Gain-of-function of mir-277 ameliorates Aβ42 mediated neurodegeneration in Drosophila eye model of AD
Prajakta D. Deshpande, Catherine Jean Yeates
Alzheimer’s disease (AD), an age-related progressive neurodegenerative disorder, exhibits reduced cognitive functions with no cure to date. One of the reasons for AD is the accumulation of extracellular Amyloid-beta 42 peptide (Aβ42) plaques that triggers oxidative stress, aberrant signaling, and finally results in the death of the neurons. The exact mechanism of neurodegeneration is still not well-understood. We misexpressed human Aβ42 protein in the developing fly retina, which triggers the neuronal cell death and exhibits AD-like neuropathology. Several studies have implicated the antiapoptotic role of microRNAs, post-transcriptionally regulate the gene expression by degrading mRNA of the target. In a forward genetic screen, we identified mir-277 as a genetic modifier of Aβ42 mediated neurodegeneration. The gain of function of mir-277 suppresses the Aβ42 mediated neurodegeneration whereas loss of function of mir-277 enhances the Aβ42 mediated neurodegeneration. We looked for the targets of mir-277 to understand the genetic mechanism of mir-277 mediated neuroprotection against Aβ42 plaques. Here we present the mechanism by which micro RNA provides neuroprotection to the neurons expressing high levels of Aβ42.
Madhuri Kango-Singh, Amit Singh
Primary Advisor's Department
Stander Symposium project, College of Arts and Sciences
United Nations Sustainable Development Goals
Good Health and Well-Being
"Gain-of-function of mir-277 ameliorates Aβ42 mediated neurodegeneration in Drosophila eye model of AD" (2020). Stander Symposium Projects. 2009.