Amit Singh, Ph.D.
Alzheimer’s disease (AD) is an age related progressive neurodegenerative disease. The exact mechanisms that lead to cell death are not entirely understood. It has been shown that accumulation of amyloid-beta-42 (Aβ42) plaques generated by mis-cleavage of amyloid-precursor-protein is the cause of neurodegeneration seen in AD. This is due to the hydrophobic nature of Aβ42 due to extra two amino acids added to the typical and naturally occurring Aβ40 in the body. These Aβ42 plaques trigger neuronal death because of the toxic nature and stress they exert on the neurons. In this study, Drosophila melanogaster transgenic model where human Aβ42 coding cDNA is ectopically expressed in the developing fly retina comprising of retinal neurons to study the effect of ultrasound waves. Our hypothesis is to employ ultrasound wave exposure as a possible treatment to Alzheimer’s Disease. Ultrasound is a high frequency and lower energy sound wave, which may have less deleterious effect on cells in the tissue. In theory, using energy emitted from these waves would break down the plaques limiting damage due to degeneration. The wild type will be used as a control to see any side effects of the ultrasound treatment, while an AD affected fly will be used to determine effectiveness of the treatments. The goal of this project is to standardize the optimum ultrasound treatment, to observe the effects on survival rates, prevent neurodegeneration by removing or decreasing plaque damage. By varying the height, medium, time, and number of treatments, the survival rate and rescue can be tracked. Further studies using larval imaging approach can be used to see early stage effects of the ultrasound. These studies will allow testing the efficacy of commonly used treatment in sports related tissue injuries to cure inflammation and also to dislodge protein aggregations in Alzheimer’s disease where accumulation of Aβ42 plaques is the hallmark.
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Biology | Life Sciences
Byrne, Sarah, "Effects of Ultrasound on Amyloid Beta 42 (Aβ42) Mediated Neurodegeneration" (2017). Honors Theses. 94.