Artykuły w czasopismach na temat „Neurodevelopment”
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Hamis, Amy Azira, Muhammad Al Amin Shaharuddin, Nazmeen Adline Fawwazah A Fauzi i Mohd Rizal Abdul Manaf. "Prenatal PM2.5 Exposure and Its Association with Neurodevelopmental Impairment in Children: A Narrative Review". International Journal of Public Health Research 13, nr 2 (3.09.2023): 1743–55. http://dx.doi.org/10.17576/ijphr.1302.2023.02.13.
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Air pollutants including PM2.5 are an increasing threat to public health. Studies have reported the adverse effect of PM2.5 exposure during pregnancy on neurodevelopment in children. We performed a narrative review using the PubMed, Web of Science and Scopus databases using keywords such as prenatal, particulate matter, neurodevelopment, and children. This review aims to identify symptoms of impaired neurodevelopment in children associated with prenatal PM2.5 exposure, the association between the timing of prenatal exposure PM2.5 and symptoms of impaired neurodevelopment in children as well as other factors that may influence the association of prenatal PM2.5 exposure and symptoms of impaired neurodevelopment in children. 25 papers were included in this review. There are ranges of symptoms of neurodevelopmental impairment associated with prenatal exposure of PM2.5, including language, speech, and communication symptoms; motor skills; behaviour and social skills; memory as well as learning/cognitive symptoms. Neurodevelopmental impairments were associated with exposure to PM2.5 across all three trimesters with impairment in communication and behavioural domains predominate in those exposed during the first trimester. Generally, male was more susceptible to having neurodevelopmental impairment symptoms compared to females. More information regarding the effect of prenatal PM2.5 exposure towards neurodevelopmental domains of the children will support public health policies that reduce air pollution and improve children’s health.
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Blomkvist, Eli Anne Myrvoll, Elisabet Rudjord Hillesund, Sissel Heidi Helland, Indra Simhan i Nina Cecilie Øverby. "Diet and Neurodevelopmental Score in a Sample of One-Year-Old Children—A Cross-Sectional Study". Nutrients 11, nr 7 (21.07.2019): 1676. http://dx.doi.org/10.3390/nu11071676.
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Environmental factors in the first years of life are crucial for a child’s neurodevelopment. Research on the association between breastfeeding and neurodevelopment is inconclusive, while research on the possible association between other dietary factors and neurodevelopment is inadequate in children as young as one year of age. The aim of the present study was to investigate associations between both breastfeeding and other dietary factors and the neurodevelopment of one-year-old children in Norway. Methods: Participants were recruited from kindergartens in four Norwegian counties in 2017. A questionnaire including questions about dietary factors and breastfeeding, and a standardised age-related questionnaire on neurodevelopment (the Ages and Stages Questionnaire), were completed by parents of one-year-olds. Linear regressions adjusting for relevant covariates were conducted to explore the associations. Results: In our sample of 212 one-year-old children, a longer duration of breastfeeding was associated with higher neurodevelopmental scores. Dietary intake of fish, fruits and vegetables was also strongly associated with higher neurodevelopmental scores, even after adjustment for breastfeeding and maternal education. Conclusion: Our results indicate that healthy dietary factors are important for neurodevelopment in young children, with measurable effects already at the age of one year.
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Malin, Ashley J., Stefanie A. Busgang, Alejandra J. Cantoral, Katherine Svensson, Manuela A. Orjuela, Ivan Pantic, Lourdes Schnaas i in. "Quality of Prenatal and Childhood Diet Predicts Neurodevelopmental Outcomes among Children in Mexico City". Nutrients 10, nr 8 (15.08.2018): 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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Given, Joanne, Rebecca L. Bromley, Florence Coste, Sandra Lopez-Leon i 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, nr 10 (14.10.2022): 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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Miller, Thomas A., Anjali Sadhwani, Jacqueline Sanz, Erica Sood, Dawn Ilardi, Jane W. Newburger, Caren S. Goldberg, David Wypij, J. William Gaynor i Bradley S. Marino. "Variations in practice in cardiac neurodevelopmental follow-up programs". Cardiology in the Young 30, nr 11 (23.10.2020): 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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Favilla, Emmanuelle, Jennifer A. Faerber, Lyla E. Hampton, Vicky Tam, Grace DeCost, Chitra Ravishankar, J. William Gaynor, Alisa Burnham, Daniel J. Licht i Laura Mercer-Rosa. "Early Evaluation and the Effect of Socioeconomic Factors on Neurodevelopment in Infants with Tetralogy of Fallot". Pediatric Cardiology 42, nr 3 (3.02.2021): 643–53. http://dx.doi.org/10.1007/s00246-020-02525-6.
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AbstractNeurodevelopmental sequelae are prevalent among patients with congenital heart defects (CHD). In a study of infants and children with repaired tetralogy of Fallot (TOF), we sought to identify those at risk for abnormal neurodevelopment and to test associations between socioeconomic and medical factors with neurodevelopment deficits. Single-center retrospective observational study of patients with repaired TOF that were evaluated at the institution’s Cardiac Kids Developmental Follow-up Program (CKDP) between 2012 and 2018. Main outcomes included neurodevelopmental test scores from the Bayley Infant Neurodevelopmental Screener (BINS), Peabody Developmental Motor Scale (PDMS), and Bayley Scales of Infant and Toddler Development, Third Edition (Bayley-III). Mixed effects linear regression and marginal logistic regression models tested relationships between patient characteristics and outcomes. Sub-analyses were conducted to test correlations between initial and later neurodevelopment tests. In total, 49 patients were included, predominantly male (n = 33) and white (n = 28), first evaluated at a median age of 4.5 months. Forty-three percent of patients (n = 16) had deficits in the BINS, the earliest screening test. Several socioeconomic parameters and measures of disease complexity were associated with neurodevelopment, independently of genetic syndrome. Early BINS and PDMS performed in infancy were associated with Bayley-III scores performed after 1 year of age. Early screening identifies TOF patients at risk for abnormal neurodevelopment. Socioeconomic factors and disease complexity are associated with abnormal neurodevelopment and should be taken into account in the risk stratification and follow-up of these patients. Early evaluation with BINS and PDMS is suggested for detection of early deficits.
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Chebet, Martin, Milton W. Musaba, David Mukunya, Brian Makoko, Agnes Napyo, Ritah Nantale, Proscovia Auma i in. "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, nr 4 (16.02.2023): 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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Lovey, Oriane, Myriam Bickle-Graz, Mathilde Morisod Harari, Antje Horsch i Juliane Schneider. "The Joint Observation in Neonatology and Neurodevelopmental Outcome of Preterm Infants at Six Months Corrected Age: Secondary Outcome Data from a Randomised Controlled Trial". Children 9, nr 9 (13.09.2022): 1380. http://dx.doi.org/10.3390/children9091380.
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This study aimed to evaluate the impact of a standardised joint observation (JOIN) performed in the neonatal intensive care unit (NICU) on the neurodevelopment of preterm infants at six months corrected age (CA) compared with a preterm control group. In this monocentric interventional randomised controlled trial, we allocated 76 mothers and their preterm neonates to either JOIN, an early one-session intervention, or standard care during the NICU hospitalisation. The neurodevelopment of the preterm infants was assessed by standardised developmental tests at six months CA and compared between the intervention and the control groups. This randomised controlled trial was registered on clinicaltrials.gov (NCT02736136) in April 2016. Sixty-five infants underwent neurodevelopmental assessment at six months CA. There were no significant differences between the two groups in neurodevelopmental outcome measures. The JOIN intervention was not associated with significant improvement in neurodevelopment at six months CA in preterm infants.
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Derbyshire, Emma, i Michael Maes. "The Role of Choline in Neurodevelopmental Disorders—A Narrative Review Focusing on ASC, ADHD and Dyslexia". Nutrients 15, nr 13 (25.06.2023): 2876. http://dx.doi.org/10.3390/nu15132876.
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Neurodevelopmental disorders appear to be rising in prevalence, according to the recent Global Burden of Disease Study. This rise is likely to be multi-factorial, but the role of certain nutrients known to facilitate neurodevelopment should be considered. One possible contributing factor could be attributed to deficits in choline intake, particularly during key stages of neurodevelopment, which includes the first 1000 days of life and childhood. Choline, a key micronutrient, is crucial for optimal neurodevelopment and brain functioning of offspring. The present narrative review discusses the main research, describing the effect of choline in neurodevelopmental disorders, to better understand its role in the etiology and management of these disorders. In terms of findings, low choline intakes and reduced or altered choline status have been reported in relevant population subgroups: pregnancy (in utero), children with autism spectrum disorders, people with attention deficit hyperactivity disorder and those with dyslexia. In conclusion, an optimal choline provision may offer some neuronal protection in early life and help to mitigate some cognitive effects in later life attributed to neurodevelopmental conditions. Research indicates that choline may act as a modifiable risk factor for certain neurodevelopmental conditions. Ongoing research is needed to unravel the mechanisms and explanations.
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Turan, Soeren, Tom Boerstler, Atria Kavyanifar, Sandra Loskarn, André Reis, Beate Winner i Dieter Chichung Lie. "A novel human stem cell model for Coffin–Siris syndrome-like syndrome reveals the importance of SOX11 dosage for neuronal differentiation and survival". Human Molecular Genetics 28, nr 15 (29.04.2019): 2589–99. http://dx.doi.org/10.1093/hmg/ddz089.
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AbstractThe SOXC transcription factors Sox4, Sox11 and Sox12, are critical neurodevelopmental regulators that are thought to function in a highly redundant fashion. Surprisingly, heterozygous missense mutations or deletions of SOX11 were recently detected in patients with Coffin–Siris syndrome-like syndrome (CSSLS), a neurodevelopmental disorder associated with intellectual disability, demonstrating that in humans SOX11 haploinsufficiency cannot be compensated and raising the question of the function of SOX11 in human neurodevelopment. Here, we describe the generation of SOX11+/− heterozygous human embryonic stem cell (hESC) lines by CRISPR/Cas9 genome engineering. SOX11 haploinsufficiency impaired the generation of neurons and resulted in a proliferation/differentiation imbalance of neural precursor cells and enhanced neuronal cell death. Using the SOX11+/− hESC model we provide for the first time experimental evidence that SOX11 haploinsufficiency is sufficient to impair key processes of human neurodevelopment, giving a first insight into the pathophysiology of CSSLS and SOX11 function in human neurodevelopment.
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Cormack, Barbara E., Jane E. Harding, Steven P. Miller i Frank H. Bloomfield. "The Influence of Early Nutrition on Brain Growth and Neurodevelopment in Extremely Preterm Babies: A Narrative Review". Nutrients 11, nr 9 (30.08.2019): 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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Madlala, Hlengiwe P., Landon Myer, Thokozile R. Malaba i Marie-Louise Newell. "Neurodevelopment of HIV-exposed uninfected children in Cape Town, South Africa". PLOS ONE 15, nr 11 (18.11.2020): e0242244. http://dx.doi.org/10.1371/journal.pone.0242244.
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Background Evidence shows that antiretroviral (ART) exposure is associated with neurodevelopmental delays in human immunodeficiency virus (HIV)-exposed uninfected (HEU) children. However, there are few insights into modifiable maternal and child factors that may play a role in improving neurodevelopment in HEU children. We used a parent-centric neurodevelopment tool, Ages & Stages Questionnaire (ASQ) to examined neurodevelopment in HEU children at 12–24 months of age, and associations with maternal and child factors. Methods 505 HIV-infected women (initiated ART pre- or during pregnancy) with live singleton births attending primary health care were enrolled; 355 of their HEU children were assessed for neurodevelopment (gross motor, fine motor, communication, problem solving and personal-social domains) at 12–24 months using age-specific ASQ administered by a trained fieldworker. Associations with maternal and child factors were examined using logistic regression models. Results Among mothers (median age 30 years, IQR, 26–34), 52% initiated ART during pregnancy; the median CD4 count was 436 cells/μl (IQR, 305–604). Most delayed neurodevelopment in HEU children was in gross (9%) and fine motor (5%) functions. In adjusted models, maternal socio-economic status (aOR 0.42, 95% CI 0.24–0.76) was associated with reduced odds of delayed gross-fine motor neurodevelopment. Maternal age ≥35 years (aOR 0.22, 95% CI 0.05–0.89) and maternal body mass index (BMI) <18.5 (aOR 6.76, 95% CI 1.06–43.13) were associated with delayed communication-problem-solving-personal-social neurodevelopment. There were no differences in odds for either domain by maternal ART initiation timing. Conclusions Delayed neurodevelopment was detected in both gross and fine motor functions in this cohort of HEU children, with strong maternal predictors that may be explored as potentially modifiable factors associated with neurodevelopment at one to two years of age.
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Nist, Marliese Dion, i Rita H. Pickler. "An Integrative Review of Cytokine/Chemokine Predictors of Neurodevelopment in Preterm Infants". Biological Research For Nursing 21, nr 4 (29.05.2019): 366–76. http://dx.doi.org/10.1177/1099800419852766.
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Preterm infants are at risk of brain injury and poor neurodevelopmental outcomes including impairments in cognition, behavioral functioning, sensory perception, and motor performance. Systemic inflammation has been identified as an important, potentially modifiable precursor of neurologic and neurodevelopmental impairments. Inflammation is typically measured by quantifying circulating cytokines and chemokines. However, it is unclear which specific cytokines/chemokines most consistently predict neurodevelopment in preterm infants. In this integrative review, we evaluated and analyzed the literature ( N = 37 publications) to determine the cytokines/chemokines most predictive of neurodevelopment in preterm infants, the optimal timing for these measurements, and the ideal source for collecting cytokines/chemokines. Synthesis of the findings of these studies revealed that interleukin (IL)-6, IL-1β, IL-8, and tumor necrosis factor (TNF)-α collected during the first 3 weeks of life are most predictive of subsequent neurodevelopment. Methodological variation among studies hinders more specific analysis, including the evaluation of cytokine thresholds and meta-analyses, that would allow for the use of cytokines/chemokines to predict neurodevelopment. Future research should focus on identifying explicit cytokine values, specifically for IL-6, IL-1β, IL-8, and TNF-α, that are most predictive for identifying preterm infants most at risk of impairment, keeping in mind that longitudinal measures of cytokines/chemokines may be more predictive of future outcomes than single-time point measures.
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Serván-Mori, Edson, Amado D. Quezada-Sánchez, Evelyn Fuentes-Rivera, Carlos Pineda-Antunez, María del Carmen Hernández-Chávez, Angélica García-Martínez, Raquel García-Feregrino i in. "Proximal determinants of suboptimal early child development during the first three years of life in socially deprived Mexican contexts". PLOS ONE 18, nr 11 (2.11.2023): e0291300. http://dx.doi.org/10.1371/journal.pone.0291300.
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Assessing the status and determinants of early child development (ECD) requires accurate and regularly updated measurements. Yet, little information has been published on the subject in low- and middle-income countries, particularly regarding the proximal determinants of childhood development in contexts of high social marginalization. This article analyzes the factors that favor or mitigate suboptimal ECD outcomes in Mexico. A cross-sectional study was conducted using recently collected data for 918 children aged 0–38 months from socially marginalized communities in 23 Mexican municipalities. The ECD outcomes of the children were estimated based on indicators of chronic undernutrition and neurodevelopment (normal, lagging and at risk of delay). The distribution of outcomes was described across the ECD proximal determinants analyzed, including the co-occurrence of chronic undernutrition and suboptimal neurodevelopment. Covariate-adjusted prevalence of the ECD outcomes and co-occurrences were calculated as post-estimations from a multiple multinomial logistic regression. The prevalence of chronic undernutrition was 23.5%; 45.9% of children were classified with neurodevelopmental lag, and 11% at risk of neurodevelopmental delay. The prevalence of stunting co-occurring with suboptimal neurodevelopment came to 15.4%. The results of the multinomial logistic regression model indicated that early gestational age, low birth weight, a low household socioeconomic level, being male and having numerous siblings were all associated with the co-occurrence of chronic undernutrition and suboptimal child neurodevelopment. This study identified important predictors of child development in the first three years of life, specifically in two of its principal indicators: nutritional and neurodevelopmental status. Most of the predictors observed can be improved by means of social programs and interventions. Trial registration: ClinicalTrials.gov ID: NCT04210362.
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Karantha, Sowmya C., Ravi P. Upadhyay, Abhinav Jain, Nita Bhandari, Neeta Dhabhai, Savita Sapra, Sitanshi Sharma, Ranadip Chowdhury i Sunita Taneja. "Association of fetal ultrasound anthropometric parameters with neurodevelopmental outcomes at 24 months of age". PLOS ONE 18, nr 12 (22.12.2023): e0296215. http://dx.doi.org/10.1371/journal.pone.0296215.
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Background There is a paucity of studies which have examined associations between ultrasound based fetal anthropometric parameters and neurodevelopment in all infants. We examined the association between ultrasound based fetal anthropometric parameters and neurodevelopment in all infants through a secondary analysis of data collected in a large community based randomized controlled trial. Methods A total of 1465 mother-child dyads were included. Ultrasound based fetal anthropometric parameters which included the head circumference (HC), abdominal circumference (AC), femur length (FL), biparietal diameter (BPD) and transcerebellar diameter (TCD) were collected at 26–28 weeks of gestation and their association with neurodevelopment at 24 months of age was examined. Results Only the transcerebellar diameter z score was positively associated +0.54 units (95% CI: 0.15, 0.93) with motor composite score. When the neurodevelopment outcomes were analyzed as categorical, none of the fetal variables were associated with risk of moderate to severe neurodevelopment impairment. Conclusion The findings suggest that transcerebellar diameter could be useful for early prediction of neurodevelopmental outcomes in childhood. Clinical trial registration Clinical trial registration of Women and Infants Integrated Interventions for Growth Study Clinical Trial Registry–India, #CTRI/2017/06/008908; Registered on: 23/06/2017, (http://ctri.nic.in/Clinicaltrials/pmaindet2.php?trialid=19339&EncHid=&userName=society%20for%20applied%20studies).
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Sharma, Deepak, Rekha Harish, Anuj Bhatti, Radhika Uppal i Jehangir Naseem. "Early Neurodevelopmental Outcome of Neonates with Gestation 35 Weeks or More with Serum Bilirubin in Exchange Range Without Encephalopathy: A Prospective Observational Study". Neonatal Network 40, nr 2 (1.03.2021): 66–72. http://dx.doi.org/10.1891/0730-0832/11-t-675.
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ObjectiveTo describe early neurodevelopment outcomes of neonates with severe hyperbilirubinemia without acute bilirubin encephalopathy (ABE).MethodsNeonates born at gestation ≥35 weeks, admitted to NICU with total serum bilirubin (TSB) in exchange range with no features of ABE, were followed up until the age of 6 months. Infants were assessed for impaired hearing and neurodevelopment at 3 months and 6 months of age.ResultsA total of 59 neonates were enrolled in the study. At 3 months of age, 7.6 percent of neonates were found to have hypotonia and motor delay, whereas 42.3 percent had abnormal brainstem evoked response audiometery. At 6 months, 6.4 percent of neonates were found to have persistent neurodevelopmental impairment.ConclusionSevere hyperbilirubinemia is associated with impaired neurodevelopment and hearing even in infants without ABE. Peak TSB level strongly correlates with abnormal outcomes.
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Li, Na, Yunlin Shen, Xiaohui Gong, Wenchao Hong, Juan Li i Hongzhuan Zhang. "Clinical features, management, and prognosis of Bacillus cereus sepsis in premature neonates". Medicine 102, nr 28 (14.07.2023): e34261. http://dx.doi.org/10.1097/md.0000000000034261.
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This study aimed to investigate the clinical characteristics, management and prognosis of Bacillus cereus sepsis in premature neonates. The clinical information of 8 premature neonates with B cereus sepsis who were treated in Shanghai Children Hospital from January 2015 to December 2019 was retrospectively collected from the medical records and analyzed. The neurodevelopment related conditions were collected at follow up visits at corrected age of 6 months and 12 months. Five patients developed meningitis, and cerebral magnetic resonance image showed abnormal in 5 patients. After treatment with meropenem and vancomycin, 1 patient died, and 7 patients survived and were smoothly discharged. At follow up visits, 1 patient was diagnosed with hydrocephalus and showed severely delayed neurodevelopment, 2 patients had mild delayed neurodevelopment, and the neurodevelopment was basically normal in remaining 4 patients. B cereus infection can cause severe complications of central nervous system, and affect neurodevelopmental outcome. Antibiotic treatment with meropenem and vancomycin is proven to be effective. Refreshing the central catheters is helpful for the prevention of B cereus sepsis and cerebral magnetic resonance image may be employed for the prognosis assessment.
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Viljetić, Barbara, Senka Blažetić, Irena Labak, Vedrana Ivić, Milorad Zjalić, Marija Heffer i Marta Balog. "Lipid Rafts: The Maestros of Normal Brain Development". Biomolecules 14, nr 3 (18.03.2024): 362. http://dx.doi.org/10.3390/biom14030362.
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Lipid rafts, specialised microdomains within cell membranes, play a central role in orchestrating various aspects of neurodevelopment, ranging from neural differentiation to the formation of functional neuronal networks. This review focuses on the multifaceted involvement of lipid rafts in key neurodevelopmental processes, including neural differentiation, synaptogenesis and myelination. Through the spatial organisation of signalling components, lipid rafts facilitate precise signalling events that determine neural fate during embryonic development and in adulthood. The evolutionary conservation of lipid rafts underscores their fundamental importance for the structural and functional complexity of the nervous system in all species. Furthermore, there is increasing evidence that environmental factors can modulate the composition and function of lipid rafts and influence neurodevelopmental processes. Understanding the intricate interplay between lipid rafts and neurodevelopment not only sheds light on the fundamental mechanisms governing brain development but also has implications for therapeutic strategies aimed at cultivating neuronal networks and addressing neurodevelopmental disorders.
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Millevert, Charissa, Nicholas Vidas-Guscic, Liesbeth Vanherp, Elisabeth Jonckers, Marleen Verhoye, Steven Staelens, Daniele Bertoglio i Sarah Weckhuysen. "Resting-State Functional MRI and PET Imaging as Noninvasive Tools to Study (Ab)Normal Neurodevelopment in Humans and Rodents". Journal of Neuroscience 43, nr 49 (6.12.2023): 8275–93. http://dx.doi.org/10.1523/jneurosci.1043-23.2023.
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Neurodevelopmental disorders (NDDs) are a group of complex neurologic and psychiatric disorders. Functional and molecular imaging techniques, such as resting-state functional magnetic resonance imaging (rs-fMRI) and positron emission tomography (PET), can be used to measure network activity noninvasively and longitudinally during maturation in both humans and rodent models. Here, we review the current knowledge on rs-fMRI and PET biomarkers in the study of normal and abnormal neurodevelopment, including intellectual disability (ID; with/without epilepsy), autism spectrum disorder (ASD), and attention deficit hyperactivity disorder (ADHD), in humans and rodent models from birth until adulthood, and evaluate the cross-species translational value of the imaging biomarkers. To date, only a few isolated studies have used rs-fMRI or PET to study (abnormal) neurodevelopment in rodents during infancy, the critical period of neurodevelopment. Further work to explore the feasibility of performing functional imaging studies in infant rodent models is essential, as rs-fMRI and PET imaging in transgenic rodent models of NDDs are powerful techniques for studying disease pathogenesis, developing noninvasive preclinical imaging biomarkers of neurodevelopmental dysfunction, and evaluating treatment-response in disease-specific models.
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Magai, Dorcas N., Jaya Chandna, Marie-Laure Volvert, Rachel Craik, Hawanatu Jah, Fatoumata Kongira, Kalilu Bojang i in. "The Precise-DYAD Neurodevelopmental substudy protocol: neurodevelopmental risk in children of mothers with placental complications". Wellcome Open Research 8 (9.11.2023): 508. http://dx.doi.org/10.12688/wellcomeopenres.19689.1.
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Background: Over 250 million children are not reaching their developmental potential globally. The impact of prenatal factors then influenced by postnatal environmental factors on child neurodevelopment, is still unclear—particularly in low- and middle-income settings. This study aims to understand the impact of placental complications as well as environmental, psychosocial, and biological predictors on neurodevelopmental trajectories. Methods: This is an observational cohort study of female and male children (≈3,950) born to women (≈4,200) with and without placental disorders (pregnancy-induced hypertension, foetal growth restriction, and premature birth) previously recruited into PREgnancy Care Integrating Translational Science, Everywhere study with detailed biological data collected in intrapartum and post-partum periods. Children will be assessed at six weeks to 6 months, 11-13 months, 23-25 months and 35-37 months in rural and semi-urban Gambia (Farafenni, Illiasa, and Ngayen Sanjal) and Kenya (Mariakani and Rabai). We will assess children's neurodevelopment using Prechtls General Movement Assessment, the Malawi Development Assessment Tool (primary outcome), Observation of Maternal-Child Interaction, the Neurodevelopmental Disorder Screening Tool, and the Epilepsy Screening tool. Children screening positive will be assessed with Cardiff cards (vision), Modified Checklist for Autism in Toddlers Revised, and Pediatric Quality of Life Inventory Family Impact. We will use multivariate logistic regression analysis to investigate the impact of placental complications on neurodevelopment and conduct structural equation modelling using latent class growth to study trajectories and relationships between biological, environmental, and psychosocial factors on child development. Conclusions: We aim to provide information regarding the neurodevelopment of infants and children born to women with and without placental complications at multiple time points during the first three years of life in two low-resource African communities. A detailed evaluation of developmental trajectories and their predictors will provide information on the most strategic points of intervention to prevent and reduce the incidence of neurodevelopmental impairments.
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Weber, Ashley M., Tondi M. Harrison i Deborah K. Steward. "Schore’s Regulation Theory". Biological Research For Nursing 14, nr 4 (23.07.2012): 375–86. http://dx.doi.org/10.1177/1099800412453760.
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Premature infants confront numerous physiologic and environmental stressors in the neonatal intensive care unit (NICU) that have the potential to permanently alter their neurodevelopment. Schore’s regulation theory postulates that positive maternal–infant interactions can shape the infant’s developmental outcomes through inducing mechanistic changes in brain structure and function. The purposes of this article are to explain the regulation of infant neurobiological processes during interactions between mothers and healthy infants in the context of Schore’s theory, to identify threats to these processes for premature infants, and to propose principles of clinical practice and areas of research necessary to establish a supportive environment and prevent or reduce maladaptive consequences for these vulnerable infants. A premature birth results in the disruption of neurodevelopment at a critical time. Chronic exposure to stressors related to the NICU environment overwhelms immature physiologic and stress systems, resulting in significant allostatic load, as measured by long-term neurodevelopmental impairments in the premature infant. Positive maternal–infant interactions during NICU hospitalization and beyond have the potential to reduce neurologic deficits and maximize positive neurodevelopmental outcomes in premature infants. The quality of the maternal–infant interaction is affected not only by the infant’s developing neurobiology but also by the mother’s responses to the stressors surrounding a premature birth and mothering an infant in the NICU environment. Nurses can empower mothers to overcome these stressors, promote sensitive interactions with their infants, and facilitate neurodevelopment. Research is critically needed to develop and test nursing interventions directed at assisting mothers in supporting optimal neurodevelopment for their infants.
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Hopkins, Stephen, Jeremy Turk, Adeniyi Daramola i 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, nr 3 (29.04.2014): 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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Rains, Marcelo E., Colin B. Muncie, Yi Pang, Lir-Wan Fan, Lu-Tai Tien i Norma B. Ojeda. "Oxidative Stress and Neurodevelopmental Outcomes in Rat Offspring with Intrauterine Growth Restriction Induced by Reduced Uterine Perfusion". Brain Sciences 11, nr 1 (8.01.2021): 78. http://dx.doi.org/10.3390/brainsci11010078.
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Intrauterine growth restriction (IUGR) is a major cause of morbidity and mortality and is worldwide associated with delayed neurodevelopment. The exact mechanism involved in delayed neurodevelopment associated with IUGR is still unclear. Reduced uterine perfusion (RUP) is among the main causes of placental insufficiency leading to IUGR, which is associated with increases in oxidative stress. This study investigated whether oxidative stress is associated with delayed neurodevelopment in IUGR rat pups. Pregnant rats were exposed to RUP surgery on gestational day 14 to generate IUGR rat offspring. We evaluated offspring’s morphometric at birth, and neurodevelopment on postnatal day 21 (PD21) as well as markers of oxidative stress in plasma and brain. Offspring from dams exposed to RUP showed significant (p < 0.05) lower birth weight compared to controls, indicating IUGR. Motor and cognitive deficits, and levels of oxidative stress markers, were significantly (p < 0.05) elevated in IUGR offspring compared to controls. IUGR offspring showed significant (p < 0.05) negative correlations between brain lipid peroxidation and neurocognitive tests (open field and novel object recognition) in comparison with controls. Our findings suggest that neurodevelopmental delay observed in IUGR rat offspring is associated with increased levels of oxidative stress markers.
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Rains, Marcelo E., Colin B. Muncie, Yi Pang, Lir-Wan Fan, Lu-Tai Tien i Norma B. Ojeda. "Oxidative Stress and Neurodevelopmental Outcomes in Rat Offspring with Intrauterine Growth Restriction Induced by Reduced Uterine Perfusion". Brain Sciences 11, nr 1 (8.01.2021): 78. http://dx.doi.org/10.3390/brainsci11010078.
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Intrauterine growth restriction (IUGR) is a major cause of morbidity and mortality and is worldwide associated with delayed neurodevelopment. The exact mechanism involved in delayed neurodevelopment associated with IUGR is still unclear. Reduced uterine perfusion (RUP) is among the main causes of placental insufficiency leading to IUGR, which is associated with increases in oxidative stress. This study investigated whether oxidative stress is associated with delayed neurodevelopment in IUGR rat pups. Pregnant rats were exposed to RUP surgery on gestational day 14 to generate IUGR rat offspring. We evaluated offspring’s morphometric at birth, and neurodevelopment on postnatal day 21 (PD21) as well as markers of oxidative stress in plasma and brain. Offspring from dams exposed to RUP showed significant (p < 0.05) lower birth weight compared to controls, indicating IUGR. Motor and cognitive deficits, and levels of oxidative stress markers, were significantly (p < 0.05) elevated in IUGR offspring compared to controls. IUGR offspring showed significant (p < 0.05) negative correlations between brain lipid peroxidation and neurocognitive tests (open field and novel object recognition) in comparison with controls. Our findings suggest that neurodevelopmental delay observed in IUGR rat offspring is associated with increased levels of oxidative stress markers.
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Keck-Kester, Terrah, i Steven D. Hicks. "Infant Saliva Microbiome Activity Modulates Nutritional Impacts on Neurodevelopment". Microorganisms 11, nr 8 (18.08.2023): 2111. http://dx.doi.org/10.3390/microorganisms11082111.
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Neurodevelopment is influenced by complex interactions between environmental factors, including social determinants of health (SDOH), nutrition, and even the microbiome. This longitudinal cohort study of 142 infants tested the hypothesis that microbial activity modulates the effects of nutrition on neurodevelopment. Salivary microbiome activity was measured at 6 months using RNA sequencing. Infant nutrition was assessed longitudinally with the Infant Feeding Practices survey. The primary outcome was presence/absence of neurodevelopmental delay (NDD) at 18 months on the Survey of Wellbeing in Young Children. A logistic regression model employing two microbial factors, one nutritional factor, and two SDOH accounted for 33.3% of the variance between neurodevelopmental groups (p < 0.001, AIC = 77.7). NDD was associated with Hispanic ethnicity (OR 18.1, 2.36–139.3; p = 0.003), no fish consumption (OR 10.6, 2.0–54.1; p = 0.003), and increased Candidatus Gracilibacteria activity (OR 1.43, 1.00–2.07; p = 0.007). Home built after 1977 (OR 0.02, 0.001–0.53; p = 0.004) and Chlorobi activity (OR 0.76, 0.62–0.93, p = 0.001) were associated with reduced risk of NDD. Microbial alpha diversity modulated the effect of fish consumption on NDD (X2 = 5.7, p = 0.017). These data suggest the benefits of fish consumption for neurodevelopment may be mediated by microbial diversity. Confirmation in a larger, randomized trial is required.
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Rodgers, Megan D., Molly J. Mead, Caroline A. McWhorter, Myla D. Ebeling, Judy R. Shary, Danforth A. Newton, John E. Baatz, Mathew J. Gregoski, Bruce W. Hollis i Carol L. Wagner. "Vitamin D and Child Neurodevelopment—A Post Hoc Analysis". Nutrients 15, nr 19 (3.10.2023): 4250. http://dx.doi.org/10.3390/nu15194250.
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Introduction: Vitamin D (VitD) has been shown to impact neurodevelopment. Studies have shown that higher 25-hydroxy-vitamin D (25(OH)D) concentrations (the indicator of vitD status) may be associated with better neurodevelopmental outcomes, although current data are conflicting. This study examined the relationship between total circulating 25(OH)D concentrations and neurodevelopmental outcomes in 3–5-year-old (3–5 yo) children. Methods: In this study, pregnant women were randomized to receive 400 (standard dose), 2000, or 4000 IU vitD3/day. Offspring then underwent the Brigance Screen at 3–5 yo. The 25(OH)D concentration was measured at birth and 3–5 yo. Relationships between Brigance scores and 25(OH)D and Brigance scores and vitamin D binding protein (VDBP) genotype were examined. Results: Higher 25(OH)D at the time of testing was associated with better overall performance on neurodevelopmental testing as measured by the Brigance quotient (B = 0.208, p = 0.049). Scores were then broken down into sub-scores. Children born to mothers in the 2000 IU/day group scored higher on the Brigance language component of the assessment versus the standard dose group (B = 4.667, p = 0.044). The group of children who had the Gc1f-1s or Gc1f-2 genotypes scored higher on the Brigance academic component (B = 9.993, p < 0.001) and lower on the Brigance language component versus the 1f1f genotype (B = −9.313, p < 0.001). Children with the Gc1s-1s, Gc1s-2, or Gc2-2 genotypes also scored lower than the Gc1f-1f genotype (B = −6.757, p = 0.003). Conclusion: These results suggest that higher 25(OH)D concentrations early in life and higher doses of maternal vitamin D supplementation during pregnancy may have a positive association with neurodevelopmental outcomes. This study also suggests that the VDBP genotype is associated with neurodevelopment and differentially affects various fields of neurodevelopment.
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Heath, Rory J., Susanna Klevebro i Thomas R. Wood. "Maternal and Neonatal Polyunsaturated Fatty Acid Intake and Risk of Neurodevelopmental Impairment in Premature Infants". International Journal of Molecular Sciences 23, nr 2 (9.01.2022): 700. http://dx.doi.org/10.3390/ijms23020700.
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The N3 and N6 long chain polyunsaturated fatty acids (LCPUFA) docosahexaenoic acid (DHA) and arachidonic acid (AA) are essential for proper neurodevelopment in early life. These fatty acids are passed from mother to infant via the placenta, accreting into fetal tissues such as brain and adipose tissue. Placental transfer of LCPUFA is highest in the final trimester, but this transfer is abruptly severed with premature birth. As such, efforts have been made to supplement the post-natal feed of premature infants with LCPUFA to improve neurodevelopmental outcomes. This narrative review analyzes the current body of evidence pertinent to neurodevelopmental outcomes after LCPUFA supplementation in prematurely born infants, which was identified via the reference lists of systematic and narrative reviews and PubMed search engine results. This review finds that, while the evidence is weakened by heterogeneity, it may be seen that feed comprising 0.3% DHA and 0.6% AA is associated with more positive neurodevelopmental outcomes than LCPUFA-deplete feed. While no new RCTs have been performed since the most recent Cochrane meta-analysis in 2016, this narrative review provides a wider commentary; the wider effects of LCPUFA supplementation in prematurely born infants, the physiology of LCPUFA accretion into preterm tissues, and the physiological effects of LCPUFA that affect neurodevelopment. We also discuss the roles of maternal LCPUFA status as a modifiable factor affecting the risk of preterm birth and infant neurodevelopmental outcomes. To better understand the role of LCPUFAs in infant neurodevelopment, future study designs must consider absolute and relative availabilities of all LCPUFA species and incorporate the LCPUFA status of both mother and infant in pre- and postnatal periods.
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Kaushik, Jaya Shankar. "Theme: Neurodevelopment". Indian Pediatrics 56, nr 9 (wrzesień 2019): 798. http://dx.doi.org/10.1007/s13312-019-1628-x.
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Spear, Linda Patia. "Adolescent Neurodevelopment". Journal of Adolescent Health 52, nr 2 (luty 2013): S7—S13. http://dx.doi.org/10.1016/j.jadohealth.2012.05.006.
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McLaughlin, Katie A., David Weissman i Debbie Bitrán. "Childhood Adversity and Neural Development: A Systematic Review". Annual Review of Developmental Psychology 1, nr 1 (24.12.2019): 277–312. http://dx.doi.org/10.1146/annurev-devpsych-121318-084950.
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An extensive literature on childhood adversity and neurodevelopment has emerged over the past decade. We evaluate two conceptual models of adversity and neurodevelopment—the dimensional model of adversity and stress acceleration model—in a systematic review of 109 studies using MRI-based measures of neural structure and function in children and adolescents. Consistent with the dimensional model, children exposed to threat had reduced amygdala, medial prefrontal cortex (mPFC), and hippocampal volume and heightened amygdala activation to threat in a majority of studies; these patterns were not observed consistently in children exposed to deprivation. In contrast, reduced volume and altered function in frontoparietal regions were observed consistently in children exposed to deprivation but not children exposed to threat. Evidence for accelerated development in amygdala-mPFC circuits was limited but emerged in other metrics of neurodevelopment. Progress in charting neurodevelopmental consequences of adversity requires larger samples, longitudinal designs, and more precise assessments of adversity.
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Tian, Yuan, Chuncao Zhang, Guangjun Yu, Xiangying Hu, Zheng Pu i Liyu Ma. "Influencing factors of the neurodevelopment of high-risk infants". General Psychiatry 31, nr 3 (grudzień 2018): e100034. http://dx.doi.org/10.1136/gpsych-2018-100034.
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BackgroundHigh-risk infants refer to newborns exposed to high-risk factors in the prenatal, natal or postnatal period. High-risk infants are at high risk of developmental retardation, and early identification of developmental abnormalities plays a vital role in improving high-risk infants’ quality of life.AimsTo describe the neurodevelopment of high-risk infants aged less than 1 year old, and to analyse the incidences and influencing factors of neurodevelopmental abnormalities in order to provide a basis for neurodevelopment monitoring and management of high-risk infants.MethodsHigh-risk infants born between January 2016 and December 2016 in the maternity and infant health hospitals of three districts in Shanghai were followed up. The Gesell Developmental Scale was used to assess the neurodevelopmental level at the time of recruitment (0–2 months) and at 9 months. Univariate and multivariate analyses of the influencing factors were conducted.Results484 high-risk infants (male 51%, female 49%) with an average gestation age of 36.5±2.2 weeks were recruited. At the time of recruitment, the average age was 2.1 (0.8) months, and the developmental quotient (DQ) scores of full-term high-risk infants in motor (t=3.542,p=0.001), cognitive (t=3.125,p=0.002), language (t=3.189,p=0.002) and social (t=3.316,p=0.001) areas were higher than those of preterm infants. The incidences of developmental abnormalities of full-term high-risk infants in motor (χ2=9.452,p=0.002), cognitive (χ2=6.258,p=0.012), language (χ2=12.319,p=0.001) and social (χ2=6.811,p=0.009) areas were lower than the preterm infants. At 9 months, there was no difference in the DQ scores and incidences of developmental abnormalities in four areas between full-term and preterm high-risk infants, and the incidence of developmental abnormalities was around 10%.ConclusionThe incidence of neurodevelopmental abnormalities in high-risk infants aged less than 1 year old is high. Preterm birth and parental bad habits are significant factors affecting the neurodevelopment. Monitoring and early interventions help to improve high-risk infants’ neurodevelopment.
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Bleker, de Rooij i Roseboom. "Programming Effects of Prenatal Stress on Neurodevelopment—the Pitfall of Introducing a Self-Fulfilling Prophecy". International Journal of Environmental Research and Public Health 16, nr 13 (28.06.2019): 2301. http://dx.doi.org/10.3390/ijerph16132301.
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There is increasing interest for the potential harmful effects of prenatal stress on the developing fetal brain, both in scientific literature and in public press. Results from animal studies suggest that gestational stress leads to an altered offspring neurodevelopment with adverse behavioral and cognitive consequences. Furthermore, there are indications in human studies that severe prenatal stress has negative consequences for the child’s neurodevelopment. However, stress is an umbrella term and studies of maternal stress have focused on a wide range of stress inducing situations, ranging from daily hassles to traumatic stress after bereavement or a natural disaster. Mild to moderate stress, experienced by many women during their pregnancy, has not consistently been shown to exert substantial negative effects on the child’s neurodevelopment. Additionally, the vast majority of human studies are observational cohort studies that are hampered by their fundamental inability to show a causal relationship. Furthermore, our limited knowledge on the possible underlying mechanisms and the effects of interventions for prenatal stress on child neurodevelopmental outcomes emphasize our incomplete understanding of the actual effects of prenatal stress on child neurodevelopment. Until we have a better understanding, it seems counterproductive to alarm all pregnant women for possible harmful effects of all sorts of prenatal stress, if only to avoid the induction of stress itself.
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Irfan B. Bhat, Muzafar Jan i Abdus S. Bhat. "Neurodevelopmental outcome of children with severe acute malnutrition". International Journal of Contemporary Pediatrics 10, nr 2 (24.01.2023): 238–40. http://dx.doi.org/10.18203/2349-3291.ijcp20230091.
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Background: Severe acute malnutrition is known to be a major risk factor for impaired motor, cognitive, and socio-emotional development. Not much work has been done to study the neuro development of these patients. The aim of this study was to assess the neurodevelopment and outcome of children between 1 and 30 months with diagnosis of SAM Methods: The study was an observational prospective study conducted from November 2018 to April 2020. A total of 61 patients were enrolled in our study. Patients admitted in NRC with diagnosis of SAM were assessed for neurodevelopment after stabilization. Developmental assessment scale of Indian infants was used to calculate the motor developmental quotient and mental developmental quotient. Patients were followed till 6 months and after 6 months, they were again assessed by DASII to see the improvement in neurodevelopment status. Developmental quotient of less 70 was taken as delayed. Results: Mean DMeQ after stabilization and at 6 months after discharge was 53.672 and 72.591 respectively. Mean DMoQ after stabilization and at 6 months after discharge was 50.50 and 68.23 respectively. Mean DQ after stabilization and at 6 months after discharge was 52.186 and 70.4105 respectively. Conclusions: Severe acute malnutrition results in neurodevelopmental impairment in children but early and effective intervention results in significant improvement in neurodevelopment status.
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Korček, Peter, Zuzana Korčeková, Ivan Berka, Jáchym Kučera i Zbyněk Straňák. "Corpus Callosum Growth and Neurodevelopmental Outcome Are Negatively Influenced by Systemic Infection in Very Low-Birth-Weight Infants". Journal of Child Neurology 36, nr 10 (28.05.2021): 883–87. http://dx.doi.org/10.1177/08830738211016239.
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Systemic infection may negatively modulate the development of cerebral white matter and long-term outcome of neonates. We analyzed the growth of corpus callosum (using cranial ultrasonography) and neurodevelopment (Bayley Scales of Infant Development, Third Edition) in 101 very low-birth-weight newborns. We observed significantly reduced corpus callosum length at 3 months of corrected age (44.5 mm vs 47.7 mm, P = .004) and diminished corpus callosum growth (0.07 mm/d vs 0.08 mm/d, P = .028) in infants who experienced systemic infection. The subgroup exhibited inferior neurodevelopmental outcomes with predominant motor impairment. The results suggest that length and growth of corpus callosum might be affected by systemic inflammatory response in preterm newborns. The changes in corpus callosum can contribute to adverse neurodevelopment at 2 years of corrected age. Serial ultrasonographic measurements of the corpus callosum may be suitable to identify preterm infants with increased risk of neurodevelopmental impairment.
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Fong, Jeanette, Juanita Lewis, Melanie Lam i Kalpashri Kesavan. "Developmental Outcomes after Opioid Exposure in the Fetus and Neonate". NeoReviews 25, nr 6 (1.06.2024): e325-e337. http://dx.doi.org/10.1542/neo.25-6-e325.
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The overall prevalence of opiate use has been increasing, currently affecting approximately 0.6% of the global population and resulting in a significant proportion of infants being born with prenatal opioid exposure. Animal and human models of prenatal opioid exposure demonstrate detrimental effects on brain anatomy as well as neurodevelopment. Less is known about the neurologic sequelae of postnatal opioid exposure in hospitalized infants. In this review, we summarize our current understanding of the impact of prenatal and postnatal opioid exposure on the brain and on neurodevelopment outcomes. We also identify resources and management strategies that may help mitigate neurodevelopmental delays and deficits associated with opioid exposure in this vulnerable population.
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Kordopati-Zilou, Kalliopi, Theodoros Sergentanis, Panagiota Pervanidou, Danai Sofianou-Petraki, Konstantinos Panoulis, Nikolaos Vlahos i Makarios Eleftheriades. "Neurodevelopmental Outcomes in Tetralogy of Fallot: A Systematic Review". Children 9, nr 2 (15.02.2022): 264. http://dx.doi.org/10.3390/children9020264.
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BACKGROUND: Tetralogy of Fallot (TOF) represents between 7 and 10% of the total cases of congenital heart defects (CHD) and is estimated to be the most common cyanotic CHD, requiring medical or surgical intervention within the first year of life. Current advances in prenatal screening and fetal echocardiography led to increased rates of prenatal diagnosis of TOF. Furthermore, improvements in initial medical care, surgical repair, and long-term care are associated with excellent long-term survival until adulthood. Consequently, issues of morbidity have come under the spotlight, specifically neurodevelopmental and psychiatric adverse outcomes, which affect the quality of life of TOF survivors. METHOD: This study is a systematic review of English articles, using PUBMED and applying the following search terms, Tetralogy of Fallot, neurodevelopment, autism, cerebral palsy, attention-deficit hyperactivity disorder. Data were extracted by two authors. RESULTS: Most researchers suggest that TOF survivors score lower in neurodevelopmental tests than healthy populations of the same age and are in danger of neurodevelopmental impairments. Furthermore, it is suggested that TOF adolescents show higher rates of psychiatric disorders. CONCLUSIONS: The neurodevelopment of TOF survivors is not intensively studied. Existing studies in TOF survivors focus on different developmental aspects, using different evaluation methods and thus making conclusions for either one of the four aspects of neurodevelopment (executive function, cognition, and adaptive function, speech-language and motor function, or neuropsychiatric domain). The poor outcomes of these isolated studies indicate the need for future research as well as for continuous neuropsychological assessment and close monitoring of children and adolescents with TOF.
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Kim, Mi Ju, Hyun Mi Kim, Hyun-Hwa Cha, Haemin Kim, Hyo-Shin Kim, Bong Seon Lim i Won Joon Seong. "Perinatal Outcomes and Neurodevelopment 1 Year after Birth in Discordant Twins According to Chorionicity". Medicina 59, nr 3 (2.03.2023): 493. http://dx.doi.org/10.3390/medicina59030493.
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Background and Objectives: This study aimed to compare maternal complications, perinatal outcomes, and neurodevelopment 1 year after the birth between concordant and discordant twins in monochorionic and dichorionic twins. Materials and Methods: This retrospective study included twin pregnancies delivered between 24 + 1 and 38 + 2 weeks of gestation between January 2011 and September 2019. Chorionicity was confirmed by ultrasonography and was categorized into monochorionic and dichorionic. Each was then divided into two groups (concordant and discordant) according to birth weight discordancy. Maternal complications and neonatal outcomes, including neurodevelopmental delays, were compared between the two groups. Results: A total of 298 pairs of twin pregnancies were enrolled, of which 58 (19.26%) women were pregnant with monochorionic diamniotic twins and 240 (80.54%) with dichorionic diamniotic twins. In both monochorionic and dichorionic twins, the discordant twins had a greater incidence of emergency deliveries because of iatrogenic causes than the concordant twins. Among dichorionic twins, discordant twins had lower birth weight rates and higher hospitalization rates and morbidities than concordant twins. Among monochorionic twins, discordant twins had a lower birth weight and higher neonatal mortality than concordant twins. The neonatal size was not a predictor of neurodevelopment in this group. Based on the logistic regression analysis, male sex, respiratory distress syndrome, and bronchopulmonary dysplasia were risk factors for the neurodevelopmental delay; birth weight discordancy was significant only in dichorionic twins. Conclusions: Perinatal outcomes in discordant twins may be poor, and neurodevelopment 1 year after birth was worse in discordant twins than in concordant twins. Discordancy in twins can be a risk factor for neurodevelopmental delay.
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Patti, Marisa A., Karl T. Kelsey, Amanda J. MacFarlane, George D. Papandonatos, Tye E. Arbuckle, Jillian Ashley-Martin, Mandy Fisher i in. "Maternal Folate Status and the Relation between Gestational Arsenic Exposure and Child Health Outcomes". International Journal of Environmental Research and Public Health 19, nr 18 (9.09.2022): 11332. http://dx.doi.org/10.3390/ijerph191811332.
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Gestational arsenic exposure adversely impacts child health. Folate-mediated 1-carbon metabolism facilitates urinary excretion of arsenic and may prevent arsenic-related adverse health outcomes. We investigated the potential for maternal folate status to modify associations between gestational arsenic exposure and child health. We used data from 364 mother–child pairs in the MIREC study, a prospective pan-Canadian cohort. During pregnancy, we measured first trimester urinary arsenic concentrations, plasma folate biomarkers, and folic acid supplementation intake. At age 3 years, we evaluated twelve neurodevelopmental and anthropometric features. Using latent profile analysis and multinomial regression, we developed phenotypic profiles of child health, estimated covariate-adjusted associations between arsenic and these phenotypic profiles, and evaluated whether folate status modified these associations. We identified three phenotypic profiles of neurodevelopment and three of anthropometry, ranging from less to more optimal child health. Gestational arsenic was associated with decreased odds of optimal neurodevelopment. Maternal folate status did not modify associations of arsenic with neurodevelopmental phenotypic profiles, but gestational arsenic was associated with increased odds of excess adiposity among those who exceed recommendations for folic acid (>1000 μg/day). However, arsenic exposure was low and folate status was high. Gestational arsenic exposure may adversely impact child neurodevelopment and anthropometry, and maternal folate status may not modify these associations; however, future work should examine these associations in more arsenic-exposed or lower folate-status populations.
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McColl, Eliza R., Jeffrey T. Henderson i Micheline Piquette-Miller. "Dysregulation of Amino Acid Transporters in a Rat Model of TLR7-Mediated Maternal Immune Activation". Pharmaceutics 15, nr 7 (1.07.2023): 1857. http://dx.doi.org/10.3390/pharmaceutics15071857.
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Maternal immune activation (MIA) during pregnancy is linked to neurodevelopmental disorders in humans. Similarly, the TLR7 agonist imiquimod alters neurodevelopment in rodents. While the mechanisms underlying MIA-mediated neurodevelopmental changes are unknown, they could involve dysregulation of amino acid transporters essential for neurodevelopment. Therefore, we sought to determine the nature of such transporter changes in both imiquimod-treated rats and human placentas during infection. Pregnant rats received imiquimod on gestational day (GD)14. Transporter expression was measured in placentas and fetal brains via qPCR (GD14.5) and immunoblotting (GD16). To monitor function, fetal brain amino acid levels were measured by HPLC on GD16. Gene expression in the cortex of female fetal brains was further examined by RNAseq on GD19. In human placentas, suspected active infection was associated with decreased ASCT1 and SNAT2 protein expression. Similarly, in imiquimod-treated rats, ASCT1 and SNAT2 protein was also decreased in male placentas, while EAAT2 was decreased in female placentas. CAT3 was increased in female fetal brains. Consistent with this, imiquimod altered amino acid levels in fetal brains, while RNAseq demonstrated changes in expression of several genes implicated in autism. Thus, imiquimod alters amino acid transporter levels in pregnant rats, and similar changes occur in human placentas during active infection. This suggests that changes in expression of amino acid transporters may contribute to effects mediated by MIA toward altered neurodevelopment.
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Newbury, Dianne F., Nuala H. Simpson, Paul A. Thompson i Dorothy V. M. Bishop. "Stage 1 Registered Report: Variation in neurodevelopmental outcomes in children with sex chromosome trisomies: protocol for a test of the double hit hypothesis". Wellcome Open Research 3 (12.02.2018): 10. http://dx.doi.org/10.12688/wellcomeopenres.13828.1.
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Background: The presence of an extra sex chromosome is associated with an increased rate of neurodevelopmental difficulties involving language. Group averages, however, obscure a wide range of outcomes. Hypothesis: The 'double hit' hypothesis proposes that the adverse impact of the extra sex chromosome is amplified when genes that are expressed from the sex chromosomes interact with autosomal variants that usually have only mild effects. Neuroligin-4 genes are expressed from X and Y chromosomes; they play an important role in synaptic development and have been implicated in neurodevelopment. We predict that the impact of an additional sex chromosome on neurodevelopment will be correlated with common autosomal variants involved in related synaptic functions. We describe here an analysis plan for testing this hypothesis using existing data. The analysis of genotype-phenotype associations will be conducted after this plan is published and peer-reviewed Methods: Neurodevelopmental data and DNA are available for 130 children with sex chromosome trisomies (SCTs: 42 girls with trisomy X, 43 boys with Klinefelter syndrome, and 45 boys with XYY). Children from a twin study using the same phenotype measures will form two comparison groups (Ns = 184 and 186). Three indicators of a neurodevelopment disorder phenotype will be used: (i) Standard score on a test of nonword repetition; (ii). A language factor score derived from a test battery; (iii) A general scale of neurodevelopmental challenges based on all available information. Autosomal genes were identified by literature search on the basis of prior association with (a) speech/language/reading phenotypes and (b) synaptic function. Preselected regions of two genes scoring high on both criteria, CNTNAP2 and NRXN1, will be tested for association with neurodevelopmental outcomes using Generalised Structural Component Analysis. We predict the association with one or both genes will be detectable in children with SCTs and stronger than in the comparison samples.
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Newbury, Dianne F., Nuala H. Simpson, Paul A. Thompson i Dorothy V. M. Bishop. "Stage 1 Registered Report: Variation in neurodevelopmental outcomes in children with sex chromosome trisomies: protocol for a test of the double hit hypothesis". Wellcome Open Research 3 (24.04.2018): 10. http://dx.doi.org/10.12688/wellcomeopenres.13828.2.
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Background: The presence of an extra sex chromosome is associated with an increased rate of neurodevelopmental difficulties involving language. Group averages, however, obscure a wide range of outcomes. Hypothesis: The 'double hit' hypothesis proposes that the adverse impact of the extra sex chromosome is amplified when genes that are expressed from the sex chromosomes interact with autosomal variants that usually have only mild effects. Neuroligin-4 genes are expressed from X and Y chromosomes; they play an important role in synaptic development and have been implicated in neurodevelopment. We predict that the impact of an additional sex chromosome on neurodevelopment will be correlated with common autosomal variants involved in related synaptic functions. We describe here an analysis plan for testing this hypothesis using existing data. The analysis of genotype-phenotype associations will be conducted after this plan is published and peer-reviewed Methods: Neurodevelopmental data and DNA are available for 130 children with sex chromosome trisomies (SCTs: 42 girls with trisomy X, 43 boys with Klinefelter syndrome, and 45 boys with XYY). Children from a twin study using the same phenotype measures will form two comparison groups (Ns = 184 and 186). Three indicators of a neurodevelopment disorder phenotype will be used: (i) Standard score on a test of nonword repetition; (ii). A language factor score derived from a test battery; (iii) A general scale of neurodevelopmental challenges based on all available information. Autosomal genes were identified by literature search on the basis of prior association with (a) speech/language/reading phenotypes and (b) synaptic function. Preselected regions of two genes scoring high on both criteria, CNTNAP2 and NRXN1, will be tested for association with neurodevelopmental outcomes using Generalised Structural Component Analysis. We predict the association with one or both genes will be detectable in children with SCTs and stronger than in the comparison samples.
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Ying, Yilin, Xuefei Hu, Peng Han, Aaron Mendez-Bermudez, Serge Bauwens, Rita Eid, Li Tan i in. "The non-telomeric evolutionary trajectory of TRF2 in zebrafish reveals its specific roles in neurodevelopment and aging". Nucleic Acids Research 50, nr 4 (12.02.2022): 2081–95. http://dx.doi.org/10.1093/nar/gkac065.
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Abstract The shelterin protein complex is required for telomere protection in various eukaryotic organisms. In mammals, the shelterin subunit TRF2 is specialized in preventing ATM activation at telomeres and chromosome end fusion in somatic cells. Here, we demonstrate that the zebrafish ortholog of TRF2 (encoded by the terfa gene) is protecting against unwanted ATM activation genome-wide. The terfa-compromised fish develop a prominent and specific embryonic neurodevelopmental failure. The heterozygous fish survive to adulthood but exhibit a premature aging phenotype. The recovery from embryonic neurodevelopmental failure requires both ATM inhibition and transcriptional complementation of neural genes. Furthermore, restoring the expression of TRF2 in glial cells rescues the embryonic neurodevelopment phenotype. These results indicate that the shelterin subunit TRF2 evolved in zebrafish as a general factor of genome maintenance and transcriptional regulation that is required for proper neurodevelopment and normal aging. These findings uncover how TRF2 links development to aging by separate functions in gene expression regulation and genome stability control.
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Hui, Kelvin K., Noriko Takashima, Akiko Watanabe, Thomas E. Chater, Hiroshi Matsukawa, Yoko Nekooki-Machida, Per Nilsson i in. "GABARAPs dysfunction by autophagy deficiency in adolescent brain impairs GABAA receptor trafficking and social behavior". Science Advances 5, nr 4 (kwiecień 2019): eaau8237. http://dx.doi.org/10.1126/sciadv.aau8237.
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Dysfunctional mTOR signaling is associated with the pathogenesis of neurodevelopmental and neuropsychiatric disorders. However, it is unclear what molecular mechanisms and pathogenic mediators are involved and whether mTOR-regulated autophagy continues to be crucial beyond neurodevelopment. Here, we selectively deleted Atg7 in forebrain GABAergic interneurons in adolescent mice and unexpectedly found that these mice showed a set of behavioral deficits similar to Atg7 deletion in forebrain excitatory neurons. By unbiased quantitative proteomic analysis, we identified γ-aminobutyric acid receptor–associated protein-like 2 (GABARAPL2) to differentially form high–molecular weight species in autophagy-deficient brains. Further functional analyses revealed a novel pathogenic mechanism involving the p62-dependent sequestration of GABARAP family proteins, leading to the reduction of surface GABAA receptor levels. Our work demonstrates a novel physiological role for autophagy in regulating GABA signaling beyond postnatal neurodevelopment, providing a potential mechanism for the reduced inhibitory inputs observed in neurodevelopmental and neuropsychiatric disorders with mTOR hyperactivation.
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Smolińska, Katarzyna, Aleksandra Szopa, Jan Sobczyński, Anna Serefko i Piotr Dobrowolski. "Nutritional Quality Implications: Exploring the Impact of a Fatty Acid-Rich Diet on Central Nervous System Development". Nutrients 16, nr 7 (8.04.2024): 1093. http://dx.doi.org/10.3390/nu16071093.
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Given the comprehensive examination of the role of fatty acid-rich diets in central nervous system development in children, this study bridges significant gaps in the understanding of dietary effects on neurodevelopment. It delves into the essential functions of fatty acids in neurodevelopment, including their contributions to neuronal membrane formation, neuroinflammatory modulation, neurogenesis, and synaptic plasticity. Despite the acknowledged importance of these nutrients, this review reveals a lack of comprehensive synthesis in current research, particularly regarding the broader spectrum of fatty acids and their optimal levels throughout childhood. By consolidating the existing knowledge and highlighting critical research gaps, such as the effects of fatty acid metabolism on neurodevelopmental disorders and the need for age-specific dietary guidelines, this study sets a foundation for future studies. This underscores the potential of nutritional strategies to significantly influence neurodevelopmental trajectories, advocating an enriched academic and clinical understanding that can inform dietary recommendations and interventions aimed at optimizing neurological health from infancy.
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Foubert, R., S. Devroe, L. Foubert, M. Van de Velde i S. Rex. "Anesthetic neurotoxicity in the pediatric population: a systematic review of the clinical evidence". Acta Anaesthesiologica Belgica 71, nr 2 (czerwiec 2020): 51–65. http://dx.doi.org/10.56126/71.2.2.
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Background: Exposure to general anesthesia (GA) in early life is known to be neurotoxic to animals. Objectives: To evaluate the risk of GA inducing long-term neurodevelopmental deficits in human children. Design: Systematic review. Methods: We included observational and randomized studies that compared the long-term neurodevelopment of postnatal children exposed to GA to the long-term neurodevelopment of children not exposed to GA. We searched MEDLINE, Embase and Web of Science for relevant studies published in the year 2000 or later. We screened all the identified studies on predetermined inclusion and exclusion criteria. A risk of bias assessment was made for each included study. We identified 9 neurodevelopmental domains for which a sub-analysis was made: intelligence; memory; learning; language/speech; motor function; visuospatial skills; development/emotions/behavior; ADHD/attention; autistic disorder. Results: We included 26 studies involving 605.391 participants. Based on AHRQ-standards 11 studies were of poor quality, 7 studies were of fair quality and 8 studies were of good quality. The major causes of potential bias were selection and comparability bias. On 2 neurodevelopmental domains (visuospatial skills and autistic disorder), the available evidence showed no association with exposure to GA. On 7 other neurodevelopmental domains, the available evidence showed mixed results. The 4 studies that used a randomized or sibling-controlled design showed no association between GA and neurodevelopmental deficits in their primary endpoints. Limitations: The absence of a meta-analysis and funnel plot. Conclusions: Based on observational studies, we found an association between GA in childhood and neuro-developmental deficits in later life. Randomized and sibling-matched observational studies failed to show the same association and therefore no evidence of a causal relationship exists at present. Since GA seems to be a marker, but not a cause of worse neurodevelopment, we argue against delaying or avoiding interventional or diagnostic procedures requiring GA in childhood based on the argument of GA-induced neurotoxicity.
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Morris, Johnathan, Elizabeth J. Bealer, Ivan D. S. Souza, Lauren Repmann, Hannah Bonelli, Joseph F. Stanzione III i Mary M. Staehle. "Chemical Exposure-Induced Developmental Neurotoxicity in Head-Regenerating Schmidtea mediterranea". Toxicological Sciences 185, nr 2 (13.11.2021): 220–31. http://dx.doi.org/10.1093/toxsci/kfab132.
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Abstract The growing number of commercially used chemicals that are under-evaluated for developmental neurotoxicity (DNT) combined with the difficulty in describing the etiology of exposure-related neurodevelopmental toxicity has created a reticent threat to human health. Current means of screening chemicals for DNT are limited to expensive, time-consuming, and labor-intensive traditional laboratory animal models. In this study, we hypothesize that exposed head-regenerating planarian flatworms can effectively and efficiently categorize DNT in known developmental neurotoxins (ethanol and bisphenol A [BPA]). Planarian flatworms are an established alternative animal model for neurodevelopmental studies and have remarkable regenerative abilities allowing neurodevelopment to be induced via head resection. Here, we observed changes in photophobic behavior and central nervous system (CNS) morphology to evaluate the impact of exposure to low concentrations of ethanol, BPA, and BPA industry alternatives bisphenol F, and bisguaiacol on neurodevelopment. Our studies show that exposure to 1% v/v ethanol during regeneration induces a recoverable 48-h delay in the development of proper CNS integrity, which aligns with behavioral assessments of cognitive ability. Exposure to BPA and its alternatives induced deviations to neurodevelopment in a range of severities, distinguished by suppressions, delays, or a combination of the 2. These results suggest that quick and inexpensive behavioral assessments are a viable surrogate for tedious and costly immunostaining studies, equipping more utility and resolution to the planarian model for neurodevelopmental toxicity in the future of mass chemical screening. These studies demonstrate that behavioral phenotypes observed following chemical exposure are classifiable and also temporally correlated to the anatomical development of the CNS in planaria. This will facilitate and accelerate toxicological screening assays with this alternative animal model.
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Morton, Sarah U., Brian J. Leyshon, Eleonora Tamilia, Rutvi Vyas, Michaela Sisitsky, Imran Ladha, John B. Lasekan, Matthew J. Kuchan, P. Ellen Grant i Yangming Ou. "A Role for Data Science in Precision Nutrition and Early Brain Development". Frontiers in Psychiatry 13 (23.06.2022). http://dx.doi.org/10.3389/fpsyt.2022.892259.
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Multimodal brain magnetic resonance imaging (MRI) can provide biomarkers of early influences on neurodevelopment such as nutrition, environmental and genetic factors. As the exposure to early influences can be separated from neurodevelopmental outcomes by many months or years, MRI markers can serve as an important intermediate outcome in multivariate analyses of neurodevelopmental determinants. Key to the success of such work are recent advances in data science as well as the growth of relevant data resources. Multimodal MRI assessment of neurodevelopment can be supplemented with other biomarkers of neurodevelopment such as electroencephalograms, magnetoencephalogram, and non-imaging biomarkers. This review focuses on how maternal nutrition impacts infant brain development, with three purposes: (1) to summarize the current knowledge about how nutrition in stages of pregnancy and breastfeeding impact infant brain development; (2) to discuss multimodal MRI and other measures of early neurodevelopment; and (3) to discuss potential opportunities for data science and artificial intelligence to advance precision nutrition. We hope this review can facilitate the collaborative march toward precision nutrition during pregnancy and the first year of life.
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Nagai, Takahisa, Yoshiko Yoda, Narumi Tokuda, Yasuhiro Takeshima, Munetaka Hirose, Masayuki Shima, Michihiro Kamijima i in. "Association between general anesthesia in early childhood and neurodevelopment up to 4 years of age: the Japan Environment and Children’s Study". Journal of Anesthesia, 7.06.2024. http://dx.doi.org/10.1007/s00540-024-03359-9.
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Abstract Purpose The effects of general anesthesia on neurodevelopment in children remain controversial. We explored the relationship between general anesthesia and neurodevelopment in children participating in the Japan Environment and Children’s Study (JECS). Methods This study enrolled children born between 37 and 41 weeks of pregnancy via single-vaginal delivery to pregnant women registered in the JECS between January 2011 and March 2014. Data were collected from mother-completed questionnaires and medical transcripts. Neurodevelopment in five domains was assessed every 6 months between 12 and 48 months of age, using the Ages and Stages Questionnaires. The associations between general anesthesia exposure during early childhood and neurodevelopment in children were evaluated at each time point. Adjusted odds ratios and 95% confidence intervals were estimated after covariate adjustment using logistic regression models. Results Children who received general anesthesia before age 1 year had higher risks of neurodevelopmental delay in all five domains throughout the observational period. The largest risk was for gross motor delay at 18 months (adjusted odds ratio: 3.51; 95% confidence interval: 2.75–4.49). The effects on the incidence of neurodevelopmental delays after age 3 were not observed except for problem solving at 48 months. The risk of neurodevelopmental delay in children who first received general anesthesia after age 1 was considerably small. Conclusions This study suggests that general anesthesia administration before age 1 is associated with neurodevelopmental delay during 1–4 years of age. The risk of general anesthesia after age 1 may be small.
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Frye, Richard E., Janet Cakir, Shannon Rose, Leanna Delhey, Sirish C. Bennuri, Marie Tippett, Stepan Melnyk i in. "Prenatal air pollution influences neurodevelopment and behavior in autism spectrum disorder by modulating mitochondrial physiology". Molecular Psychiatry, 22.09.2020. http://dx.doi.org/10.1038/s41380-020-00885-2.
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Abstract We investigate the role of the mitochondrion, an organelle highly sensitive to environmental agents, in the influence of prenatal air pollution exposure on neurodevelopment and behavior in 96 children with autism spectrum disorder (ASD) [45 with neurodevelopmental regression (NDR); 76% Male; mean (SD) age 10 y 9 m (3 y 9 m)]. Mitochondrial function was assessed using the Seahorse XFe96 in fresh peripheral blood mononuclear cells. Second and third trimester average and maximal daily exposure to fine air particulate matter of diameter ≤2.5 µm (PM2.5) was obtained from the Environmental Protection Agency’s Air Quality System. Neurodevelopment was measured using the Vineland Adaptive Behavior Scale 2nd edition and behavior was assessed using the Aberrant Behavior Checklist and Social Responsiveness Scale. Prenatal PM2.5 exposure influenced mitochondrial respiration during childhood, but this relationship was different for those with (r = 0.25–0.40) and without (r = −0.07 to −0.19) NDR. Mediation analysis found that mitochondrial respiration linked to energy production accounted for 25% (SD = 2%) and 10% (SD = 2%) of the effect of average prenatal PM2.5 exposure on neurodevelopment and behavioral symptoms, respectively. Structural equation models estimated that PM2.5 and mitochondrial respiration accounted for 34% (SD = 4%) and 36% (SD = 3%) of the effect on neurodevelopment, respectively, and that behavior was indirectly influenced by mitochondrial respiration through neurodevelopment but directly influenced by prenatal PM2.5. Our results suggest that prenatal exposure to PM2.5 disrupts neurodevelopment and behavior through complex mechanisms, including long-term changes in mitochondrial respiration and that patterns of early development need to be considered when studying the influence of environmental agents on neurodevelopmental outcomes.
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Urbonaite, Gintare, Agne Knyzeliene, Fanny Sophia Bunn, Adomas Smalskys i Urte Neniskyte. "The impact of maternal high-fat diet on offspring neurodevelopment". Frontiers in Neuroscience 16 (22.07.2022). http://dx.doi.org/10.3389/fnins.2022.909762.
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A maternal high-fat diet affects offspring neurodevelopment with long-term consequences on their brain health and behavior. During the past three decades, obesity has rapidly increased in the whole human population worldwide, including women of reproductive age. It is known that maternal obesity caused by a high-fat diet may lead to neurodevelopmental disorders in their offspring, such as autism spectrum disorder, attention deficit hyperactivity disorder, anxiety, depression, and schizophrenia. A maternal high-fat diet can affect offspring neurodevelopment due to inflammatory activation of the maternal gut, adipose tissue, and placenta, mirrored by increased levels of pro-inflammatory cytokines in both maternal and fetal circulation. Furthermore, a maternal high fat diet causes gut microbial dysbiosis further contributing to increased inflammatory milieu during pregnancy and lactation, thus disturbing both prenatal and postnatal neurodevelopment of the offspring. In addition, global molecular and cellular changes in the offspring’s brain may occur due to epigenetic modifications including the downregulation of brain-derived neurotrophic factor (BDNF) expression and the activation of the endocannabinoid system. These neurodevelopmental aberrations are reflected in behavioral deficits observed in animals, corresponding to behavioral phenotypes of certain neurodevelopmental disorders in humans. Here we reviewed recent findings from rodent models and from human studies to reveal potential mechanisms by which a maternal high-fat diet interferes with the neurodevelopment of the offspring.