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Microglia and aging: the role of the TREM2-DAP12 and CX3CL1-CX3CR1 axes

Mecca, Carmen, Giambanco, Ileana, Donato, Rosario, Arcuri, Cataldo·2018·International Journal of Molecular Sciences
DOI 10.3390/ijms19010318PMC PMC5796261
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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.

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Metadata

Authors
Mecca, C., Giambanco, I., Donato, R., & Arcuri, C.
Affiliations
Department of Experimental Medicine, Perugia Medical School, University of Perugia, Piazza Lucio Severi 1, 06132 Perugia, Italy
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2018-01-22
Volume
19
Issue
1
Pages
318
ISSN
1422-0067
DOI
10.3390/ijms19010318
PMC
PMC5796261
Cited by
258
References
55
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • Ministero dell’Istruzione, dell’Università e della Ricerca, Italy (SIR RBSI144EUA)
  • Fondazione Cassa di Risparmio di Perugia (2014.0254.021)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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