Evidence map›Paper›PMID 29361745›Full record

ReviewInternational journal of molecular sciences2018

Microglia and Aging: The Role of the TREM2-DAP12 and CX3CL1-CX3CR1 Axes.

Carmen Mecca, Ileana Giambanco, Rosario Donato, Cataldo Arcuri

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

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed, 3 pooled it
11.4field-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

154 citing papers in PubMed, 3 syntheses or guidelines pooled it, 254 citations in OpenAlex.

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94 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 1 institution in 1 country.

Carmen MeccaDepartment of Experimental Medicine, Perugia Medical School, University of Perugia, Piazza Lucio Severi 1, 06132 Perugia, Italy. carmen.mecca@unipg.it.
Ileana GiambancoDepartment of Experimental Medicine, Perugia Medical School, University of Perugia, Piazza Lucio Severi 1, 06132 Perugia, Italy. ileana.giambanco@unipg.it.
Rosario DonatoDepartment of Experimental Medicine, Perugia Medical School, University of Perugia, Piazza Lucio Severi 1, 06132 Perugia, Italy. rosario.donato@unipg.it.
Cataldo ArcuriDepartment of Experimental Medicine, Perugia Medical School, University of Perugia, Piazza Lucio Severi 1, 06132 Perugia, Italy. cataldo.arcuri@unipg.it.
University of Perugia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Depending on the species, microglial cells represent 5-20% of glial cells in the adult brain. As the innate immune effector of the brain, microglia are involved in several functions: regulation of inflammation, synaptic connectivity, programmed cell death, wiring and circuitry formation, phagocytosis of cell debris, and synaptic pruning and sculpting of postnatal neural circuits. Moreover, microglia contribute to some neurodevelopmental disorders such as Nasu-Hakola disease (NHD), and to aged-associated neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), and others. There is evidence that human and rodent microglia may become senescent. This event determines alterations in the microglia activation status, associated with a chronic inflammation phenotype and with the loss of neuroprotective functions that lead to a greater susceptibility to the neurodegenerative diseases of aging. In the central nervous system (CNS), Triggering Receptor Expressed on Myeloid Cells 2-DNAX activation protein 12 (TREM2-DAP12) is a signaling complex expressed exclusively in microglia. As a microglial surface receptor, TREM2 interacts with DAP12 to initiate signal transduction pathways that promote microglial cell activation, phagocytosis, and microglial cell survival. Defective TREM2-DAP12 functions play a central role in the pathogenesis of several diseases. The CX3CL1 (fractalkine)-CX3CR1 signaling represents the most important communication channel between neurons and microglia. The expression of CX3CL1 in neurons and of its receptor CX3CR1 in microglia determines a specific interaction, playing fundamental roles in the regulation of the maturation and function of these cells. Here, we review the role of the TREM2-DAP12 and CX3CL1-CX3CR1 axes in aged microglia and the involvement of these pathways in physiological CNS aging and in age-associated neurodegenerative diseases.

Indexed as

Adaptor Proteins, Signal TransducingAgingAnimalsBrainCentral Nervous SystemChemokine CX3CL1CX3C Chemokine Receptor 1Gene Expression RegulationHumansMembrane GlycoproteinsMembrane ProteinsMicrogliaNeurodegenerative DiseasesReceptors, ImmunologicSignal TransductionAdaptor Proteins, Signal TransducingChemokine CX3CL1CX3C Chemokine Receptor 1Membrane GlycoproteinsMembrane ProteinsReceptors, ImmunologicTREM2 protein, humanTYROBP protein, humanaged microgliaagingCX3CL1CX3CR1DAP12TREM2

Identifiers

PMID29361745
PMCPMC5796261
OpenAlexW2785783433

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.