on Signal Processing and Integrated Networks (SPIN). IEEE, 2019. http://dx.doi.org/10.1109/spin.2019.8711674.

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Trickett, Jayne, Caroline Richards, Mary Heald, Hayley Denyer, and Chris Oliver. "Sleep disordered breathing in children with neurodevelopmental disorders." In ERS/ESRS Sleep and Breathing Conference 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/23120541.sleepandbreathing-2017.p59.

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Schallner, Jens, Lena Becker, Nataliya Di Donato, and Maja von der Hagen. "Dyneinopathies - Phenotypic Insights in DYNC1H1 Related Neurodevelopmental Disorders." In Abstracts of the 45th Annual Meeting of the Society for Neuropediatrics. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1698252.

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Cipollini, Ben, and Garrison W. Cottrell. "Patchy Connectivity and Visual Processing Asymmetries: A Neurodevelopmental Hypothesis." In 14th Neural Computation and Psychology Workshop. WORLD SCIENTIFIC, 2016. http://dx.doi.org/10.1142/9789814699341_0001.

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Stracina, Tibor, Marina Ronzhina, Tibor Stark, Jana Ruda, Eva Olsanska, Petr Vesely, Vincenzo Micale, and Marie Novakova. "Prolonged QT Interval in Neurodevelopmental Rat Model of Schizophrenia." In 2016 Computing in Cardiology Conference. Computing in Cardiology, 2016. http://dx.doi.org/10.22489/cinc.2016.302-288.

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Saftić, Vanja Slijepčević. "477 Toxic stress and neurodevelopmental trajectories – oportunity for intervention." In 10th Europaediatrics Congress, Zagreb, Croatia, 7–9 October 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.477.

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Gray, P., A. Molnar, and B. Firman. "Early High-Dose Caffeine Citrate: Neonatal and Neurodevelopmental Outcomes." In 7th International Conference on Clinical Neonatology—Selected Abstracts. Thieme Medical Publishers, 2018. http://dx.doi.org/10.1055/s-0038-1647088.

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Beccaluva, Eleonora Aida, Andrea Bonarini, Roberto Cerabolini, Francesco Clasadonte, Franca Garzotto, Mirko Gelsomini, Vito Antonio Iannelli, Francesco Monaco, and Leonardo Viola. "Exploring engagement with robots among persons with neurodevelopmental disorders." In 2017 26th IEEE International Symposium on Robot and Human Interactive Communication (RO-MAN). IEEE, 2017. http://dx.doi.org/10.1109/roman.2017.8172410.

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Reports on the topic "Neurodevelopmental"

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Nelson, III, Coman Charles A., and Nicole. Defining Early Markers of Neurodevelopmental Disorders in Infants With TSC. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada592777.

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Shen, Lijun. Bevacizumab for retinopathy of prematurity in Neurodevelopmental Outcomes: A Bayesian Meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0053.

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White, Roberta, Joseph Braun, John Bucher, Leonid Kopylev, Deborah Segal, Christopher Sibrizzi, Alexander Lindahl, and Pamela Hartman. NIEHS Report on Evaluating Features and Application of Neurodevelopmental Tests in Epidemiological Studies. National Institute of Environmental Health Sciences, June 2022. http://dx.doi.org/10.22427/niehs-01.

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Bonnin, Alexandre, Nick Goeden, Brett Lund, and George Anderson. Altered Placental Tryptophan Metabolism: A Crucial Molecular Pathway for the Fetal Programming of Neurodevelopmental Disorders. Fort Belvoir, VA: Defense Technical Information Center, July 2014. http://dx.doi.org/10.21236/ada611000.

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Basu, Sayani. Minibrains: A New Dimension in Organoid Research. Gratis Research, December 2020. http://dx.doi.org/10.47496/gr.blog.06.

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Zhao, Jing-yi, Zi-xiang Zhan, Meng-juan Lu, Fang-biao Tao, De Wu, and Hui Gao. A systematic review of epidemiological studies on the association between organophosphate flame retardants and neurotoxicity. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0083.

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Review question / Objective: This study aims to collect published or unpublished related studies systematically and comprehensively, and screen out the articles that meets the quality standards for qualitative combination, so as to draw a relatively reliable comprehensive conclusion on the relationship of organophosphate flame retardants (OPFRs) with neurodevelopmental toxicity. Eligibility criteria: In brief, epidemiological studies including cohort study, case-control study and cross-sectional survey were screened. Studies regarding relationships between human exposure to organophosphate esters and neurotoxicity were possible eligible for the present systematic review. The adverse neurodevelopmental outcomes included development of cognition, behavior, motor, brain change, emotion, etc. Studies that did not meet the above criteria were not included in this systematic review.
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Feng, Xiang, Keshang Li, Quanrui Jiang, Yuxing Zhang, Zhichao Gong, Hui Zhi, Wu Li, and Jiangshan Li. Chinese medicine intervention for autism spectrum disorders:A protocol for systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0137.

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Review question / Objective: This study will help patients recover better, provide clinical evidence for practitioners, and promote the use of TCM in ASD interventions. Condition being studied: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impairments in social communication and/or social interaction as well as restrictive and/or repetitive behaviors. TCM has been clinically practiced in the intervention of ASD, especially in mainland China where studies have shown promising efficacy. However, it remains to be further explored and elaborated. Therefore, the purpose of this study was to evaluate the effectiveness and safety of conventional treatment-based TCM intervention modalities for ASD.
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Li, Yinhua, Wanting Lan, and Xiaohui Hou. The effectiveness of physical activities on children with autism spectrum disorder: A systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0034.

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Review question / Objective: The purpose of this meta-analysis was to evaluate the efficacy of different physical activity interventions and to determine which physical activity interventions are most effective for children with autism spectrum disorder. Condition being studied: Autism is a set of heterogeneous neurodevelopmental conditions, characterized by early-onset difficulties in social communication and unusually restricted, repetitive behavior and interests. Autism affects more male than female individuals, and comorbidity is common (>70% have concurrent conditions). Exercise has increasingly emerged as one of the promising compensation methods that can positively affect autistic symptoms. The positive effects of various physical activity interventions have been reported, but it is unclear which interventions are most effective at improving symptoms of autism.
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Kittana, Monia, Asma Ahmadani, Keith Williams, and Amita Attlee. Nutritional status and feeding behavior of children with autism spectrum disorder in the Middle East and North Africa Region: A systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0066.

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Review question / Objective: To elucidate the literature available regarding the nutritional status and feeding behavior in children with Autism Spectrum Disorder (ASD) in Middle East and North Africa (MENA) region. Condition being studied: Autism spectrum disorder (ASD), a neurodevelopmental condition characterized by persistent challenges in social interaction, speech, nonverbal communication, and repetitive/restrictive behavior. Eligibility criteria: Children from the MENA region diagnosed with ASD, of both genders, ages 2-19 years. Outcomes reporting either anthropometrics, serum nutrient levels, nutrient intakes, and/or feeding behaviors. Other inclusion criteria include the availability of full-length published articles in either English or Arabic. Articles presented in conferences, magazines, or newspapers are excluded. If the data are reported in more than one publication, the more recent is included.
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Gao, Hui, Chen Gong, Shi-chun Shen, Jia-ying Zhao, Dou-dou Xu, Fang-biao Tao, Yang Wang, and Xiao-chen Fan. A systematic review on the associations between prenatal phthalate exposure and childhood glycolipid metabolism and blood pressure: evidence from epidemiological studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0111.

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Review question / Objective: The present systematic review was performed to obtain a summary of epidemiological evidence on the relationships of in utero exposure to phthalates with childhood glycolipid metabolism and blood pressure. Condition being studied: Childhood cardiovascular risk factors including blood pressure, lipid profile (e.g., triglycerides, total cholesterol, HDL−C, LDL−C) and glucose metabolism (e.g., insulin, insulin resistance, insulin sensitivity, glucose) were the interested outcomes. Eligibility criteria: In brief, epidemiological studies including cohort study, case-control study and cross-sectional survey were screened. Studies regarding relationships between human exposure to organophosphate esters and neurotoxicity were possible eligible for the present systematic review. The adverse neurodevelopmental outcomes included development of cognition, behavior, motor, brain change, emotion, etc. Studies that did not meet the above criteria were not included in this systematic review.
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