The document outlines the main points to be covered in a presentation about using the nematode C. elegans to study the genetic implications of Alzheimer's disease. It will introduce the speaker and why they are doing the project, provide background on Alzheimer's disease and how it differs from normal forgetfulness, explain what C. elegans is and how it can be used to study humans with Alzheimer's disease. Key genes like apl-1 and moa-1 will be described as well as an experiment using a touch habituation assay to study learning behaviors in different C. elegans genotypes that could provide insights into Alzheimer's disease.

1. Worms and Learning:
An Illustrated Investigation into the Genetic
Implications of Alzheimer’s Disease
Katie Cheng
The following is a very basic outline of the main points I would like to cover in my presentation.
It combines main points from the animations I will be making and presenting. I plan on making 3. They will be
punctuated with still shots of my illustrations.

2. Introduction
Who am I and why am I doing this project?

3. What is Alzheimer’s Disease?
Start by citing some stats and general facts about AD.

4. What is the difference between AD and
normal forgetfulness?

5. What causes AD?
Mini-biology lesson on neurons and how they function. AD is a disruption of
neuronal function that may be attributed to the presence of plaques and tangles.

6. What is Caenorhabditis elegans?
Some points to discuss:
Model organism because scientists know entire C. elegans genome

7. How can studying C. elegans teach us about
humans with AD?
Explain the APP ortholog, called apl-1 (in the worms).
What is an ortholog?

8. What is apl-1? What is moa-1?
Review diagrams explaining what these genes are and their importance.
How are they related?

9. What is the touch habituation assay? What is
its purpose?

10. Parameters of the experiment
Describe the different genotypes and their significance in modeling learning behaviors

11. Experiment results
What is the significance of these findings?

12. So what?
How do these findings relate back to humans and AD?