Journal
NEUROBIOLOGY OF DISEASE
Volume 26, Issue 1, Pages 273-281Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2007.01.004
Keywords
Alzheimer disease; amyloid beta-protein; beta-amyloid precursor protein; angiotensin-converting enzyme; A beta degradation
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Funding
- NIA NIH HHS [AG12749, R01 AG012749-12, R01 AG012749-05, R01 AG012749] Funding Source: Medline
- NINDS NIH HHS [K08 NS046324-01, K08 NS046324-03, K08 NS046324] Funding Source: Medline
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Genetic and pathologic studies have associated angiotensin-converting enzyme (ACE) with Alzheimer disease. Previously, we and others have reported that ACE degrades in vitro the amyloid beta-protein (A beta), a putative upstream initiator of Alzheimer disease. These studies support the hypothesis that deficiency in ACE-mediated A beta proteolysis could increase Alzheimer disease risk and raise the question of whether ACE inhibitors, a commonly prescribed class of anti-hypertensive medications, can elevate A beta levels in vivo. To test this hypothesis, we administered the ACE inhibitor captopril to two lines of APP transgenic mice harboring either low levels of A beta or high levels of A beta with associated plaque deposition. In both models, we show that captopril does not affect cerebral A beta levels in either soluble or insoluble pools. Furthermore, we find no change in plaque deposition or in peripheral A beta levels. Data from these Alzheimer models suggest that captopril and similar ACE inhibitors do not cause A beta accumulation in vivo. (c) 2007 Elsevier Inc. All rights reserved.
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