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As the most common progressive neurodegenerative disorder, Alzheimer’s disease (AD) has been predominantly found in people 65 years of age or older. AD is associated with a gradual decline in cognitive impairment and memory as well as effects on behavior and decision making. AD is also responsible for the most dementia cases in elderly people. As per the Alzheimer’s Association facts, over 5 million Americans were affected by AD in 2018 whereas the number is predicted to rise to approximately 14 million in 2050. One of the causes of AD is mis-cleavage of the transmembrane protein called amyloid precursor protein (APP) by the enzymes β-secretase and γ-secretase, resulting in accumulation of amyloid beta-42 polypeptide (Aβ42). These amyloid beta peptides aggregate into hydrophobic plaques in the extracellular region in the brain, altering the cellular pathways and resulting in neuronal death. In this study, we have used Drosophila as a model system and misexpressed the human Aβ42 in the photoreceptors of the Drosophila eye. The misexpression of the Aβ42 in the Drosophila eye triggers the neuronal cell death resulting in a glassy reduced eye phenotype. This study focusses on how microRNA mir-277 regulates the Aβ42 mediated neurodegeneration. MicroRNA regulate the gene expression post-transcriptionally and repress the protein formation by sequence-specific degradation of target mRNA. Earlier studies have shown the association of microRNA in AD and the role of mir-277 in AD is not clear. This study adds to our understanding of the role mir-277 may play in Aβ42 mediated neurodegeneration and its potential role as a biomarker for AD.
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Stander Symposium poster
"The potential role of mir-277 in Alzheimer’s disease" (2019). Stander Symposium Posters. 1478.