Evidence map›Paper›PMID 30995509›Full record

ReviewImmunity2019

Immune Signaling in Neurodegeneration.

Timothy R Hammond, Samuel E Marsh, Beth Stevens

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
218citing papers in PubMed, 6 pooled it
18.0field-weighted citation impact, top 1% 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

218 citing papers in PubMed, 6 syntheses or guidelines pooled it, 330 citations in OpenAlex.

  1. The Role of Hydrogen Sulfide (HInternational journal of molecular sciences · 2023
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158 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

3 authors at 2 institutions in 1 country.

Timothy R HammondBoston Children's Hospital, F.M. Kirby Neurobiology Center, Boston, MA, USA; Harvard Medical School, Boston, MA, USA; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Samuel E MarshBoston Children's Hospital, F.M. Kirby Neurobiology Center, Boston, MA, USA; Harvard Medical School, Boston, MA, USA; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Beth StevensBoston Children's Hospital, F.M. Kirby Neurobiology Center, Boston, MA, USA; Harvard Medical School, Boston, MA, USA; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA, USA; Howard Hughes Medical Institute, Boston Children's Hospital, Boston, MA, USA. Electronic address: beth.stevens@childrens.harvard.edu.
Broad Institute · USBoston Children's Hospital · US

Funding

Regulation of Synaptic engulfment by human C4P50MH112491 · NIMH · BOSTON CHILDREN'S HOSPITAL · PI Michael Craig Carroll, Beth Ann Stevens · 2017 to 2026
$29.5M
Mouse Neurodevelopmental Behavior CoreU54HD090255 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI KUNKEL, LOUIS M · 2016 to 2020
$5.2M
Investigating the Role of Complement-expressing Myeloid Cells in Synapse Loss and Vascular Compromise in Alzheimers DiseaseRF1AG051496 · NIA · JACKSON LABORATORY · PI HOWELL, GARETH R, STEVENS, BETH ANN · 2015 to 2018
$3.7M
Howard Hughes Medical InstituteNIA NIH HHS RF1 AG051496NICHD NIH HHS U54 HD090255
6 · The paper itself

Abstract

Neurodegenerative diseases of the central nervous system progressively rob patients of their memory, motor function, and ability to perform daily tasks. Advances in genetics and animal models are beginning to unearth an unexpected role of the immune system in disease onset and pathogenesis; however, the role of cytokines, growth factors, and other immune signaling pathways in disease pathogenesis is still being examined. Here we review recent genetic risk and genome-wide association studies and emerging mechanisms for three key immune pathways implicated in disease, the growth factor TGF-β, the complement cascade, and the extracellular receptor TREM2. These immune signaling pathways are important under both healthy and neurodegenerative conditions, and recent work has highlighted new functional aspects of their signaling. Finally, we assess future directions for immune-related research in neurodegeneration and potential avenues for immune-related therapies.

Indexed as

AgingAnimalsComplement ActivationDisease ProgressionGenetic Predisposition to DiseaseGenome-Wide Association StudyGliosisHumansImmunity, InnateInflammationMembrane GlycoproteinsMiceMice, KnockoutMice, TransgenicMicrogliaModels, ImmunologicalMembrane GlycoproteinsReceptors, ImmunologicTransforming Growth Factor betaTREM2 protein, humanAlzheimer’s diseaseComplementCytokineGWASInflammationInnate ImmunityMicrogliaNeurodegenerationNeuro-immuneNeuroinflammationSignalingTGF-βTREM2

Identifiers

PMID30995509
PMCPMC6822103
OpenAlexW2938743978

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.