In many neurodegenerative diseases, proteins clump in the brain, forming so-called amyloid fibrils. Yet there exists a cellular defence mechanism that counteracts this process and even dissolves fibrils already formed. The mechanism is based on the activity of molecular helpers, so-called chaperones of the heat shock protein 70 family. Heidelberg researchers studied how the Hsp70 system disaggregates fibrils of the Parkinson-specific protein α-synuclein in a test tube. The research team expects their research results to provide new insights into how Parkinson’s disease develops and what might be done to influence it.