Evidence map›Paper›PMID 27562846›Full record

ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2016

Angiotensin Converting Enzyme Inhibitors Ameliorate Brain Inflammation Associated with Microglial Activation: Possible Implications for Alzheimer's Disease.

Nofar Torika, Keren Asraf, Ella Roasso, Abraham Danon, Sigal Fleisher-Berkovich

Abstract read
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In one paragraph

Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 62 citations in OpenAlex.

  1. The Correlation between Two Angiotensin-Converting Enzyme Inhibitor's Concentrations and Cognition.International journal of environmental research and public health · 2022
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  16. Fractalkine-induced microglial vasoregulation occurs within the retina and is altered early in diabetic retinopathy.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

5 authors at 1 institution in 1 country.

Nofar TorikaDepartment of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, P.O, B 653, Beer-Sheva, Israel.
Keren AsrafDepartment of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, P.O, B 653, Beer-Sheva, Israel.
Ella RoassoDepartment of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, P.O, B 653, Beer-Sheva, Israel.
Abraham DanonDepartment of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, P.O, B 653, Beer-Sheva, Israel.
Sigal Fleisher-BerkovichDepartment of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, P.O, B 653, Beer-Sheva, Israel. fleisher@bgu.ac.il.
Ben-Gurion University of the Negev · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin converting enzyme (ACE) converts Angiotensin I to a potent vasoconstrictor angiotensin II (ANG II). ACE inhibitors (ACEIs) are widely used for the management of hypertension. All components of the renin-angiotensin system (RAS) have also been identified in the brain. In addition to cytokines, neuromodulators such as ANG II can induce neuroinflammation. Moreover, in Alzheimer's disease (AD) models, where neuroinflammation occurs and is thought to contribute to the propagation of the disease, increased levels of ANG II and ACE have been detected. However, the specific effect of ACEIs on neuroinflammation and AD remains obscure. The present study suggests that captopril and perindopril, centrally active ACEIs, may serve as modulators for microglial activation associated with AD. Our in vitro study investigated the effect of both ACEIs on nitric oxide (NO), tumor necrosis factor- α (TNF-α) release and inducible NO synthase (iNOS) expression in lipopolysaccharide (LPS)-induced BV2 microglia. Exposure of BV2 microglia to ACEIs significantly attenuated the LPS-induced NO and TNF-α release. In vivo, short term intranasal administration of perindopril or captopril to 5 Familial AD (5XFAD) mice significantly reduced amyloid burden and CD11b expression (a microglial marker) or only CD11b expression respectively, in the cortex of 5XFAD. Long-term intranasal administration of captopril to mice reduced amyloid burden with no effect on CD11b expression. We provide evidence that intranasal delivery of ACEI may serve as an efficient alternative for their systemic administration, as it results in the attenuation of microglial accumulation and even the reduction of Amyloid β (Aβ) plaques.

Indexed as

Alzheimer DiseaseAngiotensin-Converting Enzyme InhibitorsAnimalsCell LineEncephalitisHumansMiceMice, Inbred C57BLMice, TransgenicMicrogliaAngiotensin-Converting Enzyme InhibitorsAmyloid βAngiotensin converting enzyme (ACE)CaptoprilMicrogliaNeuroinflammationPerindopril

Identifiers

PMID27562846
OpenAlexW2513016061

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.