Investigating the Effect of Comorbid Conditions on the Development of Alzheimer's Disease in Caenorhabditis elegans

Location

Poster #9

Start Date

2-5-2025 10:00 AM

Department

Biology

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that commonly affects elderly populations, leading to cognitive decline, memory impairment, rapid mood oscillations, and in severe cases, death. Previous literature has highlighted the impact of comorbidities on AD progression; however, there exists a gap regarding the dual impact of chronic stressors and comorbidities. This study aims to investigate how oxidative stress and diabetes influence AD development and progression through shared molecular pathways using the popular Caenorhabditis elegans as a model organism. We hypothesize that, under chronic oxidative stress and diabetes, neurodegeneration is accelerated by decreasing locomotor function and increasing Aβ1-42 peptide accumulation. Using different strains of C. elegans, including a strain with impaired insulin-like receptor signaling (diabetic-like strain), we set out to investigate the combined effect of a chronic oxidative stress and the comorbidity in the progression of AD markers. Each strain was chronically exposed to paraquat, a known inducer of oxidative stress, and assessed for neurodegenerative outcomes. Locomotor function was evaluated by measuring the mean speeds of C. elegans worms using the software WormLab, while biochemical analysis of Aβ1-42 levels was performed using SDS-PAGE and immunoblotting.

Faculty Sponsor

Gabriel Guzman

Faculty Sponsor

Beth Cliffel

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May 2nd, 10:00 AM

Investigating the Effect of Comorbid Conditions on the Development of Alzheimer's Disease in Caenorhabditis elegans

Poster #9

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that commonly affects elderly populations, leading to cognitive decline, memory impairment, rapid mood oscillations, and in severe cases, death. Previous literature has highlighted the impact of comorbidities on AD progression; however, there exists a gap regarding the dual impact of chronic stressors and comorbidities. This study aims to investigate how oxidative stress and diabetes influence AD development and progression through shared molecular pathways using the popular Caenorhabditis elegans as a model organism. We hypothesize that, under chronic oxidative stress and diabetes, neurodegeneration is accelerated by decreasing locomotor function and increasing Aβ1-42 peptide accumulation. Using different strains of C. elegans, including a strain with impaired insulin-like receptor signaling (diabetic-like strain), we set out to investigate the combined effect of a chronic oxidative stress and the comorbidity in the progression of AD markers. Each strain was chronically exposed to paraquat, a known inducer of oxidative stress, and assessed for neurodegenerative outcomes. Locomotor function was evaluated by measuring the mean speeds of C. elegans worms using the software WormLab, while biochemical analysis of Aβ1-42 levels was performed using SDS-PAGE and immunoblotting.