While there is a strong evidence for neural tissue destruction mediated by adaptive autoimmune responses, it is still debated how innate immune responses contribute to neuroinflammatory and neurodegenerative diseases such as multiple sclerosis and Alzheimer's disease. Recently, it was shown that loss-of-function mutations of the innate microglial immune receptor triggering receptor expressed on myeloid cells-2 (TREM2) led to a chronic neurodegenerative disease, named Nasu-Hakola disease or polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL). PLOSL is a recessively inherited disease characterized by early onset adult dementia associated with bone cysts. Since microglial cells are the major TREM2-producing cell type in the central nervous system (CNS), they appear to be plausible candidates for the neurodegenerative pathogenesis of PLOSL. Indeed, TREM2 of microglia fulfils important function of tissue debris clearance and resolution of latent inflammatory reactions. Absence of TREM2 expression on microglia impairs their capacity to phagocytose cell membrane debris and increases their gene transcription of pro-inflammatory cytokines. The disease PLOSL and the finding that TREM2 of microglia is requ...Continue Reading
Developmental regulation of TREM2 and DAP12 expression in the murine CNS: implications for Nasu-Hakola disease
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Expression of the phagocytosis-essential protein TREM2 is down-regulated by an aluminum-induced miRNA-34a in a murine microglial cell line
Triggering Receptor Expressed on Myeloid Cells-2 Correlates to Hypothermic Neuroprotection in Ischemic Stroke
Attenuation of MCP-1/CCL2 expression ameliorates neuropathy in a mouse model for Charcot-Marie-Tooth 1X
Attenuated inflammatory response in triggering receptor expressed on myeloid cells 2 (TREM2) knock-out mice following stroke
Analysis of the host transcriptome from demyelinating spinal cord of murine coronavirus-infected mice
Upregulation of TREM2 ameliorates neuropathology and rescues spatial cognitive impairment in a transgenic mouse model of Alzheimer's disease
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TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer's disease mouse models
RNA sequencing of microglia and monocyte-derived macrophages from mice with experimental autoimmune encephalomyelitis illustrates a changing phenotype with disease course
Minocycline Transiently Reduces Microglia/Macrophage Activation but Exacerbates Cognitive Deficits Following Repetitive Traumatic Brain Injury in the Neonatal Rat
Polycystic Lipomembranous Osteodysplasia with Sclerosing Leukoencephalopathy (PLOSL): a new report of an Italian woman and review of the literature
TREM2 Overexpression has No Improvement on Neuropathology and Cognitive Impairment in Aging APPswe/PS1dE9 Mice
Inflammation in Alzheimer's disease: amyloid-beta oligomers trigger innate immunity defence via pattern recognition receptors
Opposing roles of the triggering receptor expressed on myeloid cells 2 and triggering receptor expressed on myeloid cells-like transcript 2 in microglia activation
Immunomodulation by transplanted human embryonic stem cell-derived oligodendroglial progenitors in experimental autoimmune encephalomyelitis
Overexpression of the immunoreceptor CD300f has a neuroprotective role in a model of acute brain injury
DJ-1 deficiency triggers microglia sensitivity to dopamine toward a pro-inflammatory phenotype that is attenuated by rasagiline
TREM2 Protein Expression Changes Correlate with Alzheimer's Disease Neurodegenerative Pathologies in Post-Mortem Temporal Cortices
Transient activation of microglia following acute alcohol exposure in developing mouse neocortex is primarily driven by BAX-dependent neurodegeneration
What happens to microglial TREM2 in Alzheimer's disease: Immunoregulatory turned into immunopathogenic?
CD300f immunoreceptor contributes to peripheral nerve regeneration by the modulation of macrophage inflammatory phenotype
Characterisation of microglia during de- and remyelination: can they create a repair promoting environment?
Microglia: a new frontier for synaptic plasticity, learning and memory, and neurodegenerative disease research
Transcriptomics and mechanistic elucidation of Alzheimer's disease risk genes in the brain and in vitro models
Selective capacity of metreleptin administration to reconstitute CD4+ T-cell number in females with acquired hypoleptinemia
Regulating amyloidogenesis through the natural triggering receptor expressed in myeloid/microglial cells 2 (TREM2)
Proteomic analysis of lymphoblastoid cells from Nasu-Hakola patients: a step forward in our understanding of this neurodegenerative disorder
A novel ligand-independent peptide inhibitor of TREM-1 suppresses tumor growth in human lung cancer xenografts and prolongs survival of mice with lipopolysaccharide-induced septic shock
TREM-2 promotes acquired cholesteatoma-induced bone destruction by modulating TLR4 signaling pathway and osteoclasts activation
Opposing Functions of Microglial and Macrophagic TNFR2 in the Pathogenesis of Experimental Autoimmune Encephalomyelitis
Heterozygote galactocerebrosidase (GALC) mutants have reduced remyelination and impaired myelin debris clearance following demyelinating injury
Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease.
Increased expression of TREM2 in peripheral cells from mild cognitive impairment patients who progress into Alzheimer's disease
DNAX Activating Protein of 12 kDa/Triggering Receptor Expressed on Myeloid Cells 2 Expression by Mouse and Human Liver Dendritic Cells: Functional Implications and Regulation of Liver Ischemia-Reperfusion Injury
Validation of Flow Cytometry and Magnetic Bead-Based Methods to Enrich CNS Single Cell Suspensions for Quiescent Microglia
Microglia roles in synaptic plasticity and myelination in homeostatic conditions and neurodevelopmental disorders
Migration and Phagocytic Ability of Activated Microglia During Post-natal Development is Mediated by Calcium-Dependent Purinergic Signalling
The Triggering Receptor Expressed on Myeloid Cells 2: A Molecular Link of Neuroinflammation and Neurodegenerative Diseases.
Adult onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) and Nasu-Hakola disease: lesion staging and dynamic changes of axons and microglial subsets
The putative role of environmental aluminium in the development of chronic neuropathology in adults and children. How strong is the evidence and what could be the mechanisms involved?
Heterozygous carriers of galactocerebrosidase mutations that cause Krabbe disease have impaired microglial function and defective repair of myelin damage
Lipid transporter Spns2 promotes microglia pro-inflammatory activation in response to amyloid-beta peptide
Triggering receptor expressed on myeloid cells-2 expression in the brain is required for maximal phagocytic activity and improved neurological outcomes following experimental stroke
Differential effects of partial and complete loss of TREM2 on microglial injury response and tauopathy
TREM2 Regulates Heat Acclimation-Induced Microglial M2 Polarization Involving the PI3K-Akt Pathway Following EMF Exposure
GABAA R α2-activated neuroimmune signal controls binge drinking and impulsivity through regulation of the CCL2/CX3CL1 balance
Ocular hypertension suppresses homeostatic gene expression in optic nerve head microglia of DBA/2 J mice.
Amyloid-beta (1-42) lesion of CA1 rat dorsal hippocampus reduces contextual fear memory and increases expression of microglial genes regulating neuroinflammation.
The P2X7 Receptor in Microglial Cells Modulates the Endolysosomal Axis, Autophagy, and Phagocytosis.
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