Many neurodegenerative diseases are associated with the accumulation of fibrillar proteins. The unifying feature of a fibril formation is the structural transition from an initial globular or intrinsically disordered state to a β-structural form. Using molecular simulations we try to understand how the presence of ligands and of mutations affect the structural stability of proteins undergoing fibrillation in several neurodegenerative diseases. Investigations, in collaborations with a variety of experimental groups, help identifying compounds that affect fibrillation as well as uncover the role of specific cellular partners for protein fibrillation. Recently, we have started an activity also in the field of neurological diseases, including schizofrenia and depression.