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Browsing by Author "Taboada, Maria Fatima Delgado"
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Item Effects of EGCG Treatment of Ts65Dn Down Syndrome Mice on a Balance Beam Task(Office of the Vice Chancellor for Research, 2015-04-17) Taboada, Maria Fatima Delgado; Stringer, Megan; Roper, Randall J.; Goodlett, Charles R.Down syndrome (DS) is caused by trisomy of chromosome 21, and affects 1/700 live births. DS results in about 80 clinical phenotypes, including cognitive impairment. DYRK1A, a chromosome 21 gene, has been linked to alterations in morphology and function of the brain resulting in cognitive impairment. Epigallocatechin-3-gallate (EGCG), an inhibitor of DYRK1A activity, has been proposed as a possible treatment for cognitive deficits seen in individuals with DS. Using the Ts65Dn DS mouse model, we examined the effects of EGCG treatment on cerebellum dependent tasks using a balance beam test. We hypothesized that treatment with EGCG would improve Ts65Dn performance on the balance beam. In a first experiment, mice were given a dose of ~30 mg/kg/day EGCG, which showed no significant improvement in the balance beam task. In a second experiment, mice were given a dose of 100 mg/kg/day EGCG or water (control) starting at 3 weeks of age. The mice were handled two days before testing and then underwent a series of behavioral tasks including the balance beam test. The mice traversed three beams of differing widths (12, 9 and 6 mm), and three consecutive trials for each were recorded for further analysis. The balance beam recordings were scored by three independent scorers, blind to genotype and treatment, and the number of hind paw slips for each trial were scored. Our preliminary results indicate that the Ts65Dn mice are impaired at this task and have more hind paw slips compared to euploid controls. A larger number of animals should help to distinguish any differences in Ts65Dn mice due to EGCG treatment.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.