Exploring the Role of the G-protein Signaling Pathway Interaction with nAChR α 7 in D. melanogaster Alzheimer’s Models

Overview

Schmahl Science Workshops As a current treatment for Alzheimer’s Disease (AD), acetylcholinesterase inhibitors prevent the impairment of neuronal signaling pathways by retaining acetylcholine, a neurotransmitter involved in memory retention. Unfortunately, this therapy is temporary. I researched a different route for maintaining such pathways via the nAChR subunit α7/G-protein Signaling Pathway, one of the most under-studied pathways impacted in AD pathogenesis. I tested how a lack of the pathway affects learning, memory retention, locomotion, and longevity using model organism D. melanogaster . I tested nAChR- (silenced Dα7 allele PΔEY6) and GAP-43- (a key G-protein through silenced Igloo allele Igl) lacking mutants, along with AD models, double crosses Igl x PΔEY6 & Igl x AD models, and Wild-Type (WT & W118) fruit flies. The Wild-Types’ success rates were ~80% for locomotion and learning/memory retention. The mutants’ (all but Wild-Type) success rates were ~60% and ~45% for the same. Additionally, the mutants displayed decreased longevity by 25% compared to Wild-Types. Hence, a lack of the D. melanogaster -nAChR and GAP-43 causes learning, memory retention, locomotion, and longevity impairments, similar to those observed in AD models, suggesting that these two reside in the same pathway. This interaction should be further studied as a potential therapeutic target in AD.

Competition history

• JSHS 2020 Category not listed

Resources

• National JSHS abstract book ↗

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