Evidence map›Paper›PMID 33294639›Full record

ArticleBiochemistry and biophysics reports2020

Short-term treatment with dabigatran alters protein expression patterns in a late-stage tau-based Alzheimer's disease mouse model.

Jaclyn Iannucci, Shelby L Johnson, Mark Majchrzak, Benjamin J Barlock, Fatemeh Akhlaghi, Navindra P Seeram, Abhik Sen, Paula Grammas

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biochemistry and biophysics reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

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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 1 institution in 1 country.

Jaclyn IannucciGeorge & Anne Ryan Institute for Neuroscience, University of Rhode Island, Kingston, RI, 02881, USA.
Shelby L JohnsonGeorge & Anne Ryan Institute for Neuroscience, University of Rhode Island, Kingston, RI, 02881, USA.
Mark MajchrzakGeorge & Anne Ryan Institute for Neuroscience, University of Rhode Island, Kingston, RI, 02881, USA.
Benjamin J BarlockClinical Pharmacokinetics Research Laboratory, Department of Biomedical and Pharmaceutical Sciences, College of Pharmacy, University of Rhode Island, Kingston, RI, 02881, USA.
Fatemeh AkhlaghiClinical Pharmacokinetics Research Laboratory, Department of Biomedical and Pharmaceutical Sciences, College of Pharmacy, University of Rhode Island, Kingston, RI, 02881, USA.
Navindra P SeeramGeorge & Anne Ryan Institute for Neuroscience, University of Rhode Island, Kingston, RI, 02881, USA.
Abhik SenGeorge & Anne Ryan Institute for Neuroscience, University of Rhode Island, Kingston, RI, 02881, USA.
Paula GrammasGeorge & Anne Ryan Institute for Neuroscience, University of Rhode Island, Kingston, RI, 02881, USA.
University of Rhode Island · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteins that regulate the coagulation cascade, including thrombin, are elevated in the brains of Alzheimer's disease (AD) patients. While studies using amyloid-based AD transgenic mouse models have implicated thrombin as a protein of interest, the role of thrombin in tau-based animal models has not been explored. The current study aims to determine how inhibiting thrombin could alter oxidative stress, inflammation, and AD-related proteins in a tau-based mouse model, the Tg4510. Aged Tg4510 mice were treated with the direct thrombin inhibitor dabigatran or vehicle for 7 days, brains collected, and western blot and data-independent proteomics using mass spectrometry with SWATH-MS acquisition performed to evaluate proteins related to oxidative stress, intracellular signaling, inflammation, and AD pathology. Dabigatran reduced iNOS, NOX4, and phosphorylation of tau (S396, S416). Additionally, dabigatran treatment increased expression of several signaling proteins related to cell survival and synaptic function. Increasing evidence supports a chronic procoagulant state in AD, highlighting a possible pathogenic role for thrombin. Our data demonstrate that inhibiting thrombin produces alterations in the expression of proteins involved in oxidative stress, inflammation, and AD-related pathology, suggesting that thrombin-mediated signaling affects multiple AD-related pathways providing a potential future therapeutic target.

Indexed as

Alzheimer's diseaseCell signalingOxidative stressThrombin

Identifiers

PMID33294639
PMCPMC7689047
OpenAlexW3098156269

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.