Abstract

A mutant strain of Caenorhabditis elegans overexpresses a protein, amyloid precursor‐like protein (APL‐1), that is similar to the human amyloid precursor protein (APP) linked to early‐onset Alzheimer's disease (AD). AD is characterized by amyloid plaques which accumulate and contribute to the progressive neurodegeneration. The mutant strain of C. elegans (ynIs‐79) overexpresses APL‐1 specifically in neurons. Overexpression in C. elegans causes molting issues, motor dysfunction, and disrupts morphogenesis in the nematode. Ginkgo biloba (GB) extract is a popular herbal supplement which may delay or improve the memory problems associated with AD. We hypothesize that individual flavonoids, like quercetin, are likely to be the positive contributing factors because of known protective roles in preventing oxidative stress. After purifying an extract from GB leaves, we determined the concentration of quercetin using HPLC analysis and then using a standard analytical grade solution of quercetin we applied a similar concentration to both the mutant and wild type C. elegans strains. Anterior and posterior tap habituation was used to determine the ability of each stain to recognize a nonthreatening stimulus. We expected that exposing the mutant nematodes to quercetin would decrease the number of taps needed for habituation, and our results show a significant decrease, suggesting increased memory retention and rescue of neurodegenerative dysfunction for the ynIs‐79 strain.Support or Funding InformationGail Dillard Faculty Development FundThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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