Evidence map›Paper›PMID 29873184›Full record

ArticleAging cell2018

Carbonic anhydrase inhibition selectively prevents amyloid β neurovascular mitochondrial toxicity.

María E Solesio, Pablo M Peixoto, Ludovic Debure, Stephen M Madamba, Mony J de Leon, Thomas Wisniewski, Evgeny V Pavlov, Silvia Fossati

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
4.6field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 90 citations in OpenAlex.

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  12. Cerebral proteome adaptations to amyloid angiopathy are prevented by carbonic anhydrase inhibitors.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

8 authors at 2 institutions in 1 country.

María E SolesioDepartment of Basic Sciences, New York University College of Dentistry, New York, New York.ORCID 0000-0002-8105-1701
Pablo M PeixotoDepartment of Natural Sciences, Baruch College, Graduate Center, The City University of New York, New York, New York.
Ludovic DebureDepartment of Psychiatry, New York University School of Medicine, New York, New York.
Stephen M MadambaDepartment of Natural Sciences, Baruch College, Graduate Center, The City University of New York, New York, New York.
Mony J de LeonDepartment of Psychiatry, New York University School of Medicine, New York, New York.
Thomas WisniewskiDepartment of Neurology, Center for Cognitive Neurology, New York University School of Medicine, New York, New York.
Evgeny V PavlovDepartment of Basic Sciences, New York University College of Dentistry, New York, New York.
Silvia FossatiDepartment of Psychiatry, New York University School of Medicine, New York, New York.ORCID 0000-0002-2047-222X
New York University · USThe Graduate Center, CUNY · US

Funding

PSYCHOSOCIAL COREP30AG008051 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SHAO, YONGZHAO · 1990 to 2019
$36.1M
PREDICTORS OF COGNITIVE DECLINE IN NORMAL AGINGR01AG012101 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DE LEON, MONY J., RUSINEK, HENRY · 1993 to 2015
$6.7M
CLINICAL CORRELATES OF LONGITUDINAL PET CHANGES IN ADR01AG013616 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DE LEON, MONY J. · 1995 to 2013
$6.2M
Biomarkers in Early Alzheimer's Disease (AD).R01AG022374 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DE LEON, MONY J., RUSINEK, HENRY · 2004 to 2015
$5.2M
PET Measures of CSF Clearance in Preclinical Alzheimer's DiseaseRF1AG057570 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI DE LEON, MONY J. · 2017 to 2017
$4.1M
Therapeutic Targeting of Abnormal Conformation in Neurodegenerative DiseaseR01NS073502 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WISNIEWSKI, THOMAS M · 2010 to 2019
$3.7M
Alzheimer's Association NIRG-12-240372NIA NIH HHS P30 AG008051NIA NIH HHS R01 AG012101NIA NIH HHS R01 AG013616NIA NIH HHS R01 AG022374NIA NIH HHS RF1 AG057570NINDS NIH HHS R01 NS073502
6 · The paper itself

Abstract

Mounting evidence suggests that mitochondrial dysfunction plays a causal role in the etiology and progression of Alzheimer's disease (AD). We recently showed that the carbonic anhydrase inhibitor (CAI) methazolamide (MTZ) prevents amyloid β (Aβ)-mediated onset of apoptosis in the mouse brain. In this study, we used MTZ and, for the first time, the analog CAI acetazolamide (ATZ) in neuronal and cerebral vascular cells challenged with Aβ, to clarify their protective effects and mitochondrial molecular mechanism of action. The CAIs selectively inhibited mitochondrial dysfunction pathways induced by Aβ, without affecting metabolic function. ATZ was effective at concentrations 10 times lower than MTZ. Both MTZ and ATZ prevented mitochondrial membrane depolarization and H

Indexed as

AcetazolamideAmyloid beta-PeptidesCarbonic Anhydrase InhibitorsDose-Response Relationship, DrugEndothelium, VascularHumansMethazolamideMitochondriaTumor Cells, CulturedAcetazolamideAmyloid beta-PeptidesCarbonic Anhydrase InhibitorsMethazolamideacetazolamideAlzheimer's diseaseamyloid βcarbonic anhydrase inhibitorsmethazolamidemitochondria

Identifiers

PMID29873184
PMCPMC6052473
OpenAlexW2806856966

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.