Evidence map›Paper›PMID 17321748›Full record

ArticleNeurobiology of disease2007

Effects of prolonged angiotensin-converting enzyme inhibitor treatment on amyloid beta-protein metabolism in mouse models of Alzheimer disease.

Matthew L Hemming, Dennis J Selkoe, Wesley Farris

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

  1. Drug repositioning for Alzheimer's disease.Nature reviews. Drug discovery · 2012
    Pooled it
  2. Current updates on latest basic research of scientific relevance in hypertensive dementia.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Review
  3. Perturbations in the neuroactive ligand-receptor interaction and renin angiotensin system pathways are associated with cancer-related cognitive impairment.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2025
    Article
  4. Review
  5. Article
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  7. Article
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  9. Article
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  11. Article
  12. Review
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  14. Article
  15. Modifiable Risk Factors for Alzheimer's Disease.Frontiers in aging neuroscience · 2019
    Article
  16. Article
  17. Article
  18. Review
  19. Microglial Activation Is Modulated by Captopril:Frontiers in cellular neuroscience · 2018
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Matthew L HemmingCenter for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Dennis J Selkoe
Wesley Farris
Brigham and Women's Hospital · USHarvard University · US

Funding

PROTEIN/PROTEIN INTERACTIONS IN THE BIOLOGY OF BETA APPR01AG012749 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI SELKOE, DENNIS J · 1995 to 2012
$4.2M
Role of ABeta-Degrading Proteases in Alzheimer's DiseaseK08NS046324 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FARRIS, WESLEY · 2003 to 2007
$876k
NIA NIH HHS AG12749NIA NIH HHS R01 AG012749NINDS NIH HHS K08 NS046324
6 · The paper itself

Abstract

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 (Abeta), a putative upstream initiator of Alzheimer disease. These studies support the hypothesis that deficiency in ACE-mediated Abeta proteolysis could increase Alzheimer disease risk and raise the question of whether ACE inhibitors, a commonly prescribed class of anti-hypertensive medications, can elevate Abeta 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 Abeta or high levels of Abeta with associated plaque deposition. In both models, we show that captopril does not affect cerebral Abeta levels in either soluble or insoluble pools. Furthermore, we find no change in plaque deposition or in peripheral Abeta levels. Data from these Alzheimer models suggest that captopril and similar ACE inhibitors do not cause Abeta accumulation in vivo.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAngiotensin-Converting Enzyme InhibitorsAnimalsBrain ChemistryCaptoprilEnzyme-Linked Immunosorbent AssayHumansImage Interpretation, Computer-AssistedImmunohistochemistryMiceMice, Inbred C57BLMice, Inbred DBAMice, TransgenicNeprilysinPeptidyl-Dipeptidase AAmyloid beta-PeptidesAngiotensin-Converting Enzyme InhibitorsCaptoprilNeprilysinPeptidyl-Dipeptidase A

Identifiers

PMID17321748
PMCPMC2377010
OpenAlexW2133361358

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.