It was twenty ?ve years ago this year that for the ?rst time a protein under- ing a form of human cerebral amyloidosis, the Icelandic-type hereditary cerebral haemorrhage was identi?ed. This, together with the recognition that an amino acid substitution can transform the wild type cystatin C into a disease-associated amyloid-forming protein in this condition, was only a prelude to a series of imp- tant discoveries that followed. As a result, pathologically altered proteins have been brought into the centre stage of research into the pathomechanism of a n- ber of neurodegenerative diseases,...

It was twenty ?ve years ago this year that for the ?rst time a protein under- ing a form of human cerebral amyloidosis, the Icelandic-type hereditary cerebral haemorrhage was identi?ed. This, together with the recognition that an amino acid substitution can transform the wild type cystatin C into a disease-associated amyloid-forming protein in this condition, was only a prelude to a series of imp- tant discoveries that followed. As a result, pathologically altered proteins have been brought into the centre stage of research into the pathomechanism of a n- ber of neurodegenerative diseases,...