The isoforms with 40 and 42 amino acids (Aβ40/42) are the main constituents of amyloid plaques in the brains of Alzheimer's disease patients.

Research on laboratory rats suggest that the soluble form of this peptide is a causative agent in the development of Alzheimer's.

[3] Phase III double-blind clinical trials started in March 2008 with the IDENTITY study (Interrupting Alzheimer's dementia by evaluating treatment of amyloid pathology), including 1500 patients from 22 countries.

[5] The open-label trial IDENTITY-XT, which included patients who have completed one of the two studies, started in December 2009.

Preliminary findings show that not only did semagacestat fail to slow disease progression, but that it was actually associated with “worsening of clinical measures of cognition and the ability to perform activities of daily living”.