• Sam Gandy.
• Departments of Neurology and Psychiatry, and the Mount Sinai Alzheimer's Disease Research Center, Icahn School of Medicine at Mount Sinai, and James J. Peters VA Medical Center, New York, New York. Electronic address: samuel.gandy@mssm.edu.
• Biol. Psychiatry. 2014 Apr 1;75(7):553-7.

AbstractDespite compelling genetic evidence indicating that cerebral amyloidosis can be, at least sometimes, the primary cause of Alzheimer's disease (AD), clinical trials for symptomatic AD with amyloid-reducing agents have succeeded at target engagement but failed to cause clinical benefit. In a landmark shift, the U.S. Food and Drug Administration now proposes to approve prophylaxis that alters the trajectory of what is now believed to be typical AD biomarker evolution. The first prevention trials are now beginning in patients with genetic guarantees for or high genetic risks for AD. The expectation is that clues to their outcomes will begin to emerge from these trials in approximately 2018. In the meantime, new strategies point to nonneuronal cells and to system pathology. A review of the current state of the art of AD science follows herein.© 2013 Published by Society of Biological Psychiatry on behalf of Society of Biological Psychiatry.

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