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Amyloid plaque pathology is a defining characteristic of Alzheimer disease (AD), and the amyloid cascade hypothesis remains a central focus of AD research. Yet at least a dozen treatment trials have achieved target engagement by reducing fibrillar amyloid or its production, but have shown no clinical benefit. The article by Liu et al.1 shows that the monoclonal anti‐Aβ antibody bapineuzumab diminished binding of 11C–Pittsburgh compound B (PiB) in mild to moderate AD dementia, most notably in persons with APOE ε4.
Footnotes
Study funding: No targeted funding reported.
Disclosure: Dr. Breitner has no relevant financial or other competing interests. Within the past 3 years he has been a paid speaker for Lilly, and has consulted to Lundbeck and CereSpir Pharmaceuticals, but on topics unrelated to the content of this article. Go to Neurology.org for full disclosures.
- © 2015 American Academy of Neurology
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