Presentation Title

Identifying the Impact of Glial Engulfment on Aβ42-induced Nervous System Dysfunction

Presenter's Name(s)

Zoë A. PaigeFollow

Project Collaborators

Jaeda Coutinho-Budd (Primary Investigator), Toby B. Lanser (Collaborating Undergraduate)

Abstract

Alzheimer’s Disease (AD) is a well-known neurodegenerative condition characterized by the accumulation of Tau proteins (tangles) and beta amyloid (Aβ, plaques) in the brain, forming aggregations that impair neuronal communication and memory. When the toxic Aβ fragment (Aβ42) is expressed in Drosophila neurons, Drosophila recapitulate AD pathophysiology seen in mammals, such as motor deficits and premature death. We can therefore use this system to test for molecular modifiers of the symptoms to better understand the fundamental cell biology of the disease. Glial morphology and cross-talk with neurons (the focus of our lab) along with glial regulation of Aβ plaques in the context of AD is woefully understudied, and we hope to further elucidate the extent of this communication within Aβ42 Drosophila. Given the recent identification of the role of p38 kinases in Multiple Sclerosis, another glial-based neurodegenerative disease, our lab hopes to elucidate the role of p38 kinases in AD by reducing their glial expression in an Aβ42 background. Additionally, we will explore the role of a potential upstream activator of the glial engulfment receptor, Draper, which is necessary for the clearance of cellular debris . We hope to further delineate the molecular signaling involved in cortex glial removal of Aβ42 and dying neurons.

Primary Faculty Mentor Name

Jaeda Coutinho-Budd

Status

Undergraduate

Student College

College of Arts and Sciences

Program/Major

Neuroscience

Primary Research Category

Biological Sciences

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Identifying the Impact of Glial Engulfment on Aβ42-induced Nervous System Dysfunction

Alzheimer’s Disease (AD) is a well-known neurodegenerative condition characterized by the accumulation of Tau proteins (tangles) and beta amyloid (Aβ, plaques) in the brain, forming aggregations that impair neuronal communication and memory. When the toxic Aβ fragment (Aβ42) is expressed in Drosophila neurons, Drosophila recapitulate AD pathophysiology seen in mammals, such as motor deficits and premature death. We can therefore use this system to test for molecular modifiers of the symptoms to better understand the fundamental cell biology of the disease. Glial morphology and cross-talk with neurons (the focus of our lab) along with glial regulation of Aβ plaques in the context of AD is woefully understudied, and we hope to further elucidate the extent of this communication within Aβ42 Drosophila. Given the recent identification of the role of p38 kinases in Multiple Sclerosis, another glial-based neurodegenerative disease, our lab hopes to elucidate the role of p38 kinases in AD by reducing their glial expression in an Aβ42 background. Additionally, we will explore the role of a potential upstream activator of the glial engulfment receptor, Draper, which is necessary for the clearance of cellular debris . We hope to further delineate the molecular signaling involved in cortex glial removal of Aβ42 and dying neurons.