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Subjects

Alzheimer's disease -- Cytopathology, Neuroglia -- Effect on early stage Alzheimer's disease, Neurophysiology, Immunohistochemistry

Abstract

Glial cells, the resident immune cells of the brain, are important for brain health as they represent a critical function both in brain injury as well as in brain development and maintenance. Following brain injury, glia quickly respond by cleaning up neuronal and synaptic debris. In addition to their role as the cleaning cell of the brain, recent research has shown that during development, glia also shape and fine-tune neural connections by eliminating weak synapses fated for removal. However, whether glial cells also continue to remodel synaptic architecture in the adult brain is unclear. Moreover, synaptic pruning and loss are early hallmarks of Alzheimer’s disease (AD), but whether glial cells play a role in this pathophysiology remains mysterious. We will investigate the role of glial cells in AD-related synaptic loss using a Drosophila melanogaster model of AD. First, we will establish when synaptic loss occurs in AD model flies. Subsequently, we will explore the role of the glial engulfment receptor Draper, which is essential for glial clearance of neuronal debris after injury, and evaluate its effect on synaptic loss in the AD fly model. For these studies, we will use immunohistochemistry and western blotting techniques, as well as the power of Drosophila genetics. Through this project, we hope to 1) determine similarities and differences between the Drosophila AD model and human disease, 2) identify glial signals that may contribute to synaptic loss in this model and 3) identify molecular targets, which can potentially be manipulated to prevent or delay the first signs of AD.

DOI

10.15760/mcnair.2016.8

Creative Commons License

Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License
This work is licensed under a Creative Commons Attribution-NonCommercial-Share Alike 4.0 International License.

Persistent Identifier

http://archives.pdx.edu/ds/psu/17452

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