The Effect of Polyphenols on Amyloid Beta Disaggregation for Alzheimer’s Disease

Christine W. Chen
Dr. Andrew Kauffmann and Dr. Bill Miller III (A.T. Still University), Faculty Mentors

Alzheimer’s Disease (AD) is a neurodegenerative disorder resulting in memory loss and decline of a person’s ability to function independently. Currently, there is no cure; therefore, further research is needed. Scientists believe AD occurs due to the buildup of protein fragments, called Amyloid Beta (Aβ), on nerve cells. Aβ is a 42 amino acid peptide (Aβ1-42). Many Aβ peptides interact and form strong interactions due to the hydrophobic effect, which causes aggregation and plaques to form in the brain.

Thus, the goal of this research is to discover a molecule that disrupts interactions between Aβ peptides. Currently, polyphenols are hypothesized to inhibit Aβ aggregation. Computationally modeling the interactions in physiological conditions between the polyphenol and Aβ provides an atomistic understanding of results from wet labs and helps determine the efficiency of these polyphenols as aggregation inhibitors of Aβ.  

Keywords: Alzheimer's Disease, computational chemistry, Amyloid ß, drug discovery, molecular dynamics, mechanisms, molecular docking, neuroscience

Topic(s):Biochemistry and Molecular Biology
Chemistry
Biology

Presentation Type: Oral Presentation

Session: TBA
Location: TBA
Time: TBA