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Alzheimer’s disease is a progressive neurodegenerative disorder that affects cognitive function and memory of the patient. It results from plaques formed by the abnormal cleavage of the Amyloid Precursor Protein (APP), which result in the formation of 42 amino acid polypeptide, also known as amyloid beta 42 (Aβ42). Accumulation of Aβ42 peptide triggers cell death in the neuronal cell population of central nervous system. However, the trigger for this abnormal cell death is unknown. I will investigate the role of mitochondrial dysfunction as the trigger for neurodegeneration. Since the mitochondria is the site for triggering neurodegeneration, its malfunction or loss could lead to loss of dendritic branches and alteration of dendritic spines. I will employ Drosophila melanogaster eye model of Alzheimer’s disease for my studies. The GAL4/UAS system will be utilized to misexpress the human Aβ42 polypeptide in the photoreceptor neurons of the fly retina. The mitochondrial genes pentatricopeptide repeat containing protein (ppr), pyruvate dehydrogenase, and citrate synthase will be investigated in the photoreceptor cells of the Drosophila. Loss-of-Function (LOF) and Gain-of- Function (GOF) techniques will be used to determine whether or not the death of photoreceptor and neurodegeneration can be rescued from flies expressing human Aβ42 polypeptide. My proposed studies will shed light on how these mitochondrial genes can affect the survival of Drosophila photoreceptor neurons where high levels of human Aβ42 polypeptide are expressed.
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Payton, Lydia C. and Sarkar, Ankita, "Investigation of the Role of Mitochondrial Dysfunction as a Trigger for Neurodegeneration in Alzheimer’s Disease" (2016). Stander Symposium Posters. 741.
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