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https://www.readbyqxmd.com/read/29663649/trem2-inhibits-inflammatory-responses-in-mouse-microglia-by-suppressing-the-pi3k-nf-%C3%AE%C2%BAb-signaling
#1
Caixia Li, Bing Zhao, Caizhao Lin, Zhiping Gong, Xiaoxia An
This study aimed to investigate the effects of triggering receptor expressed on myeloid cell-2 (TREM2) on the production of pro-inflammatory mediators and cytokines induced by lipopolysaccharide (LPS) in BV2 microglia. TREM2 expression or TREM2-specific siRNA were used to induce TREM2 overexpression or silencing. The BV2 cells were pre-treated with the PI3K inhibitor of LY294002 for1 h and stimulated with LPS for 24 h. Then, the cell viability, apoptosis, phagocytosis, nitric oxide (NO), lactate dehydrogenase (LDH) and cytokine production, as well as the activation of AKT and NF-kB were determined, respectively...
April 16, 2018: Cell Biology International
https://www.readbyqxmd.com/read/29655369/trem2-regulates-innate-immunity-in-alzheimer-s-disease
#2
REVIEW
Jiang-Tao Li, Ying Zhang
Recent research has shown that the triggering receptor expressed on myeloid cells 2 (TREM2) in microglia is closely related to the pathogenesis of Alzheimer's disease (AD). The mechanism of this relationship, however, remains unclear. TREM2 is part of the TREM family of receptors, which are expressed primarily in myeloid cells, including monocytes, dendritic cells, and microglia. The TREM family members are cell surface glycoproteins with an immunoglobulin-like extracellular domain, a transmembrane region and a short cytoplasmic tail region...
April 14, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29623914/heterozygous-carriers-of-galactocerebrosidase-mutations-that-cause-krabbe-disease-have-impaired-microglial-function-and-defective-repair-of-myelin-damage
#3
REVIEW
Nicole J Scott-Hewitt, Christopher J Folts, Mark D Noble
This review addresses two puzzling findings related to mutations in galactocerebrosidase (GALC) that cause Krabbe disease (KD), a severe lysosomal storage disorder characterized by extensive myelin damage in children with mutations in both GALC alleles. First, heterozygous carriers of KD-causing mutations, which include the biological parents of children with KD, exhibit increased risk for developing other diseases. Second, variants in the GALC locus increase the risk of developing multiple sclerosis (MS), another disease characterized by extensive myelin damage...
March 2018: Neural Regeneration Research
https://www.readbyqxmd.com/read/29621548/trem2-modulates-microglia-phenotypes-in-the-neuroinflammation-of-parkinson-s-disease
#4
Youwen Zhang, Shujun Feng, Kun Nie, Yan Li, Yuyuan Gao, Rong Gan, Limin Wang, Bing Li, Xuegang Sun, Lijuan Wang, Yuhu Zhang
Neuroinflammation and overactivated microglia underlies the pathogenesis of Parkinson's disease (PD). Furthermore, microglia could polarize into classic inflammatory M1 and immunosuppressive M2 phenotype. Thus, inhibiting the overactivated inflammatory M1 microglia by promoting the transformation of microglia to the protective M2 phenotype provides potential therapy for PD, but the mechanism that modulates microglia polarization remains unknown. Triggering receptor expressed on myeloid cells-2 (TREM2) is a recently identified immune receptor expressed by the microglia in the brain...
April 2, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29611543/intracellular-trafficking-of-trem2-is-regulated-by-presenilin-1
#5
Yingjun Zhao, Xiaoguang Li, Timothy Huang, Lu-Lin Jiang, Zhenqiu Tan, Muxian Zhang, Irene Han-Juo Cheng, Xin Wang, Guojun Bu, Yun-Wu Zhang, Qi Wang, Huaxi Xu
Genetic mutations in triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to a variety of neurodegenerative diseases including Alzheimer's disease, amyotrophic lateral sclerosis, frontotemporal dementia and Parkinson's disease. In the brain, TREM2 is highly expressed on the cell surface of microglia, where it can transduce signals to regulate microglial functions such as phagocytosis. To date, mechanisms underlying intracellular trafficking of TREM2 remain elusive. Mutations in the presenilin 1 (PS1) catalytic subunit of the γ-secretase complex have been associated with increased generation of the amyloidogenic Aβ (amyloid-β) 42 peptide through cleavage of the Aβ precursor amyloid precursor protein...
December 1, 2017: Experimental & Molecular Medicine
https://www.readbyqxmd.com/read/29606617/functional-studies-of-missense-trem2-mutations-in-human-stem-cell-derived-microglia
#6
Philip W Brownjohn, James Smith, Ravi Solanki, Ebba Lohmann, Henry Houlden, John Hardy, Sabine Dietmann, Frederick J Livesey
The derivation of microglia from human stem cells provides systems for understanding microglial biology and enables functional studies of disease-causing mutations. We describe a robust method for the derivation of human microglia from stem cells, which are phenotypically and functionally comparable with primary microglia. We used stem cell-derived microglia to study the consequences of missense mutations in the microglial-expressed protein triggering receptor expressed on myeloid cells 2 (TREM2), which are causal for frontotemporal dementia-like syndrome and Nasu-Hakola disease...
April 10, 2018: Stem Cell Reports
https://www.readbyqxmd.com/read/29602048/lymphoblast-derived-integration-free-ipsc-line-ad-trem2-1-from-a-67year-old-alzheimer-s-disease-patient-expressing-the-trem2-p-r47h-variant
#7
Soraia Martins, Hatice Yigit, Martina Bohndorf, Nina Graffmann, Aurelian Robert Fiszl, Wasco Wruck, Kristel Sleegers, Christine Van Broeckhoven, James Adjaye
Human lymphoblast cells from a male diagnosed with Alzheimer's disease (AD) expressing the TREM2 p.R47H variant were used to generate integration-free induced pluripotent stem cells (iPSCs) by over-expressing episomal-based plasmids harbouring OCT4, SOX2, NANOG, LIN28, c-MYC and L-MYC. AD-TREM2-1 was defined as pluripotent based on (i) expression of pluripotency-associated markers (ii) embryoid body-based differentiation into cell types representative of the three germ layers and (iii) the similarity between the transcriptome of the iPSC line and the human embryonic stem cell line H1 with a Pearson correlation of 0...
March 20, 2018: Stem Cell Research
https://www.readbyqxmd.com/read/29601944/cellular-players-that-shape-evolving-pathology-and-neurodegeneration-following-traumatic-brain-injury
#8
REVIEW
Shweta S Puntambekar, Maha Saber, Bruce T Lamb, Olga N Kokiko-Cochran
Traumatic brain injury (TBI) is one of the leading causes of death and disability worldwide, and has emerged as a critical risk factor for multiple neurodegenerative diseases, particularly Alzheimer's disease (AD). How the inflammatory cascade resulting from mechanical stress, axonal shearing and the loss of neurons and glia following initial impact in TBI, contributes to the development of AD-like disease is unclear. Neuroinflammation, characterized by blood-brain barrier (BBB) dysfunction and activation of brain-resident microglia and astrocytes, resulting in secretion of inflammatory mediators and subsequent recruitment of peripheral immune cells has been the focus of extensive research in attempts to identify drug-targets towards improving functional outcomes post TBI...
March 27, 2018: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/29599291/trem2-activating-antibodies-abrogate-the-negative-pleiotropic-effects-of-the-alzheimer-s-disease-variant-trem2-r47h-on-murine-myeloid-cell-function
#9
Qingwen Cheng, Jean Danao, Santosh Talreja, Paul Wen, Jun Yin, Ning Sun, Chi-Ming Li, Danny Chui, David Tran, Samir Koirala, Hang Chen, Ian N Foltz, Songli Wang, Shilpa Sambashivan
Triggering receptor expressed on myeloid cells 2 (TREM2) is an orphan immune receptor expressed on cells of myeloid lineage such as macrophages and microglia. The rare-variant R47H TREM2 is associated with an increased risk for Alzheimer's disease (AD), supporting the hypothesis that TREM2 loss of function may exacerbate disease progression. However, a complete knockout of the TREM2 gene in different genetic models of neurodegenerative diseases has been reported to result in both protective and deleterious effects on disease-related endpoints and myeloid cell function...
March 29, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29598827/integrated-biology-approach-reveals-molecular-and-pathological-interactions-among-alzheimer-s-a%C3%AE-42-tau-trem2-and-tyrobp-in-drosophila-models
#10
Michiko Sekiya, Minghui Wang, Naoki Fujisaki, Yasufumi Sakakibara, Xiuming Quan, Michelle E Ehrlich, Philip L De Jager, David A Bennett, Eric E Schadt, Sam Gandy, Kanae Ando, Bin Zhang, Koichi M Iijima
BACKGROUND: Cerebral amyloidosis, neuroinflammation, and tauopathy are key features of Alzheimer's disease (AD), but interactions among these features remain poorly understood. Our previous multiscale molecular network models of AD revealed TYROBP as a key driver of an immune- and microglia-specific network that was robustly associated with AD pathophysiology. Recent genetic studies of AD further identified pathogenic mutations in both TREM2 and TYROBP. METHODS: In this study, we systematically examined molecular and pathological interactions among Aβ, tau, TREM2, and TYROBP by integrating signatures from transgenic Drosophila models of AD and transcriptome-wide gene co-expression networks from two human AD cohorts...
March 29, 2018: Genome Medicine
https://www.readbyqxmd.com/read/29587871/amyloid-beta-modulates-microglial-responses-by-binding-to-the-triggering-receptor-expressed-on-myeloid-cells-2-trem2
#11
Li Zhong, Zongqi Wang, Daxin Wang, Zhe Wang, Yuka A Martens, Linbei Wu, Ying Xu, Kai Wang, Jianguo Li, Ruizhi Huang, Dan Can, Huaxi Xu, Guojun Bu, Xiao-Fen Chen
BACKGROUND: TREM2 is an innate immune receptor specifically expressed in microglia. Coding variations in TREM2 have been reported to increase the risk for Alzheimer's disease (AD) and other neurodegenerative diseases. While multiple studies support a role for TREM2 in microglial recruitment to amyloid plaques, the chemoattractant factor modulating TREM2-dependent microglial responses has not been defined. METHODS: Potential binding of oligomeric amyloid-β 1-42 (oAβ1-42 ) to TREM2 was tested by complementary approaches including solid phase binding, surface plasmon resonance and immunoprecipitation assays...
March 27, 2018: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29578490/frontotemporal-dementia-and-chorea-associated-with-a-compound-heterozygous-trem2-mutation
#12
Veronica Redaelli, Ettore Salsano, Lara Colleoni, Paola Corbetta, Giovanni Tringali, Angelo Del Sole, Giorgio Giaccone, Giacomina Rossi
Frontotemporal dementia (FTD) is clinically characterized by behavioral changes, language impairment, and executive dysfunction. FTD usually belongs to the frontotemporal lobar degeneration (FTLD) disease group, and its familial forms are dominantly inherited and linked to a group of genes relevant to frontal and temporal brain pathology, such as MAPT, GRN, C9ORF72, TARDBP, CHMP2B, VCP, and FUS. However, FTD can also be associated with different clinical or pathological phenotypes caused by mutations in other genes, whose heredity can be dominant or recessive...
March 23, 2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29575797/airway-cells-from-protracted-bacterial-bronchitis-and-bronchiectasis-share-similar-gene-expression-profiles
#13
Alice C-H Chen, Olga M Pena, Hendrik J Nel, Stephanie T Yerkovich, Anne B Chang, Katherine J Baines, Peter G Gibson, Helen L Petsky, Susan J Pizzutto, Sandra Hodge, Ian B Masters, Helen L Buntain, John W Upham
AIM: Protracted bacterial bronchitis (PBB) is a common cause of prolonged cough in young children, and may be a precursor of bronchiectasis. Bacteria are often present in the lower airways in both PBB and bronchiectasis and may cause persistent infections. However, there is a paucity of information available on the pathogenesis of PBB and the factors associated with persistent bacterial infection and progression to bronchiectasis. This study hypothesised that lung immune cells in recurrent PBB and bronchiectasis differentially express genes related to immune cell dysfunction compared to lung immune cells from control subjects...
March 24, 2018: Pediatric Pulmonology
https://www.readbyqxmd.com/read/29557178/trem2-variants-in-neurodegenerative-disorders-in-the-polish-population-homozygosity-and-compound-heterozygosity-in-ftd-patients
#14
Beata Peplonska, Mariusz Berdynski, Monika Mandecka, Anna Barczak, Magdalena Kuzma-Kozakiewicz, Maria Barcikowska, Cezary Zekanowski
Activation of the TREM2 receptor on microglia stimulates phagocytosis and decreases the microglial proinflammatory response. Mutations in exon 2 of the TREM2 gene have been reported to be associated with various neurodegenerative diseases characterized by chronic inflammation. The aim of our study was to evaluate exon 2 of TREM2 gene variants as a putative genetic risk factor for Alzheimer's disease (AD), frontotemporal dementia (FTD), and amyotrophic lateral sclerosis (ALS) in the Polish population. The results were interpreted using previously published data, especially highlighting differences in the prevalence of the variants among Caucasian subpopulations across different geographic regions...
March 20, 2018: Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration
https://www.readbyqxmd.com/read/29552443/alzheimer-s-disease-pathology-in-nasu-hakola-disease-brains
#15
Jun-Ichi Satoh, Yoshihiro Kino, Motoaki Yanaizu, Yuko Saito
Nasu-Hakola disease (NHD) is a rare autosomal recessive disorder, characterized by progressive presenile dementia and formation of multifocal bone cysts, caused by genetic mutations of either triggering receptor expressed on myeloid cells 2 ( TREM2 ) or TYRO protein tyrosine kinase binding protein ( TYROBP ), alternatively named DNAX-activation protein 12 ( DAP12 ), both of which are expressed on microglia in the brain and form the receptor-adaptor complex that chiefly recognizes anionic lipids. TREM2 transmits the signals involved in microglial survival, proliferation, chemotaxis, and phagocytosis...
February 2018: Intractable & Rare Diseases Research
https://www.readbyqxmd.com/read/29552013/differential-phagocytic-properties-of-cd45-low-microglia-and-cd45-high-brain-mononuclear-phagocytes-activation-and-age-related-effects
#16
Srikant Rangaraju, Syed Ali Raza, Noel Xiang'An Li, Ranjita Betarbet, Eric B Dammer, Duc Duong, James J Lah, Nicholas T Seyfried, Allan I Levey
In the central nervous system (CNS), microglia are innate immune mononuclear phagocytes (CNS MPs) that can phagocytose infectious particles, apoptotic cells, neurons, and pathological protein aggregates, such as Aβ in Alzheimer's disease (AD). While CD11b+ CD45low microglia account for the majority of CNS MPs, a small population of CD11b+ CD45high CNS MPs is also recognized in AD that surround Aβ plaques. These transcriptionally and pathologically unique CD45high cells have unclear origin and undefined phagocytic characteristics...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29545365/single-cell-rna-seq-reveals-the-transcriptional-landscape-and-heterogeneity-of-aortic-macrophages-in-murine-atherosclerosis
#17
Clément Cochain, Ehsan Vafadarnejad, Panagiota Arampatzi, Pelisek Jaroslav, Holger Winkels, Klaus Ley, Dennis Wolf, Antoine-Emmanuel Saliba, Alma Zernecke
<u>Rationale:</u> It is assumed that atherosclerotic arteries contain several macrophage subsets endowed with specific functions. The precise identity of these subsets is poorly characterized as they ha ve been defined by the expression of a restricted number of markers. <u>Objective:</u> We have applied single-cell RNA-seq as an unbiased profiling strategy to interrogate and classify aortic macrophage heterogeneity at the single-cell level in atherosclerosis. <u>Methods and Results:</u> We performed single-cell RNA sequencing of total aortic CD45+ cells extracted from the non-diseased (chow fed) and atherosclerotic (11 weeks of high fat diet) aorta of Ldlr-/- mice...
March 15, 2018: Circulation Research
https://www.readbyqxmd.com/read/29523800/cerebrospinal-fluid-neurogranin-and-trem2-in-huntington-s-disease
#18
Lauren M Byrne, Filipe B Rodrigues, Eileanoir B Johnson, Enrico De Vita, Kaj Blennow, Rachael Scahill, Henrik Zetterberg, Amanda Heslegrave, Edward J Wild
Biomarkers of Huntington's disease (HD) in cerebrospinal fluid (CSF) could be of value in elucidating the biology of this genetic neurodegenerative disease, as well as in the development of novel therapeutics. Deranged synaptic and immune function have been reported in HD, and concentrations of the synaptic protein neurogranin and the microglial protein TREM2 are increased in other neurodegenerative diseases. We therefore used ELISAs to quantify neurogranin and TREM2 in CSF samples from HD mutation carriers and controls...
March 9, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29518360/trem2-and-amyloid-beta-a-love-hate-relationship
#19
Joe Udeochu, Faten A Sayed, Li Gan
Mutations in TREM2 increase risk for late-onset AD. In this issue of Neuron, Zhao et al. (2018) show that TREM2 binds Aβ to enhance its clearance and Lee et al. (2018) demonstrate that human TREM2 expression in AD mice ameliorates Aβ-associated deficits.
March 7, 2018: Neuron
https://www.readbyqxmd.com/read/29518357/elevated-trem2-gene-dosage-reprograms-microglia-responsivity-and-ameliorates-pathological-phenotypes-in-alzheimer-s-disease-models
#20
C Y Daniel Lee, Anthony Daggett, Xiaofeng Gu, Lu-Lin Jiang, Peter Langfelder, Xiaoguang Li, Nan Wang, Yingjun Zhao, Chang Sin Park, Yonatan Cooper, Isabella Ferando, Istvan Mody, Giovanni Coppola, Huaxi Xu, X William Yang
Variants of TREM2 are associated with Alzheimer's disease (AD). To study whether increasing TREM2 gene dosage could modify the disease pathogenesis, we developed BAC transgenic mice expressing human TREM2 (BAC-TREM2) in microglia. We found that elevated TREM2 expression reduced amyloid burden in the 5xFAD mouse model. Transcriptomic profiling demonstrated that increasing TREM2 levels conferred a rescuing effect, which includes dampening the expression of multiple disease-associated microglial genes and augmenting downregulated neuronal genes...
March 7, 2018: Neuron
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