Companies are taking steps -- baby steps -- to test new targets in pathways such as neuroinflammation and neuroprotection as a means to treat Alzheimer’s disease.
The failure of aducanumab won’t be the final nail in the coffin of the β amyloid hypothesis, but it certainly sends a clarion call for investment in other mechanisms. The good news is that compounds against newer mechanisms are trickling into the clinic, and more lie behind them in preclinical studies.
Thursday’s announcement by Biogen Inc. and Eisai Co. Ltd. that they would stop the Phase III ENGAGE and EMERGE trials of aducanumab in AD was the latest in a series of hits over the last three years for the hypothesis that holds that β amyloid is somehow causative for the disease, or at least that removing it will improve cognition. At least six agents targeting the β amyloid pathway have had Phase III misses or trial discontinuations since 2012.
The aducanumab decision followed an interim futility analysis and IDMC recommendation that the