Evidence map›Paper›PMID 30555470›Full record

ArticleFrontiers in immunology2018

Tuftsin Combines With Remyelinating Therapy and Improves Outcomes in Models of CNS Demyelinating Disease.

Kaitlyn K Thompson, Jillian C Nissen, Amanda Pretory, Stella E Tsirka

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022
    Review
  7. Tuftsin: A Natural Molecule Against SARS-CoV-2 Infection.Frontiers in molecular biosciences · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
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

4 authors at 2 institutions in 1 country.

Kaitlyn K ThompsonProgram in Molecular and Cellular Pharmacology, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States.
Jillian C NissenProgram in Molecular and Cellular Pharmacology, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States.
Amanda PretoryProgram in Molecular and Cellular Pharmacology, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States.
Stella E TsirkaProgram in Molecular and Cellular Pharmacology, Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States.
Stony Brook University · USSUNY Old Westbury · US

Funding

IRACDA - The New York Consortium for the Advancement of Postdoctoral Scholars (NY CAPS)Phase IIK12GM102778 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI Carol A. Carter, Karian Janice Wright · 2012 to 2026
$13.1M
Training Program in Pharmacological SciencesT32GM007518 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI GARCIA-DIAZ, MIGUEL · 1985 to 2021
$5.4M
NIGMS NIH HHS K12 GM102778NIGMS NIH HHS T32 GM007518
6 · The paper itself

Abstract

Though promoting remyelination in multiple sclerosis (MS) has emerged as a promising therapeutic strategy, it does not address inflammatory signals that continue to induce neuronal damage and inhibit effectiveness of repair mechanisms. Our lab has previously characterized the immunomodulatory tetrapeptide, tuftsin, which induces an anti-inflammatory shift in microglia and macrophages. This targeted anti-inflammatory agent improves physical deficits in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Here, we sought to determine whether tuftsin is also effective in combination with benztropine, an FDA-approved drug that stimulates remyelination, in both EAE and in the cuprizone model of demyelination. We show that combining these two agents to promote anti-inflammatory and remyelinating mechanisms alleviates symptoms in EAE and lessens pathological hallmarks in both MS models. Importantly, tuftsin is required to transform the inflammatory CNS environment normally present in EAE/MS into one of an anti-inflammatory nature, and benztropine is required in the cuprizone model to improve remyelination. Our data further support tuftsin's beneficial immunomodulatory activity in the context of EAE, and show that when studying remyelination in the absence of an autoimmune insult, tuftsin still activated microglia toward an anti-inflammatory fate, but benztropine was necessary for significant repair of the damaged myelin. Overall, tuftsin effectively combined with benztropine to significantly improve MS-like pathologies in both models.

Indexed as

AnimalsBenztropineCuprizoneDisease Models, AnimalDrug Therapy, CombinationEncephalomyelitis, Autoimmune, ExperimentalMiceMultiple SclerosisMyelin SheathTuftsinBenztropineCuprizoneTuftsinanti-inflammatoryautoimmunitycombinationmicrogliaremyelinationtherapytuftsin

Identifiers

PMID30555470
PMCPMC6283261
OpenAlexW2903446135

What OpenQuestion holds

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LicenceCC BY
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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.