Exciting recent progress in deciphering the molecular basis of Alzheimer's
disease points to a crucial role of amyloid in the pathogenesis of this dis
order. As a consequence, preventing and reversing cerebral amyloid depositi
on have become attractive therapeutic strategies for Alzheimer's disease. B
iophysical and biochemical studies have shown that amyloidosis is, in essen
ce, a problem of protein folding in which the normally soluble unstructured
amyloid-beta peptide becomes organised in neurotoxic beta-pleated sheet fi
brils. Compounds with the ability to stabilise the normal form of amyloid-b
eta peptide and/or to destabilise the pathological fibrillar structure coul
d represent novel drugs for this devastating and so far incurable disease.