Angiotensin II-inhibiting drugs have no effect on intraneuronal Aβ or oligomeric Aβ levels in a triple transgenic mouse model of Alzheimer's disease

Linda Ferrington, J Scott Miners, Laura E Palmer, Susan M Bond, Joanne E Povey, Paul At Kelly, Seth Love, Karen J Horsburgh, Patrick G Kehoe

Research output: Contribution to journalArticlepeer-review

Abstract

Reducing the excessive accumulation of amyloid β-protein (Aβ) in Alzheimer's disease (AD) is a key objective of most AD therapies. Several studies suggest that pharmacological inhibition of angiotensin-converting enzyme (ACE) or its by-product angiotensin II may delay onset or progression of dementia and it has been suggested that this occurs via regulation of Aβ. Intraneuronal oligomeric accumulation of Aβ is postulated to be one of the earliest pathological events. Thus this study investigated the effect of an ACE-inhibitor, captopril, and two angiotensin II receptor blockers (ARBs), eprosartan and valsartan, on intraneuronal Aβ pathology and oligomeric Aβ levels in a triple transgenic (3xTGAD) mouse model of AD.
Original languageEnglish
Pages (from-to)197-208
Number of pages12
JournalAmerican journal of translational research
Volume3
Issue number2
Publication statusPublished - 2011

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