Semagacestat's fall: where next for AD therapies?
Nat Med. 2013 Oct;19(10):1214-5.
| Authors/Editors: |
Kaj Blennow Henrik Zetterberg Christian Haass Thomas Finucane |
|---|---|
| Type of Publication: | Review |
Community Corner
Many attempts to develop Alzheimer’s disease (AD) therapies have focused on targeting the formation of the toxic amyloid-β (Aβ) species. A recent paper by Doody et al.1 describes the phase 3 trial of one such strategy, the γ-secretase inhibitor semagacestat, which acts by blocking one of the cleavage steps of amyloid precursor protein into Aβ. However, the trial was discontinued early owing to a high occurrence of adverse effects. In addition, patients with AD receiving the drug did not show an improvement in symptoms; to the contrary they showed a worsening of functional ability. We asked the experts for their opinion of this study and how Alzheimer’s researchers should move forward after this disappointing result.
