Amyloid aggregation inhibitors

Amongst the 4,700 presentations at the 215th National Meeting of the American Chemical Society (ACS), were fourteen research papers on Alzheimer's disease (AD) and related issues. The dementia associated with AD is a progressive and common neuro-degenerative disorder producing widespread brain destruction, with no curative therapies. The brains of AD patients have an abundance of amyloid plaques and neurofibrillary tangles. The major protein component of the amyloid plaques is the beta-peptide that exists in two predominant forms: the shorter, 40-residue beta(1-40), and the longer, 42-residue beta(1-42). Recent genetic studies have established that amyloid deposition, particularly by the longer beta(1-42), is directly linked to early onset cases of AD. As a result, major research efforts are focused on uncovering effective therapeutic strategies to prevent or slow down the aggregation and the associated precipitation of the beta-peptide into amyloid. In the amyloid deposits, the beta-peptide adopts a beta-sheet structure which is proposed to be neurotoxic.