The amyloid hypothesis has led to a greater understanding of Alzheimer’s disease and has provided a foundation for the development of drugs to tackle the disease.  Two large clinical trials investigating the clinical effects of two such novel compounds, bapineuzimab and tarenflurbil, on Alzheimer’s disease, have been recently published.  Both drugs were designed to modulate the pathophysiology of the disease by interfering with the beta-amyloid metabolism, albeit through different modes of action, but both trials have disappointingly yielded negative findings, leading to questions being asked of the respective study designs and dosing regimes.

In a commentary published recently in Alzheimer’s Research & Therapy, Prins et al. discuss the lessons that can be learnt from these studies. They suggest that the failure of these trials can be attributed not just to problems in study design, but also our incomplete understanding of the mechanisms involved. These trial results may help shape our understanding of the pathogenesis of Alzheimer’s disease and in particular, the amyloid beta mechanism, vital in the search for novel therapeutics for this disease.

Alex Kroll – Senior Assistant Editor