Ludwig-Maximilians-Universität, Chair of Metabolic Biochemistry

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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.

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