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Browsing by Subject "cognitive development"
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Item Adversity in Infancy and Childhood Cognitive Development: Evidence From Four Developing Countries(Frontiers, 2022-12-12) Manalew, W. Samuel; Tennekoon, Vidhura S.; Lee, Jusung; O'Connell, Bethesda; Quinn, Megan; Economics, School of Liberal ArtsObjectives: We investigated whether adverse experiences at age 1 (AE-1) affect the level of and change in cognition during childhood using harmonized data from four developing countries. Methods: Data included children born in 2001/2002 and were followed longitudinally in 2006/2007 and in 2009/2010 by Young Lives study in Ethiopia, India, Peru, and Vietnam. Childhood cognition was measured using the Peabody Picture Vocabulary Test (PPVT) at ages 5 (PPVT-5) and 8 (PPVT-8). We also examined the effect on a change in cognition between age 5–8 (PPVT-Change). The AE-1 scores were constructed using survey responses at age 1. The ordinary least squares regression was used for estimation. Results: We found that children with higher adversities as infants had lower cognition scores at ages 5 and 8. The change in cognition between the two ages was also generally smaller for those with severe adversities at infancy. The negative association between adversities and childhood cognition was strongest for India. Conclusion: The results provide policy relevant information for mitigation of undesirable consequences of early life adversities through timely interventions.Item EGCG Treatment on Ts65Dn Mice Suggests a Possible Correlation in Cognitive Development Deficit Reduction(Office of the Vice Chancellor for Research, 2014-04-11) Taboada, Maria Fatima Delgado; Abeysekera, Irushi S.; Roper, Randall J.Down syndrome (DS) is caused by trisomy of human chromosome 21 (Ts21), affecting 1 in 700 live births. Ts21 results in about 80 phenotypes of which intellectual disability (ID) is one of the most debilitating. DYRK1A, found in 3 copies in individuals with Ts21 has been linked to alterations in morphology and function of the brain resulting in ID. Epigallocatechin-3-gallate (EGCG), a specific inhibitor of Dyrk1a activity has been hypothesized as a possible treatment for the overexpression of this gene, reducing the deficits caused by Dryk1a. Using the Ts65Dn mouse model, we examined the effects on hippocampal dependent learning and memory in the novel object recognition task (NOR) using mice of 3-6 weeks of age (adolescent mice). They were given free access to EGCG (0.124 mg/mL) in their drinking water for 21 days. They were then tested for cognitive improvement through NOR. Ts65Dn and control mice (treated and untreated) were subjected to 3 days of testing with 15 minute sessions per day consisting of habituation, exposure, and test day. All procedures were recorded and analyzed to determine time spent exploring novel object in relation to familiar. Our current results suggest that s65Dn mice do not spend as much time exploring the novel object as euploid mice and there exists a genotype effect, but treatment is not correcting the learning and memory deficit. We hypothesize that continuous EGCG treatment may be needed in order to see cognitive deficit reduction in adolescent mice.