Judging Category
Basic or Experimental Research
Student Rank
Senior
College
Sciences and Mathematics
Faculty Sponsor
Edward (Ted) Schmid eschmid@astate.edu
Description
Alzheimer's disease (AD) represents one of the most prevalent neurodegenerative disorders globally. Thus far, the underlying mechanisms associated with the pathogenesis of AD are innately elusive. Two hallmarks associated with the progression of AD exist, including Amyloid-Beta 42 (Aβ42) protein plaque formation and hyperphosphorylation of tau proteins in neurons. Amyloid-beta is known to concentrate with other neuronal proteins as complexes form, including the cytoskeletal protein actin. However, whether actin contributes to neuronal decline in AD is unknown. To further understand the cellular cascades associated with AD, we investigated the role of cytoskeleton dynamics in modulating oxidative stress and neuroinflammation within a Drosophila Aβ42 induced model. Drosophila neural architecture exhibits profound evolutionary conservation when compared to that of humans; in which the neurobiological organization and synaptic structure can be observed. Using Drosophila genetics, we expressed Aβ42 in fly retinal cells. The effect of select gene interventions to offset amyloid toxicity were assessed by analyzing eye size change and/or manifestations of abnormal cell development. Through genetic screening on the effect of eye morphologies, we aim to identify potential gene therapies and molecular targets for treating AD.
Disciplines
Animal Experimentation and Research | Biology | Genetics | Molecular and Cellular Neuroscience | Systems and Integrative Physiology
License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
Recommended Citation
Sims, Shay O.; Duncan, Pierce; Abon, Malachi; and Smith, Jacob G., "Amyloid beta-42 neurotoxicity in Drosophila retinal development" (2026). Create@State. 13.
https://arch.astate.edu/evn-createstate/2026/posters/13
Included in
Animal Experimentation and Research Commons, Biology Commons, Genetics Commons, Molecular and Cellular Neuroscience Commons, Systems and Integrative Physiology Commons
Amyloid beta-42 neurotoxicity in Drosophila retinal development
Alzheimer's disease (AD) represents one of the most prevalent neurodegenerative disorders globally. Thus far, the underlying mechanisms associated with the pathogenesis of AD are innately elusive. Two hallmarks associated with the progression of AD exist, including Amyloid-Beta 42 (Aβ42) protein plaque formation and hyperphosphorylation of tau proteins in neurons. Amyloid-beta is known to concentrate with other neuronal proteins as complexes form, including the cytoskeletal protein actin. However, whether actin contributes to neuronal decline in AD is unknown. To further understand the cellular cascades associated with AD, we investigated the role of cytoskeleton dynamics in modulating oxidative stress and neuroinflammation within a Drosophila Aβ42 induced model. Drosophila neural architecture exhibits profound evolutionary conservation when compared to that of humans; in which the neurobiological organization and synaptic structure can be observed. Using Drosophila genetics, we expressed Aβ42 in fly retinal cells. The effect of select gene interventions to offset amyloid toxicity were assessed by analyzing eye size change and/or manifestations of abnormal cell development. Through genetic screening on the effect of eye morphologies, we aim to identify potential gene therapies and molecular targets for treating AD.
