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Alzheimer’s Disease (AD) is a progressive neurodegenerative disorder associated with gradual cognitive impairment and memory decline. As the most common form of dementia, AD currently affects more than 5 million Americans and is expected to affect over 16 million Americans by 2050, according to the Alzheimer’s Association. This disease is characterized by the accumulation of Amyloid-beta 42 (Aβ-42) polypeptides, resulting from the hydrophobic nature of an improperly cleaved transmembrane protein called the amyloid precursor protein (APP). When the APP is cleaved to be 42 amino acids long instead of 40, plaques are formed that alter cellular pathways, inhibit synaptic activity, and initiate neuronal death. Using Drosophila melanogaster as a transgenic model system, we misexpressed Aβ-42 in the differentiating photoreceptors of the developing Drosophila eye. Misexpression of Aβ-42 in the eye results in a strong neurodegenerative phenotype. This project focuses on the impact of a specific microRNA, mir-277, on amyloid-beta-42 mediated neurodegeneration. MicroRNAs act as post-transcriptional regulators of gene expression and work by binding to complementary sequences of mRNA to induce effects such as target degradation, or translational repression. By doing so, microRNAs are capable of preventing protein assembly associated with specific mRNA targets. The results from our studies will be presented.

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Amit Singh

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This poster reflects research conducted as part of course project designed to give students experience in the research process.