Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12202/4773
Title: Calcium-independent Phospholipase A2β is Vital in Neurons and Possibly Other Tissues to Inhibit Age-Related Motor Degeneration.
Authors: Steinhauer, Josefa
Shulman, Benjamin
Keywords: senior honors thesis
Parkinson's disease (PD)
Calcium-independent Phospholipase A2β
Issue Date: Sep-2019
Publisher: NY: Yeshiva College. Yeshiva University.
Citation: Shulman, Benjamin. (September 2019). Calcium-independent Phospholipase A2β is Vital in Neurons and Possibly Other Tissues to Inhibit Age-Related Motor Degeneration. Thesis Submitted in Partial Fulfillment of the Requirements of the Jay and Jeanie Schottenstein Honors Program Yeshiva College Yeshiva University.
Abstract: By 2020, nearly one million Americans will be living with Parkinson’s disease (PD), and nearly ten million worldwide. This number outstrips every other age-related neurodegenerative disease save for Alzheimer disease (AD). The underlying cause of PD remains elusive, as does a medical remedy. Several genes have been linked to the disease, such as PLA2G6 (also known as iPLA2, PARK14, and iPLA2-VIA), a calcium-independent phospholipase A2 (iPLA2), which has been implicated in two forms of PD: Dystonia-parkinsonism (DP) and autosomal recessive early-onset parkinsonism (AREP). PLA2G6 has also been associated with Infantile neuroaxonal dystrophy (INAD) and atypical neuroaxonal dystrophy (aNAD). The model organism Drosophila melanogaster contains one homolog for PLA2G6. Previous studies have established knockout PLA2G6 Drosophila mutants showing locomotor defects, decreased lifespan, and increased sensitivity to oxidative stress − all symptoms of PD and other PLA2G6-associated neurodegeneration (PLAN) diseases. To better understand the mechanism and cell types by which PLA2G6 works, I used the GAL4-UAS and RNAi systems to generate two fly lines: one with PLA2G6 knockdown in neuronal tissue and one with ubiquitous knockdown. I found that the while PLA2G6 was required for neuronal upkeep to prevent age-related locomotor decline, neuronal tissue alone does not explain the full extent of the disease pathology. Based on these findings, a more universal approach should be taken when dealing with PLA2G6 related diseases. I believe that this information will be insightful and useful for future therapeutic approaches combating PLAN diseases.
Description: Senior honors thesis -- Open Access per signed student consent form
URI: https://hdl.handle.net/20.500.12202/4773
Appears in Collections:Jay and Jeanie Schottenstein Honors Student Theses

Files in This Item:
File Description SizeFormat 
Benjamin Shulman OA October 2019 ThesisFinalDraft.pdfPDF OA per signed student consent form689.53 kBAdobe PDFThumbnail
View/Open


This item is licensed under a Creative Commons License Creative Commons