Journal articles: 'Lead exposure; cognitive; development'

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Massaro, E. J., and T. F. Massaro. "Low Level Lead Exposure During Neonatal Development Perturbs Cognitive Function." Journal of the American College of Toxicology 6, no. 4 (July 1987): 441–49. http://dx.doi.org/10.3109/10915818709075689.

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Complex maze learning was investigated in male neonatal and adult rats using a latent learning task. The neonates received (intragastric administration) either lead acetate (50 mg Pb/kg) or equimolar sodium acetate on days 6, 9, 12, and 18 postpartum. The adult subjects were exposed to 100 ppm Pb acetate or equimolar sodium acetate in drinking water for 112 days beginning at weaning (day 21 postpartum). Training for the latent learning task began on day 31 postpartum for the neonates and on day 143 for the young adults. The training sequence included free exploration (under conditions of satiation) of a symmetrical latent learning maze or an open field of the same shape and area by the Pb-treated and control subjects (randomly distributed). Subsequently, all subjects were food deprived and appetitively tested in the latent learning maze. Neonatal lead exposure perturbed latent learning: the Pb-treated subjects showed no evidence of latent learning. However, pretest exploratory activity was similar for Pb-exposed and control neonates. Pb exposure had no effect on exploratory activity under normal (nonappetitive) conditions or latent learning performance of young adult subjects despite the increased body burden of Pb. The results suggest that latent learning may be a particularly sensitive measure of Pb exposure in the neonatal rat model.

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MENDELSOHN, ALAN L., BENARD P. DREYER, ARTHUR H. FIERMAN, CAROLYN M. ROSEN, LORI A. LEGANO, HILLARY A. KRUGER, SYLVIA W. LIM, SUSAN BARASCH, AU LORETTA, and CHERYL D. COURTLANDT. "Low-Level Lead Exposure and Cognitive Development in Early Childhood." Journal of Developmental & Behavioral Pediatrics 20, no. 6 (December 1999): 425–31. http://dx.doi.org/10.1097/00004703-199912000-00004.

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TONG, S. "Lead exposure and cognitive development: Persistence and a dynamic pattern." Journal of Paediatrics and Child Health 34, no. 2 (April 1998): 114–18. http://dx.doi.org/10.1046/j.1440-1754.1998.00187.x.

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Tong, Shilu, Anthony J. McMichael, and Peter A. Baghurst. "Interactions between Environmental Lead Exposure and Sociodemographic Factors on Cognitive Development." Archives of Environmental Health: An International Journal 55, no. 5 (September 2000): 330–35. http://dx.doi.org/10.1080/00039890009604025.

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Lee, Haena, Mark Lee, and John Robert Warren. "Childhood Lead Exposure and Cognitive Functioning Among Older Adults: Evidence From the Health and Retirement Study." Innovation in Aging 5, Supplement_1 (December 1, 2021): 311. http://dx.doi.org/10.1093/geroni/igab046.1212.

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Abstract Many children born in the early 20th century were exposed to water-borne lead, a neurotoxin that negatively impacts brain development. While lead exposure has been linked to poor cognition among children and young adults, no population-level research has examined the long-term implications of lead exposure for cognitive functioning in later life. Our study is the first to address this gap by utilizing novel data linkages between the 1940 U.S. Census and the Health and Retirement Study (HRS). Our sample includes respondents who were under age 17 (born 1924-1940) by the time of the decennial enumeration on April 1, 1940. Given that the dominant source of lead exposure was water during this period, we assessed lead exposure by using water chemistry and piping material data for each HRS respondent’s city of residence in 1940. Late-life cognitive functioning for HRS participants (observed 1998-2016) was measured using the Telephone Interview for Cognitive Status. We find that lead exposure during childhood is significantly and negatively associated with cognitive functioning in later life. HRS participants who lived in cities with lead pipes and acidic or alkaline water—the conditions required for lead to leech into municipal water—showed lower levels of cognitive functioning decades later as compared to other participants. This association persisted net of race, gender, childhood socioeconomic status and childhood health. However, the association was largely accounted for by adjusting for educational attainment. This implies that childhood lead exposure impacts later-life cognition via its effect on educational attainment.

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Marshall, Andrew T., Rob McConnell, Bruce P. Lanphear, Wesley K. Thompson, Megan M. Herting, and Elizabeth R. Sowell. "Risk of lead exposure, subcortical brain structure, and cognition in a large cohort of 9- to 10-year-old children." PLOS ONE 16, no. 10 (October 14, 2021): e0258469. http://dx.doi.org/10.1371/journal.pone.0258469.

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Background Lead, a toxic metal, affects cognitive development at the lowest measurable concentrations found in children, but little is known about its direct impact on brain development. Recently, we reported widespread decreases in cortical surface area and volume with increased risks of lead exposure, primarily in children of low-income families. Methods and findings We examined associations of neighborhood-level risk of lead exposure with cognitive test performance and subcortical brain volumes. We also examined whether subcortical structure mediated associations between lead risk and cognitive performance. Our analyses employed a cross-sectional analysis of baseline data from the observational Adolescent Brain Cognitive Development (ABCD) Study. The multi-center ABCD Study used school-based enrollment to recruit a demographically diverse cohort of almost 11,900 9- and 10-year-old children from an initial 22 study sites. The analyzed sample included data from 8,524 typically developing child participants and their parents or caregivers. The primary outcomes and measures were subcortical brain structure, cognitive performance using the National Institutes of Health Toolbox, and geocoded risk of lead exposure. Children who lived in neighborhoods with greater risks of environmental lead exposure exhibited smaller volumes of the mid-anterior (partial correlation coefficient [rp] = -0.040), central (rp = -0.038), and mid-posterior corpus callosum (rp = -0.035). Smaller volumes of these three callosal regions were associated with poorer performance on cognitive tests measuring language and processing speed. The association of lead exposure risk with cognitive performance was partially mediated through callosal volume, particularly the mid-posterior corpus callosum. In contrast, neighborhood-level indicators of disadvantage were not associated with smaller volumes of these brain structures. Conclusions Environmental factors related to the risk of lead exposure may be associated with certain aspects of cognitive functioning via diminished subcortical brain structure, including the anterior splenium (i.e., mid-posterior corpus callosum).

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Min, Meeyoung, Lynn Singer, Sonia Minnes, H. Lester Kirchner, and Suchitra Nelson. "Cognitive development and low-level lead exposure in poly-drug exposed children." Neurotoxicology and Teratology 30, no. 3 (May 2008): 249. http://dx.doi.org/10.1016/j.ntt.2008.03.025.

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Min, Meeyoung O., Lynn T. Singer, H. Lester Kirchner, Sonia Minnes, Elizabeth Short, Zehra Hussain, and Suchitra Nelson. "Cognitive development and low-level lead exposure in poly-drug exposed children." Neurotoxicology and Teratology 31, no. 4 (July 2009): 225–31. http://dx.doi.org/10.1016/j.ntt.2009.03.002.

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Bellinger, David, Alan Leviton, Christine Waternaux, Herbert Needleman, and Michael Rabinowitz. "Longitudinal Analyses of Prenatal and Postnatal Lead Exposure and Early Cognitive Development." New England Journal of Medicine 316, no. 17 (April 23, 1987): 1037–43. http://dx.doi.org/10.1056/nejm198704233161701.

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Levitt, Miriam. "Toxic metals, preconception and early childhood development." Social Science Information 38, no. 2 (June 1999): 179–201. http://dx.doi.org/10.1177/053901899038002001.

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Exposure to lead and other heavy metals is now considered a risk factor in fetal and early childhood developmental deficits, premature birth, low cranial circumference, lower IQ, learning disabilities, attention deficit disorders (ADD) or hyperactivity (ADHD), and reduced impulse control. Studies suggest that blood lead levels as low as 10 micrograms per deciliter can result in detectable physical, cognitive, and psychobehavioral deficits in children. According to recent CDC findings, the major sources of lead exposure include deteriorated paint in older housing, and dust and soil that are contaminated with lead from old paint and from past emissions of leaded gasoline. Further, the direct effects of poor diet on children's behavior combined with exposure to toxic metals increase the likelihood of attention deficit disorder (ADD), hyperactivity, and other learning deficits. Poor urban populations and minorities are at increased risk for these effects of neurotoxicity, because the problems of poverty and broken families often co-vary with inadequate diet, housing that contains lead paint and water systems that release lead, inadequate prenatal health care, high rates of bottle feeding, and exposure to industrial pollution.

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Polanska, Kinga, Wojciech Hanke, Wojciech Sobala, Malgorzata Trzcinka-Ochocka, Danuta Ligocka, Slawomir Brzeznicki, Halina Strugala-Stawik, and Per Magnus. "Developmental Effects of Exposures to Environmental Factors: The Polish Mother and Child Cohort Study." BioMed Research International 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/629716.

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This paper estimates the effects of exposure to environmental factors, including lead, mercury, environmental tobacco smoke (ETS), and polycyclic aromatic hydrocarbons (PAH), on child psychomotor development. The study population consists of mother-child pairs in the Polish Mother and Child Cohort Study. Prenatal and postnatal exposure to environmental factors was determined from biomarker measurements as follows: for lead exposure—cord blood lead level, for mercury—maternal hair mercury level, for ETS—cotinine level in saliva and urine, and for PAH—1-hydroxypyrene (1-HP) in urine. At the age of 12 (406 subjects) and 24 months (198 subjects) children were assessed using Bayley Scales of Infant and Toddler Development. There were no statistically significant effects of prenatal exposure to mercury or 1-HP on child psychomotor development. After adjusting for potential confounders, adverse effects of prenatal exposure to ETS on motor development (β= −2.6;P=0.02) and postnatal exposure to ETS on cognitive (β= −0.2;P=0.05) and motor functions (β= −0.5;P=0.01) were found. The adverse effect of prenatal lead exposure on cognitive score was of borderline significance (β= −6.2;P=0.06). The study underscores the importance of policies and public health interventions that aim to reduce prenatal and postnatal exposure to lead and ETS.

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Bellinger, David, Alan Leviton, Jone Sloman, Michael Rabinowitz, Herbert L. Needleman, and Christine Waternaux. "Low-Level Lead Exposure and Children's Cognitive Function in the Preschool Years." Pediatrics 87, no. 2 (February 1, 1991): 219–27. http://dx.doi.org/10.1542/peds.87.2.219.

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In a cohort of 170 middle and upper-middle class children participating in a prospective study of child development and low-level lead exposure, higher blood lead levels at age 24 months were associated with lower scores at age 57 months on the McCarthy Scales of Children's Abilities. The mean blood lead level at age 24 months was 6.8 µg/dL (SD = 6.3; 75th, 90th, and 99th percentiles: 8.8, 13.7, 23.6, respectively) and for all but 1 child was less than 25 µg/dL, the current definition of an "elevated" level. After adjustment for confounding, scores on the General Cognitive Index decreased approximately 3 points (SE = 1.4) for each natural log unit increase in 24-month blood lead level. The inverse association between lead level and performance was especially prominent for visual-spatial and visual-motor integration skills. Higher prenatal exposures were not associated with lower scores at 57 months except in the subgroup of children with "high" concurrent blood lead levels (ie, ≥10 µg/dL). The concentration of lead in the dentine of shed deciduous teeth was not significantly associated with children's performance after adjustment for confounding.

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Al-Saleh, Iman, Michael Nester, Abdullah Mashhour, Lina Moncari, Neptune Shinwari, Gamal El-Din Mohamed, and Abdullah Rabah. "Prenatal and Postnatal Lead Exposure and Early Cognitive Development: Longitudinal Study in Saudi Arabia." Journal of Environmental Pathology, Toxicology and Oncology 28, no. 4 (2009): 283–302. http://dx.doi.org/10.1615/jenvironpatholtoxicoloncol.v28.i4.40.

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Kordas, Katarzyna, Graciela Ardoino, Donna L. Coffman, Elena I. Queirolo, Daniela Ciccariello, Nelly Mañay, and Adrienne S. Ettinger. "Patterns of Exposure to Multiple Metals and Associations with Neurodevelopment of Preschool Children from Montevideo, Uruguay." Journal of Environmental and Public Health 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/493471.

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While it is known that toxic metals contribute individually to child cognitive and behavioral deficits, we still know little about the effects of exposure to multiple metals, particularly when exposures are low. We studied the association between children’s blood lead and hair arsenic, cadmium, and manganese and their performance on the Bayley Scales of Infant Development III. Ninety-two preschool children (age 13–42 months) from Montevideo, Uruguay, provided a hair sample and 78 had a blood lead level (BLL) measurement. Using latent class analysis (LCA), we identified four groups of exposure based on metal concentrations: (1) low metals, (2) low-to-moderate metals, (3) high lead and cadmium, and (4) high metals. Using the four-group exposure variable as the main predictor, and fitting raw scores on the cognitive, receptive vocabulary, and expressive vocabulary scales as dependent variables, both complete-case and multiple imputation (MI) analyses were conducted. We found no association between multiple-metal exposures and neurodevelopment in covariate-adjusted models. This study demonstrates the use of LCA together with MI to determine patterns of exposure to multiple toxic metals and relate these to child neurodevelopment. However, because the overall study population was small, other studies with larger sample sizes are needed to investigate these associations.

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A, Marshall, Betts S, McConnell R, Lanphear B, Thompson W, Dowling G, Fan C, and Sowell E. "Socioeconomic adversity and risk of lead exposure is associated with brain and cognitive development in the Adolescent Brain Cognitive Development (ABCD) study." Environmental Epidemiology 3 (October 2019): 260. http://dx.doi.org/10.1097/01.ee9.0000608764.56723.3e.

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Dietrich, Kim N., Paul A. Succop, Omer G. Berger, Paul B. Hammond, and Robert L. Bornschein. "Lead exposure and the cognitive development of urban preschool children: The cincinnati lead study cohort at age 4 years." Neurotoxicology and Teratology 13, no. 2 (March 1991): 203–11. http://dx.doi.org/10.1016/0892-0362(91)90012-l.

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Z, Repp, Hertza J, Burton J, and Jupp K. "A-049 Cognitive Correlates of Childhood Lead Poisoning in a High Achieving Child." Archives of Clinical Neuropsychology 35, no. 6 (August 28, 2020): 839. http://dx.doi.org/10.1093/arclin/acaa068.049.

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Abstract Objective Individuals exposed to lead often have persistent medical issues, changes in personality, and cognitive decline, with worsening symptoms following chronic exposure. Lead poisoning in children can have lasting effects as they age. This case study examines the correlation between cognitive ability and brain damage, with demyelination, following lead exposure in an academically well performing eight-year-old. Lead poisoning was verified by medical records and neuroimaging showing demyelination is included. Method The individual was an eight-year-old male who was exposed to lead multiple times in a home environment over the course of one year starting as a two-year-old. Cognitive ability, academic achievement, and emotional development were assessed with clinical interview of the child and his mother and comprehensive test battery including cognitive and emotional measures. Testing also included appropriate imbedded and free-standing validity measures. Results Cognitive testing showed relative weakness in certain measures of verbal and visuospatial processing speed as well as indications of deficit in sustained attention. These deficits did not reach objective impairment but suggest weakness in these areas in the context of superior overall cognitive ability and academic achievement. Observation showed hyperactivity and anxious behaviors, the individual’s mother reported elevated anxiety and unusually high somatic complaints. Conclusion This pattern of scores corresponded to what is typically seen in patients with lead poisoning, suggesting an impact of lead poisoning on the individual’s neural development, potentially causing both cognitive and psychiatric deficits. This case is unique because, despite his lead poisoning, the patient performs well academically, suggesting that the brain can compensate for this impairment given the correct environment.

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Zhou, Leilei, Jian Xu, Jinsong Zhang, Chonghuai Yan, Yanfen Lin, Yinan Jia, and Wenjing Hu. "Prenatal maternal stress in relation to the effects of prenatal lead exposure on toddler cognitive development." NeuroToxicology 59 (March 2017): 71–78. http://dx.doi.org/10.1016/j.neuro.2017.01.008.

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Sasaki, Nozomi, and David O. Carpenter. "Associations between Metal Exposures and Cognitive Function in American Older Adults." International Journal of Environmental Research and Public Health 19, no. 4 (February 17, 2022): 2327. http://dx.doi.org/10.3390/ijerph19042327.

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Cognitive function frequently declines with older age, independently of the development of neurodegenerative diseases, and few interventions are known to counter this decline. Exposure to neurotoxic metals may contribute to this decline in cognitive function in older adults. Using the National Health and Nutrition Examination Survey (NHANES) data, the performance of 3042 adults aged 60 years and older on three cognitive tests for immediate, delayed, and working memory were examined in relation to blood concentrations of seven metals and metalloids and urinary concentrations of nineteen metals and metabolites. Using linear regression models, associations between cognitive tests and logarithms of metal exposures were adjusted for age, sex, ethnicity, education level, depression, diabetes, alcohol consumption, and cigarette use. Increased selenium was strongly associated with better performance on all three cognitive tests. Cadmium and lead were negatively associated with performance on all three cognitive tests. Some urinary metabolites of arsenic, urinary lead, cadmium, and tungsten were significantly associated with poor performance on some tests. In older adults, higher selenium levels were strongly associated with better cognitive performance.

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Polanska, Kinga, Wojciech Hanke, Natalia Pawlas, Ewelina Wesolowska, Agnieszka Jankowska, Marta Jagodic, Darja Mazej, et al. "Sex-Dependent Impact of Low-Level Lead Exposure during Prenatal Period on Child Psychomotor Functions." International Journal of Environmental Research and Public Health 15, no. 10 (October 16, 2018): 2263. http://dx.doi.org/10.3390/ijerph15102263.

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The impact of exposure to lead on child neurodevelopment has been well established. However, sex differences in vulnerability are still not fully explained. We aimed at evaluating the effect of a low-level lead exposure, as measured between 20 to 24 weeks of pregnancy and in cord blood, on developmental scores up to 24 months of age in 402 children from the Polish Mother and Child Cohort (REPRO_PL). Additionally, sex-dependent susceptibility to lead at this very early stage of psychomotor development was assessed. The blood lead levels were analyzed using inductively coupled plasma mass spectrometry (ICP-MS). In order to estimate the children’s neurodevelopment, the Bayley Scales of Infant and Toddler Development was applied. The geometric mean (GM) for blood lead level during 20–24 weeks of pregnancy was 0.99 ± 0.15 µg/dL and, in the cord blood, it was 0.96 ± 0.16 µg/dL. There was no statistically significant impact of lead exposure during prenatal period on the girls’ psychomotor abilities. Among the boys, we observed lower scores for cognitive functions, along with increasing cord blood lead levels (β = −2.07; p = 0.04), whereas the results for the language and motor abilities were not statistically significant (p > 0.05). Our findings show that fetal exposure to very low lead levels might affect early cognitive domain, with boys being more susceptible than girls. Education on health, higher public awareness, as well as intervention programs, along with relevant regulations, are still needed to reduce risks for the vulnerable population subgroups.

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RIS, M. DOUGLAS, KIM N. DIETRICH, PAUL A. SUCCOP, OMER G. BERGER, and ROBERT L. BORNSCHEIN. "Early exposure to lead and neuropsychological outcome in adolescence." Journal of the International Neuropsychological Society 10, no. 2 (March 2004): 261–70. http://dx.doi.org/10.1017/s1355617704102154.

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One hundred and ninety-five participants in the Cincinnati Lead Study were neuropsychologically evaluated in mid-adolescence. The neuropsychological measures yielded five factors labeled Memory, Learning/IQ, Attention, Visuoconstruction, and Fine-Motor. Prenatal, Average Childhood, and 78 month blood lead (PbB) levels were used in a series of multiple regression analyses. Following rigorous covariate pretesting and adjustment, a significant main effect of 78 month PbB on the Fine-Motor factor was found (p< .004). Significant interactions were also found between gender and lead exposure parameters for both Attention and Visuoconstruction indicating heightened risk in males. Finally, a trend toward significance was found for the PbB × SES interaction for Learning/IQ, consistent with previous evidence of increased educational and cognitive vulnerability for youth from more disadvantaged backgrounds. These results provide new evidence from the longest continuing prospective study of the remote effects of early lead exposure. They indicate the presence of selective neuropsychological effects in this population, and also that males and females are not uniformly affected. These results also underscore the complexity of models of neurobehavioral development, and the modest predictive power of any single determinant. (JINS, 2004,10, 261–270.)

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Tartaglione, Anna Maria, Melania Maria Serafini, Andrea Raggi, Francesca Iacoponi, Elisa Zianni, Alessandro Scalfari, Luisa Minghetti, et al. "Sex-Dependent Effects of Developmental Lead Exposure in Wistar Rats: Evidence from Behavioral and Molecular Correlates." International Journal of Molecular Sciences 21, no. 8 (April 11, 2020): 2664. http://dx.doi.org/10.3390/ijms21082664.

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Lead (Pb) exposure in early life affects brain development resulting in cognitive and behavioral deficits. Epidemiologic and experimental evidence of sex as an effect modifier of developmental Pb exposure is emerging. In the present study, we investigated Pb effects on behavior and mechanisms of neuroplasticity in the hippocampus and potential sex differences. To this aim, dams were exposed, from one month pre-mating to offspring weaning, to Pb via drinking water at 5 mg/kg body weight per day. In the offspring of both sexes, the longitudinal assessment of motor, emotional, and cognitive end points was performed. We also evaluated the expression and synaptic distribution of N-methyl-D-Aspartate receptor (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunits at post-natal day (pnd) 23 and 70 in the hippocampus. Neonatal motor patterns and explorative behavior in offspring were affected in both sexes. Pb effects in emotional response and memory retention were observed in adult females only, preceded by increased levels of GluN2A and GluA1 subunits at the post-synapse at pnd 23. These data suggest that Pb exposure during development affects glutamatergic receptors distribution at the post-synaptic spine in females. These effects may contribute to alterations in selected behavioral domains.

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Bihaqi, Syed Waseem, Azadeh Bahmani, Gehad M. Subaiea, and Nasser H. Zawia. "Infantile exposure to lead and late-age cognitive decline: Relevance to AD." Alzheimer's & Dementia 10, no. 2 (July 17, 2013): 187–95. http://dx.doi.org/10.1016/j.jalz.2013.02.012.

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Dietrich, K. "Lead exposure and the central auditory processing abilities and cognitive development of urban children: The cincinnati lead study cohort at age 5 years." Neurotoxicology and Teratology 14, no. 1 (February 1992): 51–56. http://dx.doi.org/10.1016/0892-0362(92)90028-9.

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Farías, Paulina, David Hernández-Bonilla, Hortensia Moreno-Macías, Sergio Montes-López, Lourdes Schnaas, José Luis Texcalac-Sangrador, Camilo Ríos, and Horacio Riojas-Rodríguez. "Prenatal Co-Exposure to Manganese, Mercury, and Lead, and Neurodevelopment in Children during the First Year of Life." International Journal of Environmental Research and Public Health 19, no. 20 (October 11, 2022): 13020. http://dx.doi.org/10.3390/ijerph192013020.

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Lead (Pb), mercury (Hg), and manganese (Mn) are neurotoxic, but little is known about the neurodevelopmental effects associated with simultaneous prenatal exposure to these metals. We aimed to study the associations of Pb, Hg, and Mn prenatal levels (jointly and separately) with neurodevelopment in the first year of life. Methods: Pb, Hg, and Mn blood lead levels were measured in 253 pregnant women. Their offspring’s neurodevelopment was assessed through the Bayley Scale of Infant Development III® at one, three, six, and twelve months. The metals’ mean blood levels (µg/L) were Pb = 11.2, Hg = 2.1, and Mn = 10.2. Mean language, cognitive, and motor development scores of the infants at each age were between low-average and average. Multilevel models’ results showed that language development coefficients of the offspring decreased by 1.5 points per 1 µg/dL increase in maternal blood lead levels (p = 0.002); the magnitude of the aforementioned association increased in children with maternal blood Mn < 9.6 µg/L (ß = −1.9, p = 0.003) or Hg > 1.9 µg/L (ß = −1.6, p = 0.013). Cognitive and motor development had negative associations with maternal blood Pb levels; the latter was statistically significant when the interaction term between Pb, Mn, and Hg was included (ß = −0.037, p = 0.03). Prenatal exposure to low Pb levels may impair infants’ neurodevelopment in the first year of life, even more so if they are exposed to Hg or deficient in Mn.

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Yin, Y., H. Li, J. Wang, Y. Kong, J. Chang, and G. Chu. "Implication of microglia in ketamine-induced long-term cognitive impairment in murine pups." Human & Experimental Toxicology 41 (January 2022): 096032712211287. http://dx.doi.org/10.1177/09603271221128739.

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Background Ketamine, a non-competitive N-methyl-D-aspartate receptor (NMDAR) antagonist, is widely applicable to anesthesia, analgesia, and sedation. However, the function and mechanisms of ketamine in the long-term learning and memory function of neonatal mice are unclear. Objective The present study aims to investigate whether long-term learning and memory function will be affected by multiple ketamine exposures in the early development period. Methods The mRNA and protein levels were measured by RT-qPCR and western blot, respectively. The Morris Water Maze test was performed to assess spatial learning and memory. Results We identified that neonatal exposure to ketamine downsized the positive neurons for microtubule-associated protein doublecortin (DCX) and Ki67 in hippocampal dentate gyrus at the juvenile and late adolescence stages. Double-labeling tests demonstrated that the counts of Iba1+ cells and Ki67+ cells were pronouncedly diminished with exposure to ketamine. Further, qPCR assays to screen the key factors predisposing the populations and maturation of microglia exhibited remarkable decline of CX3CR1 mRNA levels in ketamine group versus the control group. The close relation of microglia to synaptic plasticity was depicted by the significantly downregulated synaptic plasticity-related proteins NR2B and PSD-95 subsequent to multiple exposures to ketamine. Finally, we found that both the protein and mRNA levels of BDNF were markedly decreased in ketamine group versus the control group. Conclusion We found that multiple exposures to ketamine in neonatal mice lead to spatial learning and memory dysfunction. The alterations of microglial development and function are the possible mechanisms of long-term learning and memory impairment.

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Dou, John F., Zishaan Farooqui, Christopher D. Faulk, Amanda K. Barks, Tamara Jones, Dana C. Dolinoy, and Kelly M. Bakulski. "Perinatal Lead (Pb) Exposure and Cortical Neuron-Specific DNA Methylation in Male Mice." Genes 10, no. 4 (April 4, 2019): 274. http://dx.doi.org/10.3390/genes10040274.

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: Lead (Pb) exposure is associated with a wide range of neurological deficits. Environmental exposures may impact epigenetic changes, such as DNA methylation, and can affect neurodevelopmental outcomes over the life-course. Mating mice were obtained from a genetically invariant C57BL/6J background agouti viable yellow Avy strain. Virgin dams (a/a) were randomly assigned 0 ppm (control), 2.1 ppm (low), or 32 ppm (high) Pb-acetate water two weeks prior to mating with male mice (Avy/a), and this continued through weaning. At age 10 months, cortex neuronal nuclei were separated with NeuN+ antibodies in male mice to investigate neuron-specific genome-wide promoter DNA methylation using the Roche NimbleGen Mouse 3x720K CpG Island Promoter Array in nine pooled samples (three per dose). Several probes reached p-value < 10-5 , all of which were hypomethylated: 12 for high Pb (minimum false discovery rate (FDR) = 0.16, largest intensity ratio difference = −2.1) and 7 for low Pb (minimum FDR = 0.56, largest intensity ratio difference = −2.2). Consistent with previous results in bulk tissue, we observed a weak association between early-life exposure to Pb and DNA hypomethylation, with some affected genes related to neurodevelopment or cognitive function. Although these analyses were limited to males, data indicate that non-dividing cells such as neurons can be carriers of long-term epigenetic changes induced in development.

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Liu, Rundong, Yawei Wang, Lin Bai, Ruike Wang, Yingying Wu, Mengchen Liu, Qiong Li, et al. "Time-course miRNA alterations and SIRT1 inhibition triggered by adolescent lead exposure in mice." Toxicology Research 10, no. 4 (June 7, 2021): 667–76. http://dx.doi.org/10.1093/toxres/tfab050.

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Abstract Sirtuin 1 (SIRT1), the NAD-dependent histone deacetylase, has been extensively investigated due to its cognitive protective effect. Studies suggest microRNAs (miRNAs) and histone modifications are key epigenetic regulators of gene expression and play important role in brain development. We previously showed that cognitive impairment by lead (Pb) was associated with downregulation of SIRT1, but the epigenetic role of this is unclear. Thus, we exposed 4-week-old male mice to 0.2% lead acetate solution for three months, and subsequently extracted brain homogenate from mice cortex and hippocampus at the age of 1, 4, and 16 months, respectively. In this study, we found that the protein level of SIRT1 was inhibited in the hippocampus and cortex of 16-month-old aged mice exposed to Pb. Moreover, changes in the levels of miR-138-5p and miR-141-3p, which were considered to the mechanistic target of SIRT1 by bioinformatic analysis, were negative correlations SIRT1 protein expression. We also found miR-34c-3p expression was increased in the cortex of mice at the age of 16 months. Collectively, our results showed the expression of neural SIRT1 and three selected microRNAs at different age nodes of mice for the first time of following Pb exposure. Our results suggest that additional efforts should focus on the consequences of early Pb exposure from an epigenetic perspective.

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Ferriday, Danielle, and Jeffrey M. Brunstrom. "How does food-cue exposure lead to larger meal sizes?" British Journal of Nutrition 100, no. 6 (December 2008): 1325–32. http://dx.doi.org/10.1017/s0007114508978296.

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Exposure to the sight and smell of food influences our momentary desire to consume it. This study explored the process by which cue exposure promotes greater consumption of food. Three hypotheses were explored, cue exposure: (i) increases the planned consumption of food; (ii) increases tolerance of larger portion sizes; (iii) arrests the development of satiety. Female participants (n50) were each tested in two conditions. In a ‘cue condition’ they were exposed to the sight and smell of pizza for 60 s. Before and after this period they provided information about prospective and maximum tolerated portion sizes and their desire to eat pizza and other non-cued foods. Participants then consumed a fixed portion of pizza, rated their hunger and were finally offeredad libitumaccess to pizza. In the ‘no-cue condition’, cue exposure was replaced with a cognitive task. Cueing had little effect on tolerance of larger portion sizes or on hunger after consuming the fixed portion. Instead, it increased prospective pizza portion size and subsequent intake of pizza. Together, these results suggest that cueing increases the amount of food that people actively plan to eat. This plan is then executed, leading to greater intake. Pizza cueing also increased prospective portion size of other foods. Thus, contrary to previous reports, effects of exposure may generalise to other foods. Finally, we found evidence that restrained eaters are less ‘cue reactive’ than unrestrained eaters. In future, our approach might be adapted to consider whether heightened ‘cue reactivity’ represents a risk factor for obesity.

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Nevo-Shenker, Michal, and Shlomit Shalitin. "The Impact of Hypo- and Hyperglycemia on Cognition and Brain Development in Young Children with Type 1 Diabetes." Hormone Research in Paediatrics 94, no. 3-4 (2021): 115–23. http://dx.doi.org/10.1159/000517352.

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Human and experimental animal data suggest both hyperglycemia and hypoglycemia can lead to altered brain structure and neurocognitive function in type 1 diabetes (T1D). Young children with T1D are prone to extreme fluctuations in glucose levels. The overlap of these potential dysglycemic insults to the brain during the time of most active brain and cognitive development may cause cellular and structural injuries that appear to persist into adult life. Brain structure and cognition in persons with T1D are influenced by age of onset, exposure to glycemic extremes such as severe hypoglycemic episodes, history of diabetic ketoacidosis, persistent hyperglycemia, and glucose variability. Studies using brain imaging techniques have shown brain changes that appear to be influenced by metabolic abnormalities characteristic of diabetes, changes apparent at diagnosis and persistent throughout adulthood. Some evidence suggests that brain injury might also directly contribute to psychological and mental health outcomes. Neurocognitive deficits manifest across multiple cognitive domains. Moreover, impaired executive function and mental health can affect patients’ adherence to treatment. This review summarizes the current data on the impact of glycemic extremes on brain structure and cognitive function in youth with T1D and the use of new diabetes technologies that may reduce these complications.

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Salsabilla, Riska Oktavioni, Bagus Pratama, and Dian Isti Angraini. "The Kadar Timbal Darah pada Kesehatan Anak." Jurnal Penelitian Perawat Profesional 2, no. 2 (March 9, 2020): 119–24. http://dx.doi.org/10.37287/jppp.v2i2.54.

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Timbal merupakan logam berat yang beracun bagi banyak organ, termasuk sistem saraf pusat yang berpotensi menyebabkan kerusakan saraf dan kognitif secara persisten hingga permanen. Potensi toksisitas timbal akan meningkatkan kesadaran tentang bahaya kesehatan terkait paparan lingkungan. Literatur review ini bertujuan mengumpulkan penelitian – penelitian yang berhubungan dengan kadar timbal darah dan efeknya terhadap kesehatan anak. Metode yang digunakan berupa studi literatur dengan metode mencari, menggabungkan inti sari serta menganalisis fakta dari beberapa sumber ilmiah yang akurat dan validPada pedoman asupan mingguan konsumsi timbal yang dapat ditoleransi pada darah adalah ≤5 µg/dl. Hasil dari tinjauan pustka ini ditemukan bahwa bahaya kesehatan terkait paparan lingkungan pada anak dengan jalur masuk paparan dan asal sumber timbal telah banyak dilaporkan. Paparan timbal dalam jumlah yang sangat kecil sekalipun dapat memiliki efek jangka panjang dan lambat yang terakumulasi pada anak-anak. Penurunan fungsi kognitif dimungkinkan pada kandungan timbal lebih rendah dari pedoman asupan mingguan yang dapat ditoleransi. Secara khusus, paparan kronis terhadap konsentrasi timbal yang rendah menyebabkan gangguan perilaku kognitif pada anak-anak. Pengaruh kadar timbal darah pada kesehatan neurobehavior anak berupa pengaruh pada perilaku dan perkembangan mental, neurokognitif dan intelegensia, serta gangguan neurobehavioral pada anak. Kata kunci: anak, kadar timbal darah, neurobehavior, timbal BLOOD LEAD LEVELS IN CHILDREN'S HEALTH ABSTRACT Lead is a heavy metal that is poisonous to many organs, including the central nervous system which has the potential to cause permanent and permanent nerve and cognitive damage. Potential for lead toxicity will increase awareness about health hazards related to environmental exposure. This literature review aims to gather research related to blood lead levels and their effects on children's health. The method used in the form of a literature study with the method of searching, combining essence and analyzing facts from several scientific sources that are accurate and valid In the guidelines for weekly intake of lead consumption that can be tolerated in the blood is ≤5 µg / dl. The results of this literature review found that health hazards related to environmental exposure in children with exposure to entry and origin of lead sources have been widely reported. Even very small amounts of lead exposure can have long-term and slow effects that accumulate in children. Decreased cognitive function is possible at lead levels lower than the tolerable weekly intake guidelines. Specifically, chronic exposure to low lead concentrations causes impaired cognitive behavior in children. The influence of blood lead levels on children's neurobehavior health in the form of influences on behavior and mental development, neurocognitive and intelligence, as well as neurobehavioral disorders in children. Keywords: children, blood lead levels, neurobehavior, lead

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Dohmen, Maud, Ella Braat-Eggen, Astrid Kemperman, and Maarten Hornikx. "The Effects of Noise on Cognitive Performance and Helplessness in Childhood: A Review." International Journal of Environmental Research and Public Health 20, no. 1 (December 24, 2022): 288. http://dx.doi.org/10.3390/ijerph20010288.

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Environmental noise affects our daily functioning in many ways, and the cognitive, motivational, and emotional effects of noise are intertwined. Our task performance under noisy conditions depends on our ability to cope with the noise and our cognitive resources. The process of (failed) coping may wear us out cognitively, lead to learned helplessness, and, consequently, alter the motivation to persist in a task. The direct effect of irrelevant sounds on cognitive functioning in children is relatively well-established, however, the research on the framework of learned helplessness is limited when it comes to children. Learned helplessness can give more insight into effects of environmental noise on learning and child development and how the effects of short-term and long-term exposure interact. A systematic literature review is performed to assess to what extent the current evidence addresses the (interaction) effects of the sound environment on cognition and learned helplessness as measured by motivation in children and young adults up to the age of 21. The search resulted in 8 included papers that addressed both cognition and learned helplessness in their research. The included papers study children between 8–13 years old and show evidence for a relation between environmental noise, cognition, and helplessness individually, but none study a possible interaction. Based on the individual study designs, it could be hypothesized that cognitive fatigue may play a role in the interaction. Studies that conducted motivation tasks after cognitive tasks found stronger effects than those that conducted tasks in a random order. More research is needed using the same methods in different age groups to further assess the interaction between cognition and learned helplessness in relation to the sound environment.

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Oppenheimer, Anna, David Bellinger, Brent Coull, Marc Weisskopf, and Susan Korrick. "Prenatal Exposure to Chemical Mixtures and Cognitive Flexibility among Adolescents." Toxics 9, no. 12 (December 2, 2021): 329. http://dx.doi.org/10.3390/toxics9120329.

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Cognitive flexibility, the ability to smoothly adapt to changing circumstances, is a skill that is vital to higher-level executive functions such as problem-solving, planning, and reasoning. As it undergoes substantial development during adolescence, decrements in cognitive flexibility may not become apparent until this time. There is evidence that prenatal exposure to individual chemicals may adversely impact executive functions in children, but few studies have explored the association of co-exposure to multiple chemicals with cognitive flexibility specifically among adolescents. We investigated this association among a diverse group of adolescents living near a Superfund site in New Bedford, Massachusetts. Specifically, using Bayesian kernel machine regression (BKMR) and multivariable regression analyses, we investigated the association of biomarkers of prenatal exposure to organochlorines (DDE, HCB, PCBs) and metals (lead, manganese) with cognitive flexibility, measured with four subtests of the Delis-Kaplan Executive Function System. In BKMR models, we observed adverse joint associations of the chemical mixture with two of the four cognitive flexibility subtests. In covariate-adjusted linear regression models, a two-fold increase in cord blood Mn was associated with poorer performance on two of the subtests: Trail-Making (scaled score difference = −0.60; 95% CI: −1.16, −0.05 points) and Color-Word Interference (scaled score difference = −0.53; 95% CI: −1.08, 0.01 points). These adverse Mn-cognitive flexibility associations were supported by the results of the BKMR. There was little evidence of effect modification by sex and some evidence of effect modification by a measure of social disadvantage, particularly for the associations between HCB and cognitive flexibility. This study is among the first to provide evidence of an adverse association of prenatal exposure to a chemical mixture with cognitive flexibility in adolescence.

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Neelima, Ayyalasomayajula, Ajumeera Rajanna, Reddy G. Bhanuprakash, C. S. Chetty, and Challa Suresh. "Deleterious effects of combination of lead and β-amyloid peptides in inducing apoptosis and altering cell cycle in human neuroblastoma cells." Interdisciplinary Toxicology 10, no. 3 (November 1, 2017): 93–98. http://dx.doi.org/10.1515/intox-2017-0015.

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AbstractLead (Pb) is a toxic pollutant known to cause several abnormalities related to the brain, including cognitive dysfunction, and it is ubiquitous in nature. β-amyloid peptides (AP) are crucially involved in Alzheimer’s disease (AD). It has been reported that there is a connection between lead and amyloid peptides in exerting similar kinds of altered functions in the brain and long-term exposure to lead leads ultimately to increased beta amyloid formation in the brain, lethal to human brain cells. There is still a lack of information on the mechanism by which Pb affects AP formation, exerting combined toxicity in AD patients. To fill the gap, we have systematically analyzed the toxicity individually and in combination of Pb and AP in human brain cells. We found that the combination of Pb and AP exerted a higher toxicity than individual exposures in human neuroblastoma cells. The lower inhibitory concentration values were determined by both time and concentration dependent manner on using MTT assay. The data resulted in the development of enhanced toxicity on exposure to Pb with both the combinations of AP(1-40) or (25-35) and with all combinations in human brain cells compared to individual exposures to Pb (1-40) or AP(25-35). The severe apoptotic effect and alteration in cell cycle by arresting at the S-phase evidenced the increased toxicity of combinational exposure to Pb and AP on human neuroblastoma cells. Furthermore, the quantitative determination of LDH and caspase-3 activity indicated the induction of severe toxicity. We conclude that both are synergistically associated with effects such as arresting the cell cycle and triggering apoptosis during the progression of Alzheimer’s disease.

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Chetty, C. S., G. R. Reddy, K. S. Murthy, J. Johnson, K. Sajwan, and D. Desaiah. "Perinatal Lead Exposure Alters the Expression of Neuronal Nitric Oxide Synthase in Rat Brain." International Journal of Toxicology 20, no. 3 (May 2001): 113–20. http://dx.doi.org/10.1080/109158101317097692.

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Environmental exposure to lead (Pb) is known to affect the developing nervous system causing cognitive deficits in children. The diffusible nitric oxide (NO) is a biological messenger known to be involved in brain development. We examined the developmental changes of neuronal nitric oxide synthase (nNOS) in cerebellum and hippocampus of developing rat brain by radiometric assay, Western blot analysis and immunohistochemistry. Pb-exposure (0.2% Pb acetate) was initiated on gestation day 6 through the drinking water of the dam and continued through birth and postnatal days (PNDs) 1 to 21. The pups were never exposed to Pb directly. Pb exposure was stopped on weaning of pups from mothers on PND 21. The changes in nNOS were measured in the offspring on PNDs 7, 14, 21, and 35. The nNOS activity was increased gradually from PNDs 7 to 35 in both cerebellum and hippocampus of control rats when the enzyme activity was determined in the presence of either 0.5 or 6 μM calcium (Ca2+) in the reaction mixture. However, Pb exposure decreased the nNOS activity significantly at PNDs 21 to 35 as compared to respective controls when the enzyme activity was determined in the presence of 6 μM Ca2+. The decrease of nNOS was even greater and evident at all PNDs tested when the enzyme activity was assayed in the presence of physiological concentration of Ca2+ (0.5 μM). These findings were further strengthened by the in vitro studies. The cerebellar nNOS activity was inhibited much more at low Ca2+ (0.5 μM) as compared to 6 μM Ca2+, with IC50 values of 35 and 50 nM Pb, respectively. The nNOS protein levels and immunoreactivity in the cerebellum and hippocampus of rats perinatally exposed to Pb were decreased as compared to controls at PNDs 21 and 35. These data suggest perinatal Pb exposure decreases the nNOS in the developing brain. The decrease of nNOS activity and protein may explain the Pb-mediated cognitive deficits because NO regulates long-term potentiation (LTP) and other neurophysiological events in the developing nervous system.

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Al-Saleh, I., N. Shinwari, M. Nester, A. Mashhour, L. Moncari, G. El Din Mohamed, and A. Rabah. "Longitudinal Study of Prenatal and Postnatal Lead Exposure and Early Cognitive Development in Al-Kharj, Saudi Arabia: A Preliminary Results of Cord Blood Lead Levels." Journal of Tropical Pediatrics 54, no. 5 (March 15, 2008): 300–307. http://dx.doi.org/10.1093/tropej/fmn019.

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Koshy, Beena, Manikandan Srinivasan, Susan Mary Zachariah, Arun S. Karthikeyan, Reeba Roshan, Anuradha Bose, Venkata Raghava Mohan, et al. "Body iron and lead status in early childhood and its effects on development and cognition: a longitudinal study from urban Vellore." Public Health Nutrition 23, no. 11 (April 14, 2020): 1896–906. http://dx.doi.org/10.1017/s1368980019004622.

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AbstractObjective:Early childhood factors can have persisting effects on development and cognition in children. We propose to explore the trends of Fe deficiency and Pb toxicity in early childhood and their association with child development at 2 years of age and cognition at 5 years.Design:Longitudinal birth cohort study.Setting:Urban slum, Vellore, India.Participants:Children enrolled at birth were followed up regularly in the first 2 years with developmental and cognitive assessments at 2 and 5 years of age, respectively.Results:The birth cohort enrolled 251 children with 228 children followed up at 2 years and 212 at 5 years of age. Fe deficiency (ID) was highest at 15 months of age and improved subsequently at 24 months. Blood Pb levels (BLL) remained high at all age groups with an increasing trend with age; 97 % at 36 months having high BLL. Persistent high mean BLL at 15 and 24 months had negative association with both cognition and expressive language raw scores of 24 months, while high mean BLL at 15, 24 and 36 months had no significant association with any of the domains of cognition at 5 years of age. Early childhood cumulative body Fe status at 7, 15 and 24 months did not show any association with child development at 2 years, but was associated with verbal, performance and processing speed components of cognition at 5 years.Conclusions:Optimising body Fe status and limiting Pb exposure in early childhood can augment child development and school entry cognition.

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Abdullahi, Abubakar lema, A. A. Lema, K. Jibrin, W. Nuraddeen, and E. M. Alexander. "Ameliorative Role of Nutraceutical Quercetin and its Derivatives Against Cognitive Impairment Process Induced by Lead Exposure in Drosophila melanogaster(Fruit Fly)." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 30, no. 2 (December 11, 2021): 135–42. http://dx.doi.org/10.31351/vol30iss2pp135-142.

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Cumulative lifetime lead (Pb) exposure has been associated with accelerated declines in cognition through the free radical generation and epigenetic effects. Several pieces of literature have identified a correlation between exposure to lead and neurodegenerative disorders. Harwich strain Drosophila melanogaster was exposed to lead acetate for two weeks, and changes in pulse transmission by acetylcholinesterase and systemic redox were evaluated. Besides, molecular docking studies of acetylcholinesterase against Quercetin and its most common derivatives contained in food have been performed. Pharmacokinetic studies on Quercetin and its derivatives have also been performed in silico toxicity. The data obtained showed alterations in antioxidant enzymes and molecules such as catalase, glutathione-S-transferase, and glutathione. Upregulation of acetylcholinesterase activity was observed after treatment with Quercetin. In molecular docking tests, Quercetin and its derivatives were found to bind to acetylcholinesterase's active and peripheral pockets. Pharmacokinetic studies demonstrate moderate solubility, high therapeutic index, excellent absorption potential, hepatoprotective and non-mutagenic properties. With other antioxidant molecules, Quercetin may also play a crucial role in avoiding the development of Alzheimer's and associated antioxidant disorders.

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Consorti, Alan, Gabriele Sansevero, Claudia Torelli, Nicoletta Berardi, and Alessandro Sale. "From Basic Visual Science to Neurodevelopmental Disorders: The Voyage of Environmental Enrichment-Like Stimulation." Neural Plasticity 2019 (May 6, 2019): 1–9. http://dx.doi.org/10.1155/2019/5653180.

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Genes and environmental stimuli cooperate in the regulation of brain development and formation of the adult neuronal architecture. Genetic alterations or exposure to perturbing environmental conditions, therefore, can lead to altered neural processes associated with neurodevelopmental disorders and brain disabilities. In this context, environmental enrichment emerged as a promising and noninvasive experimental treatment for favoring recovery of cognitive and sensory functions in different neurodevelopmental disorders. The aim of this review is to depict, mainly through the much explicative examples of amblyopia, Down syndrome, and Rett syndrome, the increasing interest in the potentialities and applications of enriched environment-like protocols in the field of neurodevelopmental disorders and the understanding of the molecular mechanisms underlying the beneficial effects of these protocols, which might lead to development of pharmacological interventions.

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Molino, Paul J., Richard Bentham, Michael J. Higgins, Jason Hinds, and Harriet Whiley. "Public Health Risks Associated with Heavy Metal and Microbial Contamination of Drinking Water in Australia." International Journal of Environmental Research and Public Health 16, no. 20 (October 18, 2019): 3982. http://dx.doi.org/10.3390/ijerph16203982.

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Recently in Australia concerns have been raised regarding the contamination of municipal drinking water supplies with lead. This is of particular concern to children due to the impact of lead exposure on cognitive development and as such these findings have received much media attention. The response from legislators has been swift, and The Victorian School Building Authority has announced that all new schools and school upgrade works will only use lead-free tapware and piping systems. However, while the immediate replacement of lead-containing brass fittings may seem a logical and obvious response, it does not consider the potential implications on microbial contamination. This is particularly concerning given the increasing public health threat posed by opportunistic premise plumbing pathogens (OPPPs). This commentary explores this public health risk of lead exposure from plumbing materials compared to the potential public health risks from OPPPs. Non-tuberculous mycobacterium was chosen as the example OPPP, and the influence on plumbing material and its public health burden in Australia is explored. This commentary highlights the need for future research into the influence of plumbing material on OPPPs prior to any changes in legislation regarding plumbing material.

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Siracusano, Martina, Elisa Carloni, Assia Riccioni, Marialaura Ferrara, Chiara Scoppola, Lucrezia Arturi, Cinzia Niolu, Girolama Alessandra Marfia, and Luigi Mazzone. "Maternal Multiple Sclerosis and Offspring’s Cognitive and Behavioral Development: What Do We Know until Now?" Children 9, no. 11 (November 9, 2022): 1716. http://dx.doi.org/10.3390/children9111716.

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Multiple Sclerosis (MS) is a chronic pathological condition representing one of the main causes of neurological disability in the female young population. MS, as an immune disorder, could impact fetus development, and, considering the need for and the possibility of pharmacological treatment during pregnancy, the possible influence of medication on developmental trajectories represents a topic of great interest. We provide an overview of the available literature on the influence of maternal Multiple Sclerosis on offspring cognitive and behavioral development. A study was conducted on Pubmed, Medline and Google Scholar, considering empirical studies and reviews exclusively in the English language. Maternal MS appears not to be associated with emotional and behavioral problems, as evaluated through retrospective studies. However, a specific cognitive and behavioral phenotype, through the administration of standardized instruments, has not been delineated yet. Available studies on the topic are characterized by poor methodology and do not lead to conclusions. This overview highlights implications for further longitudinal studies which should delineate offspring developmental trajectories, taking into consideration maternal confounding factors and the exposure to pharmacological treatment in pregnancy.

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Ledda, Caterina, Emanuele Cannizzaro, Piero Lovreglio, Ermanno Vitale, Angela Stufano, Angelo Montana, Giovanni Li Volti, and Venerando Rapisarda. "Exposure to Toxic Heavy Metals Can Influence Homocysteine Metabolism?" Antioxidants 9, no. 1 (December 28, 2019): 30. http://dx.doi.org/10.3390/antiox9010030.

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Background: Homocysteine is a sulfur amino acid whose metabolism is activated in two pathways: remethylation to methionine, which requires folate and vitamin B12, and transsulfuration to cystathionine, which needs pyridoxal-5’-phosphate. High homocysteine level increases the risk of developing heart disease, stroke, peripheral vascular diseases, and cognitive impairment. Some evidence showed that exposure to these metals increased plasma homocysteine levels. Methods: A systematic review was carried out to clarify the relationship between homocysteine blood levels and exposure to toxic heavy metals (Lead, Cadmium, Mercury, and Chromium). Results: The results of this systematic review indicate that exposure to Pb, Cr, Cd, and Hg is connected with nonphysiological homocysteine levels or vitamin B12 and folate serum concentrations. Conclusions: These findings reinforce the importance of involvement in exposure to heavy metals in homocysteine metabolism. This supports the role of blood metals as potential upstream modifiable risk factors to prevent the development of other established risk factors as hyperhomocysteinemia.

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Trofimov, A. N., O. E. Zubareva, A. P. Schwarz, E. A. Veniaminova, K. Fomalont, and V. M. Klimenko. "DELAYED COGNITIVE DEFICIT AS A RESULT OF NEONATAL LIPOPOLYSACCHARIDE EXPOSURE: A PRESUMABLE IMPLICATION OF LONG-LASTING CHANGES OF NEUROPLASTIC GENE EXPRESSION." Medical academic journal 19, no. 1S (December 15, 2019): 119–20. http://dx.doi.org/10.17816/maj191s1119-120.

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Disorders of the CNS development at an early age caused by various types of perinatal pathology, such as infectious diseases, trauma, hypoxia and ischemia, often lead to the development of cognitive brain dysfunctions in adulthood. Proinflammatory cytokines play key role in these pathological processes and can affect the expression of genes involved in the regulation of neuroplasticity. This article describes the changes in the expression of fibroblast growth factor-2 (Fgf2), as well as genes encoding matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinases-1 (TIMP-1), proteins that by intercellular matrix re-modeling are involved in the regulation of neuroplasticity.

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Ahmadi, Shukrullah, Barbara Le Bot, Roméo Zoumenou, Séverine Durand, Nadine Fiévet, Pierre Ayotte, Achille Massougbodji, et al. "Follow-Up of Elevated Blood Lead Levels and Sources in a Cohort of Children in Benin." International Journal of Environmental Research and Public Health 17, no. 22 (November 23, 2020): 8689. http://dx.doi.org/10.3390/ijerph17228689.

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Lead exposure is associated with poor cognitive development in children. Very few studies in sub-Saharan Africa (SSA) have studied blood lead levels (BLLs) and non-gasoline sources of exposure in children. Data from a birth cohort in Benin (2011–2013) suggested that 58% of 1-year-old children had BLLs > 50 ug/L. We aimed to investigate the prevalence of elevated BLLs (>50 µg/L and >100 µg /L) among 425 of these children at 6 years of age in 2016–2018 and to compare BLLs between age 1 and 6 years, and study sources of lead at age 6 years. BLLs were analysed by inductively coupled plasma mass spectrometry. Multiple linear regression and quantile regressions were used to study potential sources of lead. The prevalence of BLLs > 50 µg/L in children was 59.5% (Geometric Mean (GM) 56.4 µg/L, 95% CI: 54.1–58.7) at 6 years of age compared to 54.8% (GM 56.5 µg/L, 95% CI: 53.4–59.6) at 1 year of age. The prevalence of children with BLLs > 100 µg/L decreased from 14.4% at 1 year of age to 8.2% at 6 years of age. After adjustment for all other covariates, consumption of peanuts more than once per month was significantly associated with a 22.0% (95% CI: 4.6, 42.5) increment in BLLs at age 6 years compared with no consumption. Consumption of bushmeat killed by lead bullets at age 6 years was associated with an increase in the higher percentiles of BLLs (P75) compared with the absence of this source. Other potential sources of lead associated with BLLs with marginal significance were consumption of rice, paternal occupational exposure, and the presence of activity with the potential use of lead. This prospective cohort confirms the persistently high prevalence of elevated BLLs in children residing in a rural region in the south of Benin, as well as the presence of multiple and continuous sources of lead. These results highlight the need for prevention programs to reduce and eliminate lead exposure in children.

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Chakraborty, Goutam, Alejandra Magagna-Poveda, Carolyn Parratt, Jason G. Umans, Neil J. MacLusky, and Helen E. Scharfman. "Reduced Hippocampal Brain-Derived Neurotrophic Factor (BDNF) in Neonatal Rats after Prenatal Exposure to Propylthiouracil (PTU)." Endocrinology 153, no. 3 (March 1, 2012): 1311–16. http://dx.doi.org/10.1210/en.2011-1437.

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Thyroid hormone is critical for central nervous system development. Fetal hypothyroidism leads to reduced cognitive performance in offspring as well as other effects on neural development in both humans and experimental animals. The nature of these impairments suggests that thyroid hormone may exert its effects via dysregulation of the neurotrophin brain-derived neurotrophic factor (BDNF), which is critical to normal development of the central nervous system and has been implicated in neurodevelopmental disorders. The only evidence of BDNF dysregulation in early development, however, comes from experimental models in which severe prenatal hypothyroidism occurred. By contrast, milder prenatal hypothyroidism has been shown to alter BDNF levels and BDNF-dependent functions only much later in life. We hypothesized that mild experimental prenatal hypothyroidism might lead to dysregulation of BDNF in the early postnatal period. BDNF levels were measured by ELISA at 3 or 7 d after birth in different regions of the brains of rats exposed to propylthiouracil (PTU) in the drinking water. The dose of PTU that was used induced mild maternal thyroid hormone insufficiency. Pups, but not the parents, exhibited alterations in tissue BDNF levels. Hippocampal BDNF levels were reduced at both d 3 and 7, but no significant reductions were observed in either the cerebellum or brain stem. Unexpectedly, more males than females were born to PTU-treated dams, suggesting an effect of PTU on sex determination. These results support the hypothesis that reduced hippocampal BDNF levels during early development may contribute to the adverse neurodevelopmental effects of mild thyroid hormone insufficiency during pregnancy.

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Kepka, Sabrina, François Lersy, Julien Godet, Frederic Blanc, Mathias Bilger, Anne Botzung, Catherine Kleitz, et al. "Cerebral and cognitive modifications in retired professional soccer players: TC-FOOT protocol, a transverse analytical study." BMJ Open 12, no. 11 (November 2022): e060459. http://dx.doi.org/10.1136/bmjopen-2021-060459.

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IntroductionSoccer is the most popular sport in the world. This contact sport carries the risk of exposure to repeated head impacts in the form of subconcussions, defined as minimal brain injuries following head impact, with no symptom of concussion. While it has been suggested that exposure to repetitive subconcussive events can result in long-term neurophysiological modifications, and the later development of chronic traumatic encephalopathy, the consequences of these repeated impacts remain controversial and largely unexplored in the context of soccer players.Methods and analysisThis is a prospective, single-centre, exposure/non-exposure, transverse study assessing the MRI and neuropsychological abnormalities in professional retired soccer players exposed to subconcussive impacts, compared with high-level athletes not exposed to head impacts. The primary outcome corresponds to the results of MRI by advanced MRI techniques (diffusion tensor, cerebral perfusion, functional MRI, cerebral volumetry and cortical thickness, spectroscopy, susceptibility imaging). Secondary outcomes are the results of the neuropsychological tests: number of errors and time to complete tests. We hypothesise that repeated subconcussive impacts could lead to morphological lesions and impact on soccer players’ cognitive skills in the long term.Ethics and disseminationEthics approval has been obtained and the study was approved by the Comité de Protection des Personnes (CPP) No 2021-A01169-32. Study findings will be disseminated by publication in a high-impact international journal. Results will be presented at national and international imaging meetings.Trial registration numberNCT04903015.

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Neylon, Jeremy, Jarrad N. Fuller, Chris van der Poel, Jarrod E. Church, and Sebastian Dworkin. "Organophosphate Insecticide Toxicity in Neural Development, Cognition, Behaviour and Degeneration: Insights from Zebrafish." Journal of Developmental Biology 10, no. 4 (November 21, 2022): 49. http://dx.doi.org/10.3390/jdb10040049.

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Organophosphate (OP) insecticides are used to eliminate agricultural threats posed by insects, through inhibition of the neurotransmitter acetylcholinesterase (AChE). These potent neurotoxins are extremely efficacious in insect elimination, and as such, are the preferred agricultural insecticides worldwide. Despite their efficacy, however, estimates indicate that only 0.1% of organophosphates reach their desired target. Moreover, multiple studies have shown that OP exposure in both humans and animals can lead to aberrations in embryonic development, defects in childhood neurocognition, and substantial contribution to neurodegenerative diseases such as Alzheimer’s and Motor Neurone Disease. Here, we review the current state of knowledge pertaining to organophosphate exposure on both embryonic development and/or subsequent neurological consequences on behaviour, paying particular attention to data gleaned using an excellent animal model, the zebrafish (Danio rerio).

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Kumar, Gautam, Priyadarshini Dutta, Vipan K. Parihar, Mallikarjuna R. Chamallamudi, and Nitesh Kumar. "Radiotherapy and Its Impact on the Nervous System of Cancer Survivors." CNS & Neurological Disorders - Drug Targets 19, no. 5 (November 13, 2020): 374–85. http://dx.doi.org/10.2174/1871527319666200708125741.

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Radiotherapy is routinely used for the treatment of nearly all brain tumors, but it may lead to progressive and debilitating impairments of cognitive function. The growing evidence supports the fact that radiation exposure to CNS disrupts diverse cognitive functions including learning, memory, processing speed, attention and executive functions. The present review highlights the types of radiotherapy and the possible mechanisms of cognitive deficits and neurotoxicity following radiotherapy. The review summarizes the articles from Scopus, PubMed, and Web of science search engines. Radiation therapy uses high-powered x-rays, particles, or radioactive seeds to kill cancer cells, with minimal damage to healthy cells. While radiotherapy has yielded relative success in the treatment of cancer, patients are often plagued with unwanted and even debilitating side effects from the treatment, which can lead to dose reduction or even cessation of treatment. Little is known about the underlying mechanisms responsible for the development of these behavioral toxicities; however, neuroinflammation is widely considered as one of the major mechanisms responsible for radiotherapy-induced toxicities. The present study reviews the different types of radiotherapy available for the treatment of various types of cancers and their associated neurological complications. It also summarizes the doses of radiations used in the variety of radiotherapy, and their early and delayed side effects. Special emphasis is given to the effects of various types of radiations or late side effects on cognitive impairments.

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Huang, Lianyan, and Guang Yang. "Repeated Exposure to Ketamine–Xylazine during Early Development Impairs Motor Learning–dependent Dendritic Spine Plasticity in Adulthood." Anesthesiology 122, no. 4 (April 1, 2015): 821–31. http://dx.doi.org/10.1097/aln.0000000000000579.

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Abstract Background: Recent studies in rodents suggest that repeated and prolonged anesthetic exposure at early stages of development leads to cognitive and behavioral impairments later in life. However, the underlying mechanism remains unknown. In this study, we tested whether exposure to general anesthesia during early development will disrupt the maturation of synaptic circuits and compromise learning-related synaptic plasticity later in life. Methods: Mice received ketamine–xylazine (20/3 mg/kg) anesthesia for one or three times, starting at either early (postnatal day 14 [P14]) or late (P21) stages of development (n = 105). Control mice received saline injections (n = 34). At P30, mice were subjected to rotarod motor training and fear conditioning. Motor learning–induced synaptic remodeling was examined in vivo by repeatedly imaging fluorescently labeled postsynaptic dendritic spines in the primary motor cortex before and after training using two-photon microscopy. Results: Three exposures to ketamine–xylazine anesthesia between P14 and P18 impair the animals’ motor learning and learning-dependent dendritic spine plasticity (new spine formation, 8.4 ± 1.3% [mean ± SD] vs. 13.4 ± 1.8%, P = 0.002) without affecting fear memory and cell apoptosis. One exposure at P14 or three exposures between P21 and P25 has no effects on the animals’ motor learning or spine plasticity. Finally, enriched motor experience ameliorates anesthesia-induced motor learning impairment and synaptic deficits. Conclusions: Our study demonstrates that repeated exposures to ketamine–xylazine during early development impair motor learning and learning-dependent dendritic spine plasticity later in life. The reduction in synaptic structural plasticity may underlie anesthesia-induced behavioral impairment.

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Gatzke-Kopp, Lisa M., and Kristine L. Creavey. "Unsealing Fate: Policy Practices Aimed at Reducing the Intergenerational Transmission of Poverty." Policy Insights from the Behavioral and Brain Sciences 4, no. 2 (August 24, 2017): 115–22. http://dx.doi.org/10.1177/2372732217719712.

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Enabling children born into poverty to transcend the circumstances of their birth requires ensuring that they develop the cognitive, intellectual, and behavioral skills needed to succeed at school, and eventually the workplace. Research in developmental neuroscience highlights how brain systems that support these skills are already influenced by risk factors associated with poverty during prenatal development, indicating the potential value of programs targeted at this developmental stage. Such interventions could include programs that support maternal physical and psychological health, as well as efforts to eliminate known neurotoxins from the environment, all of which are disproportionately represented among low-income families. Maternal stress, environmental nicotine, and lead exposure all represent risk factors that not only directly impact child development, but cascade to translate risk into subsequent generations.

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Journal articles on the topic 'Lead exposure; cognitive; development'

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