Alzheimer's disease is a neurodegenerative disease characterized by the buildup of amyloid-beta proteins in the brain, and degeneration caused by the death of neurons. This neuron death is suspected to be caused by the amyloid-ß protein. Neuron death causes people to slowly lose their memory and cognitive skills. There currently is not a cure for Alzheimer's, but a few different drugs, supplements, and dietary changes have been shown to delay or slow the onset of Alzheimer's.

Cholesterol is a sterol type molecule that is vital to cellular function. It is present in nearly every food. Well-known for its causation of high blood pressure, cholesterol is often seen as unhealthy and dangerous. In recent studies, high-cholesterol levels have been seen to lead to an increased risk of Alzheimer's. In studies with C. elegans, cholesterol has been seen to bind with amyloid precursor protein (APP), implicating that cholesterol could be having an effect on the aggregation of amyloid-beta.

I am testing whether cholesterol has an effect on Amyloid-B toxicity in transgenic C. elegans. I hypothesized that worms eating more cholesterol will be affected by Amyloid-B toxicity more than worms that eat less cholesterol. To test this, I am using transgenic Caenorhabditis elegans (strain CL4176). They become paralyzed as amyloid-beta builds up in their neurons, which is induced when the worms are upshifted from 16 degrees Celsius to 27 degrees celsius. To compare amyloid-B toxicities in the different plates of worms, the percentage of the worms on the plates that are paralyzed after upshift are measured. In the trials, I placed the worms in conditions that emulated high cholesterol and low cholesterol diets, all cultivated on modified nematode growth medium to account for the changing cholesterol levels. The worms were age synchronized and grown to the second larval stage. At the second larval stage, the worms were upshifted to 27 degrees celsius. After 1 day of upshift, the first worms started to be paralyzed. At 1 day and for 24 hour increments after, the percentage of the worms paralyzed on each plate was calculated for up to 4 days.

According to ANOVA, the worms treated that consumed less cholesterol were significantly different, with the worms on plates with 3 mg/ml cholesterol showing the least paralysis, and the worms on plates with 10 mg/ml cholesterol showing the most.

The lower level of cholesterol showed decreased paralysis of the transgenic C. elegans. This suggests that cholesterol is linked to the formation and aggregation of the amyloid-B peptide. These results suggest that people who are at a higher risk of Alzheimer's could benefit from a low cholesterol diet.