The researchers observed protein aggregates in the nerve tissue of Parkinson's patients, composed of the protein alpha-synuclein monomers that assemble into so-called amyloid fibrils. Similar deposits have also been found in other neurodegenerative diseases such as Alzheimer's. So researchers think these fibrils are responsible for the disease, and to test that possibility, researchers are looking for ways to stop fibrils from forming.
Professor William h.Crocker describes a class of engineered binding proteins called beta-wrapins that prevent alpha-synaptic nucleonuclear proteins from clumping together. "We studied the function of beta-wrapins and how they disrupt the process of alpha-synaptic nuclein aggregation," says William.

First, the researchers found that beta-wrapins prevented the new alpha-synuclein monomer from lengthening amyloid fibrils. Because β-wrapins capture monomers and form chemical complexes with them. In addition, the researchers studied the role of β-wrapins not only in test tubes, but also in cell culture and animal models. The researchers treated diseased flies with beta-encapsulating proteins and showed significantly improved motor skills in climbing tests.