Current Research

Design, Production, and Characterization of Beta Amyloid-Binding Proteins and Peptides

Alzheimer’s disease is characterized by neurofibrillary tangles of tau protein and intracellular plaques of beta-amyloid peptide. Sequestration and/or removal of beta-amyloid is considered a promising therapeutic strategy. The beta-amyloid peptide spontaneously self-assembles into soluble oligomers and ultimately fibrillar structures that deposit on tissue; the soluble oligomeric species are widely considered to be highly toxic. Using the ROSETTA software suite, we work to develop peptides that inhibit beta amyloid fibril formation through binding and redirect beta-amyloid towards forming protease-sensitive, nonfibrillar aggregates.