ArticleJournal of Alzheimer's disease : JAD2013
Angiotensin converting enzyme inhibitors and the reduced risk of Alzheimer's disease in the absence of apolipoprotein E4 allele.
Article in Journal of Alzheimer's disease : JAD, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Renin-angiotensin system gene expression and neurodegenerative diseases.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2016Pooled it
- Dimerization and dynamics of human angiotensin-I converting enzyme revealed by cryo-EM and MD simulations.eLife · 2025Article
- Higher Neuronal Facilitation and Potentiation with APOE4 Suppressed by Angiotensin II.Molecular neurobiology · 2024Article
- The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Higher Neuronal Facilitation and Potentiation with APOE4 Suppressed by Angiotensin II.Research square · 2023Article
- ACE and ACE2: insights fromHeliyon · 2021Review
- Blood Pressure Profiles and Cognitive Function from Adulthood to Old Age: Chasing a Golden Middle Way?Journal of clinical medicine · 2021Review
- Effects of Antihypertensive Drugs on Cognitive Function in Elderly Patients with Hypertension: A Review.Aging and disease · 2021Review
- Increased plasma bradykinin level is associated with cognitive impairment in Alzheimer's patients.Neurobiology of disease · 2020Article
- The Role of Cardiovascular Risk Factors and Stroke in Familial Alzheimer Disease.JAMA neurology · 2016Article
- Arabidopsis thaliana extracts optimized for polyphenols production as potential therapeutics for the APOE-modulated neuroinflammation characteristic of Alzheimer's disease in vitro.Scientific reports · 2016Article
- Angiotensin-(1-7) is Reduced and Inversely Correlates with Tau Hyperphosphorylation in Animal Models of Alzheimer's Disease.Molecular neurobiology · 2016Article
- An Integrated Data Driven Approach to Drug Repositioning Using Gene-Disease Associations.PloS one · 2016Article
- Examining the association between Apolipoprotein E (APOE) and self-reported sleep disturbances in non-demented older adults.Neuroscience letters · 2015Article
- APOE-modulated Aβ-induced neuroinflammation in Alzheimer's disease: current landscape, novel data, and future perspective.Journal of neurochemistry · 2015Review
- Amyloid-β pathology and APOE genotype modulate retinoid X receptor agonist activity in vivo.The Journal of biological chemistry · 2014Article
- Successful therapies for Alzheimer's disease: why so many in animal models and none in humans?Frontiers in pharmacology · 2014Review
- Oxidative stress and metabolic syndrome: cause or consequence of Alzheimer's disease?Oxidative medicine and cellular longevity · 2014Review
- Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor Blockers Rescue Memory Defects ineNeuroArticle
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Our cross-sectional study showed that the interaction between apolipoprotein E4 (ApoE4) and angiotensin converting enzyme (ACE) inhibitors was associated with Alzheimer's disease (AD). The aim of this longitudinal study was to differentiate whether ACE inhibitors accelerate or reduce the risk of AD in the context of ApoE alleles. Using the longitudinal data from the National Alzheimer's Coordinating Center (NACC) with ApoE genotyping and documentation of ACE inhibitors use, we found that in the absence of ApoE4, subjects who had been taking central ACE inhibitor use (χ2 test: 21% versus 27%, p = 0.0002) or peripheral ACE inhibitor use (χ2 test: 13% versus 27%, p < 0.0001) had lower incidence of AD compared with those who had not been taking an ACE inhibitor. In contrast, in the presence of ApoE4, there was no such association between ACE inhibitor use and the risk of AD. After adjusting for the confounders, central ACE inhibitor use (OR = 0.68, 95% CI = 0.55, 0.83, p = 0.0002) or peripheral ACE inhibitor use (OR = 0.33, 95% CI = 0.33, 0.68, p < 0.0001) still remained inversely associated with a risk of developing AD in ApoE4 non-carriers. In conclusion, ACE inhibitors, especially peripherally acting ones, were associated with a reduced risk of AD in the absence of ApoE4, but had no such effect in those carrying the ApoE4 allele. A double-blind clinical trial should be considered to determine the effect of ACE inhibitors on prevention of AD in the context of ApoE genotype.
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Registered trials
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