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Down syndrome (DS) is the most common aneuploidy in humans, and is a leading cause of genetic mental retardation and learning disabilities in children. DS is closely linked to Alzheimer’s disease (AD), as the majority of DS patients develop AD by 50 years of age. Previous studies have shown that patients with DS or AD have a higher incidence of seizures, but despite the correlations between seizures and dementia, the biological mechanisms influencing these processes are poorly understood. We used 12-month-old Dp16 mouse models of DS to identify markers of seizure activity in the hippocampus, a region of the brain that experiences neurodegeneration in AD. Markers were analyzed and included reduced expression of calbindin, increased expression of neuropeptide Y (NPY), and mossy fiber sprouting. Our results found increased expression of NPY, but no difference in calbindin or mossy fiber sprouting; consequently, it cannot be concluded that there is seizure activity in this mouse model of DS. As the results were not conclusive, more research will be required given that seizure activity may be age-dependent and may need to be explored in older animals. Another possibility is that alterations in gene expression in the trisomic mouse may alter the expression and activity of seizure-related proteins and signaling pathways. We are currently looking into these various alternatives.
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