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Down syndrome is caused by trisomy of human chromosome 21 (Hsa21) and often leads to Alzheimer’s disease in affected individuals. The Tc1 mouse model contains a copy of Hsa21 in its genome, and is therefore trisomic for the genes it contains to manifest as a Down syndrome mouse model. Transmission of Hsa21 to offspring generations occurs at a low frequency with fertility rates decreased in comparison to control mouse lines. This experiment has verified that presence of Hsa21 causes a significant increase from normal brain weight. Hsa21 carriers demonstrated reductions in the number and length of dendritic projections and the number spines on cortical neurons suggesting that the increase in brain size may have been due to changes in glial cell proliferation rather than an increase in gray matter. Some have reported increases in beta-amyloid plaques in affected persons which can induce gliosis. These observations have led us to begin a study to verify the presence of beta-amyloid plaques and cell density to better understand the changes Hsa21 produces in the brain. Despite relatively extreme pathological changes in the brain the behavior of Hsa21 carriers did not exhibit significant memory impairments as compared to controls. There was a trend towards memory impairment. However, some of the subjects appeared to be hypoactive (a trait associated with Down Syndrome) that may have confounded our test that was dependent on normal motor function. Studies of spontaneous activity are now underway.

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Final Report Form, Research Report

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Richard Deyo



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