Evidence map›Paper›PMID 29803827›Full record

ArticleExperimental neurology2018

Csf1R inhibition attenuates experimental autoimmune encephalomyelitis and promotes recovery.

Jillian C Nissen, Kaitlyn K Thompson, Brian L West, Stella E Tsirka

Abstract read
In one paragraph

Article in Experimental neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

105 citing papers in PubMed, 189 citations in OpenAlex.

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45 more citing papers are in PubMed but not listed here.

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.

Jillian C NissenPrograme in Molecular and Cellular Pharmacology, Department of Pharmacological Sciences, Stony Brook University, NY 11794-8651, United States; Department of Biological Sciences, State University of New York, College at Old Westbury, Old Westbury, NY 11568, United States.
Kaitlyn K ThompsonPrograme in Molecular and Cellular Pharmacology, Department of Pharmacological Sciences, Stony Brook University, NY 11794-8651, United States.
Brian L WestPlexxikon Inc, Berkeley, CA 94710, United States.
Stella E TsirkaPrograme in Molecular and Cellular Pharmacology, Department of Pharmacological Sciences, Stony Brook University, NY 11794-8651, United States. Electronic address: Styliani-anna.tsirka@stonybrook.edu.
Stony Brook University · USPlexxikon (United States)

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
Microglial effector pathways in the CNSR01NS042168 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI TSIRKA, STYLIANI-ANNA (STELLA) E · 2003 to 2011
$3.1M
NIGMS NIH HHS K12 GM102778NIGMS NIH HHS T32 GM007518NINDS NIH HHS R01 NS042168
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterized by progressive neuronal demyelination and degeneration. Much of this damage can be attributed to microglia, the resident innate immune cells of the CNS, as well as monocyte-derived macrophages, which breach the blood-brain barrier in this inflammatory state. Upon activation, both microglia and macrophages release a variety of factors that greatly contribute to disease progression, and thus therapeutic approaches in MS focus on diminishing their activity. We use the CSF1R inhibitor PLX5622, administered in mouse chow, to ablate microglia and macrophages during the course of experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Here, we show that ablation of these cells significantly improves animal mobility and weight gain in EAE. Further, we show that this treatment addresses the pathological hallmarks of MS, as it reduces demyelination and immune activation. White matter lesion areas in microglia/macrophage-depleted animals show substantial preservation of mature, myelinating oligodendrocytes in comparison to control animals. Taken together, these findings suggest that ablation of microglia/macrophages during the symptomatic phase of EAE reduces CNS inflammation and may also promote a more permissive environment for remyelination and recovery. This microglia and macrophage-targeted therapy could be a promising avenue for treatment of MS.

Indexed as

Administration, OralAmino Acid SequenceAnimalsEncephalomyelitis, Autoimmune, ExperimentalFemaleMiceMice, Inbred C57BLMicrogliaProtein Kinase InhibitorsReceptors, Granulocyte-Macrophage Colony-Stimulating FactorRecovery of FunctionCsf1r protein, mouseProtein Kinase InhibitorsReceptors, Granulocyte-Macrophage Colony-Stimulating FactorDemyelinationDepletionEAEMicrogliaOligodendrocytesTherapy

Identifiers

PMID29803827
PMCPMC6380683
OpenAlexW2804436811

What OpenQuestion holds

Textmetadata
LicenceTDM
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.