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Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: TREM2 dependent and independent functions of microglia in Alzheimer’s disease

Fig. 1

Microglial features in steady-state. In steady-state, microglia are maintained via paracrine colony-stimulating factor-1 receptor (CSF1R) signaling and via autocrine transforming growth factor-β (TGFβ) signaling. The two pathways endow a unique homeostatic feature of microglia, characterized by high expression levels of P2ry12, Cx3cr1, Tmem119, MerTK, Itgam and others. Microglia lineage-determining transcription factors PU.1, myocyte enhancer factor 2A (Mef2a), mothers against decapentaplegic homolog 3 (Smad3), transcription factors MafB (MafB), interferon regulatory factor 8 (Irf8), and spalt-like transcription factor 1 (Sall1) control microglia homeostasis. The features of homeostatic microglia make them well suited to the physiological functions, including neuronal trophic support via BDNF release, myelination via IGF-1 secretion, and synaptic pruning. Microglia remove excess synapses from postnatal or adult-born neuron via diverse ligand-receptor pathways including C3-CR3, PS-TREM2, Gas-MerTK, CX3CL1-CX3CR1, ADP-P2RY12, et al. OLs, oligodendrocytes; OPC, oligodendrocyte progenitor cell; IGF-1, insulin-like growth factor 1; BDNF, brain derived neurotrophic factor; CR3, complement receptor 3; TREM2, triggering receptor expressed on myeloid cells 2; MerTK, Mer tyrosine kinase; P2RY12, purinergic receptor P2Y; CX3CR1, C-X3-C motif chemokine receptor 1; C1q, complement component 1q; PS, phosphatidylserine; Gas6, growth arrest-specific 6; ADP, adenosine diphosphate; CX3CL1, C-X3-C motif chemokine ligand 1; TGFBR1/2, TGF-β receptor 1/2

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