Author Affiliation: Division of Cardiology, Johns Hopkins University, Baltimore, Maryland.
The work of Hajjar et al1 may represent a milestone in Alzheimer disease prophylaxis. However, I have a few simple questions. Since all participants who were included had clinical evidence for dementia, don't the results refer only to the relative likelihood of developing Alzheimer vs non-Alzheimer pathology? If so, wouldn't an excess of non-Alzheimer pathology in the angiotensin receptor blocker group produce identical results to a dearth of Alzheimer pathology? To consider the extreme case, if angiotensin receptor blockers cause non–Alzheimer disease dementia, these patients would predominate among the angiotensin receptor blocker–exposed patients and there would be relatively less amyloid deposition. Is this possibility excluded by your analyses?
Shapiro EP. Alzheimer Pathology and Angiotension Receptor Blockers. JAMA Neurol. 2013;70(3):414. doi:10.1001/jamaneurol.2013.1464