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https://www.readbyqxmd.com/read/29448957/brain-region-specific-enhancement-of-remyelination-and-prevention-of-demyelination-by-the-csf1r-kinase-inhibitor-blz945
#1
Nicolau Beckmann, Elisa Giorgetti, Anna Neuhaus, Stefan Zurbruegg, Nathalie Accart, Paul Smith, Julien Perdoux, Ludovic Perrot, Mark Nash, Sandrine Desrayaud, Peter Wipfli, Wilfried Frieauff, Derya R Shimshek
Multiple sclerosis (MS) is a chronic inflammatory disease affecting the central nervous system (CNS). While multiple effective immunomodulatory therapies for MS exist today, they lack the scope of promoting CNS repair, in particular remyelination. Microglia play a pivotal role in regulating myelination processes, and the colony-stimulating factor 1 (CSF-1) pathway is a key regulator for microglia differentiation and survival. Here, we investigated the effects of the CSF-1 receptor kinase inhibitor, BLZ945, on central myelination processes in the 5-week murine cuprizone model by non-invasive and longitudinal magnetic resonance imaging (MRI) and histology...
February 15, 2018: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/29443116/liver-a-protective-role-for-trem2-in-liver-injury
#2
Katrina Ray
No abstract text is available yet for this article.
February 14, 2018: Nature Reviews. Gastroenterology & Hepatology
https://www.readbyqxmd.com/read/29411406/apoe-%C3%AE%C2%B54-is-also-required-in-trem2-r47h-variant-carriers-for-alzheimer-s-disease-to-develop
#3
Christina E Murray, Andrew King, Claire Troakes, Angela Hodges, Tammaryn Lashley
In late-onset Alzheimer's disease (AD), the ε4 allele of the apolipoprotein E gene (APOE) is the major known genetic risk factor [1]. In 2013 two research groups reported the R47H variant of triggering receptor expressed on myeloid cells 2 (TREM2), is associated with AD by almost as much as APOE ε4 [2,3]. A loss-of-function R47H mutation in TREM2 is also one of the strongest single allele genetic risk factors for AD [2,3], providing a link between microglia dysfunction and AD pathogenesis. TREM2 encodes a single-pass type I membrane protein that forms a receptor-signaling complex with the TYRO protein tyrosine kinase-binding protein (TYROBP) triggering immune responses in certain macrophages and dendritic cells...
February 7, 2018: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/29407460/trem2-overexpression-attenuates-neuroinflammation-and-protects-dopaminergic-neurons-in-experimental-models-of-parkinson-s-disease
#4
Manru Ren, Ying Guo, Xinbing Wei, Shaoqi Yan, Yue Qin, Xiumei Zhang, Fan Jiang, Haiyan Lou
Triggering receptor expressed on myeloid cells-2 (TREM2) was a newly identified receptor expressed on microglia. Several observations support the hypothesis that TREM2 variation may confer susceptibility to Parkinson's disease (PD). Therefore, in this paper, we explored the role of TREM2 in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. Our results revealed that overexpression of TREM2 remarkably reduced MPTP-induced neuropathology including the dopaminergic neurodegeneration and neuroinflammation in vivo...
January 27, 2018: Experimental Neurology
https://www.readbyqxmd.com/read/29395285/the-effect-of-rare-variants-in-trem2-and-pld3-on-longitudinal-cognitive-function-in-the-wisconsin-registry-for-alzheimer-s-prevention
#5
Corinne D Engelman, Burcu F Darst, Murat Bilgel, Eva Vasiljevic, Rebecca L Koscik, Bruno M Jedynak, Sterling C Johnson
Recent studies have found an association between functional variants in TREM2 and PLD3 and Alzheimer's disease (AD), but their effect on cognitive function is unknown. We examined the effect of these variants on cognitive function in 1449 participants from the Wisconsin Registry for Alzheimer's Prevention, a longitudinal study of initially asymptomatic adults, aged 36-73 years at baseline, enriched for a parental history of AD. A comprehensive cognitive test battery was performed at up to 5 visits. A factor analysis resulted in 6 cognitive factors that were standardized into z scores (∼N [0, 1]); the mean of these z scores was also calculated...
December 29, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/29379882/alzheimer-risk-loci-and-associated-neuropathology-in-a-population-based-study-vantaa-85
#6
Mira Mäkelä, Karri Kaivola, Miko Valori, Anders Paetau, Tuomo Polvikoski, Andrew B Singleton, Bryan J Traynor, David J Stone, Terhi Peuralinna, Pentti J Tienari, Maarit Tanskanen, Liisa Myllykangas
Objective: To test the association of distinct neuropathologic features of Alzheimer disease (AD) with risk loci identified in genome-wide association studies. Methods: Vantaa 85+ is a population-based study that includes 601 participants aged ≥85 years, of which 256 were neuropathologically examined. We analyzed 29 AD risk loci in addition to APOE ε4, which was studied separately and used as a covariate. Genotyping was performed using a single nucleotide polymorphism (SNP) array (341 variants) and imputation (6,038 variants)...
February 2018: Neurology. Genetics
https://www.readbyqxmd.com/read/29377401/increased-expression-of-trem2-in-peripheral-cells-from-mild-cognitive-impairment-patients-that-progress-into-alzheimer-s-disease
#7
Martina Casati, Evelyn Ferri, Cristina Gussago, Paolo Mazzola, Carlo Abbate, Giuseppe Bellelli, Daniela Mari, Matteo Cesari, Beatrice Arosio
BACKGROUND: Neuroinflammation plays a role in the etiopathogenesis of Alzheimer's disease (AD). TREM2, a cell surface receptor of the immunoglobulin superfamily, seems to have protective anti-inflammatory activity in AD. METHODS: We analyzed TREM2 expression in peripheral blood mononuclear cells from healthy subjects (CT) and from patients with either AD or mild cognitive impairment (MCI). MCI were re-evaluated at a two-year follow-up to investigate their progression to AD (MCI-AD), or lack thereof (MCI-MCI)...
January 27, 2018: European Journal of Neurology: the Official Journal of the European Federation of Neurological Societies
https://www.readbyqxmd.com/read/29362997/trem2-ameliorates-neuronal-tau-pathology-through-suppression-of-microglial-inflammatory-response
#8
Teng Jiang, Ying-Dong Zhang, Qing Gao, Zhou Ou, Peng-Yu Gong, Jian-Quan Shi, Liang Wu, Jun-Shan Zhou
As a recently identified susceptibility gene for Alzheimer's disease (AD), triggering receptor expressed on myeloid cells 2 (TREM2) encodes an immune receptor that is uniquely expressed on microglia, functioning as a modulator of microglial functions including phagocytosis and inflammatory response. Several lines of evidence suggest that TREM2 is upregulated and positively correlates with tau pathology in the brains of AD patients. Meanwhile, our recent study showed that knockdown of TREM2 markedly exacerbated neuronal tau hyperphosphorylation in the brains of P301S-tau transgenic mice, implying that TREM2 might exert a protective role against tau pathology under AD context...
January 23, 2018: Inflammation
https://www.readbyqxmd.com/read/29361745/microglia-and-aging-the-role-of-the-trem2-dap12-and-cx3cl1-cx3cr1-axes
#9
REVIEW
Carmen Mecca, Ileana Giambanco, Rosario Donato, Cataldo Arcuri
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...
January 22, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29360998/concussion-microvascular-injury-and-early-tauopathy-in-young-athletes-after-impact-head-injury-and-an-impact-concussion-mouse-model
#10
Chad A Tagge, Andrew M Fisher, Olga V Minaeva, Amanda Gaudreau-Balderrama, Juliet A Moncaster, Xiao-Lei Zhang, Mark W Wojnarowicz, Noel Casey, Haiyan Lu, Olga N Kokiko-Cochran, Sudad Saman, Maria Ericsson, Kristen D Onos, Ronel Veksler, Vladimir V Senatorov, Asami Kondo, Xiao Z Zhou, Omid Miry, Linnea R Vose, Katisha R Gopaul, Chirag Upreti, Christopher J Nowinski, Robert C Cantu, Victor E Alvarez, Audrey M Hildebrandt, Erich S Franz, Janusz Konrad, James A Hamilton, Ning Hua, Yorghos Tripodis, Andrew T Anderson, Gareth R Howell, Daniela Kaufer, Garth F Hall, Kun P Lu, Richard M Ransohoff, Robin O Cleveland, Neil W Kowall, Thor D Stein, Bruce T Lamb, Bertrand R Huber, William C Moss, Alon Friedman, Patric K Stanton, Ann C McKee, Lee E Goldstein
The mechanisms underpinning concussion, traumatic brain injury, and chronic traumatic encephalopathy, and the relationships between these disorders, are poorly understood. We examined post-mortem brains from teenage athletes in the acute-subacute period after mild closed-head impact injury and found astrocytosis, myelinated axonopathy, microvascular injury, perivascular neuroinflammation, and phosphorylated tau protein pathology. To investigate causal mechanisms, we developed a mouse model of lateral closed-head impact injury that uses momentum transfer to induce traumatic head acceleration...
January 18, 2018: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29336840/heterozygous-tyrobp-deletion-ploslfin-is-not-a-strong-risk-factor-for-cognitive-impairment
#11
Karri Kaivola, Lilja Jansson, Elmo Saarentaus, Anna Kiviharju, Ville Rantalainen, Johan G Eriksson, Timo E Strandberg, Tuomo Polvikoski, Liisa Myllykangas, Pentti J Tienari
Biallelic loss-of-function mutations in TYROBP and TREM2 cause a rare disease that resembles early-onset frontotemporal dementia with bone lesions called polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL). Some PLOSL-causing variants in TREM2 have also been associated with Alzheimer's disease when heterozygous. Here, we studied the PLOSLFINTYROBP deletion that covers 4 of the gene's 5 exons. We genotyped 3220 older Finns (mean age 79, range 58-104) and found 11 deletion carriers (mean age 78, range 60-94)...
December 18, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/29322490/the-rs75932628-and-rs2234253-polymorphisms-of-the-trem2-gene-were-associated-with-susceptibility-to-frontotemporal-lobar-degeneration-in-caucasian-populations
#12
Wen-Hua Su, Zhi-Hong Shi, Shu-Ling Liu, Xiao-Dan Wang, Shuai Liu, Yong Ji
Polymorphisms of the triggering receptor expressed on myeloid cells 2 (TREM2) gene have been reported to be potentially associated with the risks of developing frontotemporal lobar degeneration (FTLD), with inconsistent conclusions. This study aims to comprehensively investigate the potential role of TREM2 variants in FTLD risks via a meta-analysis. We included a total of eight eligible articles. For TREM2 rs75932628, we observed a significantly increased FTLD risk in the models of T vs. C [Association Test, odds ratio (OR) = 2...
January 10, 2018: Annals of Human Genetics
https://www.readbyqxmd.com/read/29321225/humanized-trem2-mice-reveal-microglia-intrinsic-and-extrinsic-effects-of-r47h-polymorphism
#13
Wilbur M Song, Satoru Joshita, Yingyue Zhou, Tyler K Ulland, Susan Gilfillan, Marco Colonna
Alzheimer's disease (AD) is a neurodegenerative disease that causes late-onset dementia. The R47H variant of the microglial receptor TREM2 triples AD risk in genome-wide association studies. In mouse AD models, TREM2-deficient microglia fail to proliferate and cluster around the amyloid-β plaques characteristic of AD. In vitro, the common variant (CV) of TREM2 binds anionic lipids, whereas R47H mutation impairs binding. However, in vivo, the identity of TREM2 ligands and effect of the R47H variant remain unknown...
January 10, 2018: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/29278889/erythromyeloid-derived-trem2-a-major-determinant-of-alzheimer-s-disease-pathology-in-down-syndrome
#14
Ruma Raha-Chowdhury, James W Henderson, Animesh Alexander Raha, Simon R W Stott, Romina Vuono, Simona Foscarin, Liam Wilson, Tiina Annus, Robert Fincham, Kieren Allinson, Vinod Devalia, Robert P Friedland, Anthony Holland, Shahid H Zaman
BACKGROUND: Down syndrome (DS; trisomy 21) individuals have a spectrum of hematopoietic and neuronal dysfunctions, and by the time they reach the age of 40 years, almost all develop Alzheimer's disease (AD) neuropathology which includes senile plaques and neurofibrillary tangles. Inflammation and innate immunity are key players in AD and DS. Triggering receptor expressed in myeloid cells-2 (TREM2) variants have been identified as risk factors for AD and other neurodegenerative diseases...
December 16, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29259854/microglia-express-abi3-in-the-brains-of-alzheimer-s-disease-and-nasu-hakola-disease
#15
Jun-Ichi Satoh, Yoshihiro Kino, Motoaki Yanaizu, Youhei Tosaki, Kenji Sakai, Tsuyoshi Ishida, Yuko Saito
Nasu-Hakola disease (NHD) is a rare autosomal recessive leukoencephalopathy caused by a loss-of-function mutation of either TYROBP (DAP12) or TREM2 expressed in microglia. A rare variant of the TREM2 gene encoding p.Arg47His causes a 3-fold increase in the risk for late-onset Alzheimer's disease (LOAD). A recent study demonstrated that a rare coding variant p.Ser209Phe in the ABI family member 3 (ABI3) gene, a regulator of actin cytoskeleton organization, confers risk of developing of LOAD, although the pattern of ABI3 expression in AD and NHD brains with relevance to microglial pathology remains to be characterized...
November 2017: Intractable & Rare Diseases Research
https://www.readbyqxmd.com/read/29259249/comparative-profiling-of-cortical-gene-expression-in-alzheimer-s-disease-patients-and-mouse-models-demonstrates-a-link-between-amyloidosis-and-neuroinflammation
#16
Erika Castillo, Julio Leon, Guianfranco Mazzei, Nona Abolhassani, Naoki Haruyama, Takashi Saito, Takaomi Saido, Masaaki Hokama, Toru Iwaki, Tomoyuki Ohara, Toshiharu Ninomiya, Yutaka Kiyohara, Kunihiko Sakumi, Frank M LaFerla, Yusaku Nakabeppu
Alzheimer's disease (AD) is the most common form of dementia, characterized by accumulation of amyloid β (Aβ) and neurofibrillary tangles. Oxidative stress and inflammation are considered to play an important role in the development and progression of AD. However, the extent to which these events contribute to the Aβ pathologies remains unclear. We performed inter-species comparative gene expression profiling between AD patient brains and the App NL-G-F/NL-G-F and 3xTg-AD-H mouse models. Genes commonly altered in App NL-G-F/NL-G-F and human AD cortices correlated with the inflammatory response or immunological disease...
December 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29185135/disease-modifying-treatments-modulate-myeloid-cells-in-multiple-sclerosis-patients
#17
Gloria Dalla Costa, Annamaria Finardi, Livia Garzetti, Tiziana Carandini, Giancarlo Comi, Vittorio Martinelli, Roberto Furlan
The role of myeloid cells in the pathogenesis of MS is determined by the polarization they acquire after activation, and mediated by release of extracellular vesicles (MVs). We assessed the effects of treatments for MS on activation and polarization of myeloid cells. MVs levels and markers of polarization of myeloid cells have been assessed at baseline and up to 6 months after the start of a MS treatment. Patients had higher levels of MVs than controls, and these increased significantly over 6 months under natalizumab...
November 28, 2017: Neurological Sciences
https://www.readbyqxmd.com/read/29180839/triggering-receptor-expressed-on-myeloid-cells-2-overexpression-inhibits-proinflammatory-cytokines-in-lipopolysaccharide-stimulated-microglia
#18
Xiaobao Zhang, Fang Yan, Jizheng Cui, Yong Wu, Hengfei Luan, Miaomiao Yin, Zhibin Zhao, Jiying Feng, Jinwei Zhang
Microglia play an important role in mediating inflammatory processes in the central nervous system (CNS). Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglia-specific receptor and could decrease neuropathology in Alzheimer's disease (AD). However, the detailed mechanism remains unclear. This study was designed to elucidate the effect of TREM2 on microglia. We showed that lipopolysaccharide (LPS) stimulation significantly increases proinflammatory cytokines and suppressed TREM2 in microglia...
2017: Mediators of Inflammation
https://www.readbyqxmd.com/read/29177109/exome-sequencing-of-extended-families-with-alzheimer-s-disease-identifies-novel-genes-implicated-in-cell-immunity-and-neuronal-function
#19
H N Cukier, B K Kunkle, K L Hamilton, S Rolati, M A Kohli, P L Whitehead, J Jaworski, J M Vance, M L Cuccaro, R M Carney, J R Gilbert, L A Farrer, E R Martin, G W Beecham, J L Haines, M A Pericak-Vance
Objective: Alzheimer's disease (AD) is a neurodegenerative disorder for which more than 20 genetic loci have been implicated to date. However, studies demonstrate not all genetic factors have been identified. Therefore, in this study we seek to identify additional rare variants and novel genes potentially contributing to AD. Methods: Whole exome sequencing was performed on 23 multi-generational families with an average of eight affected subjects. Exome sequencing was filtered for rare, nonsynonymous and loss-of-function variants...
August 2017: Journal of Alzheimer's Disease and Parkinsonism
https://www.readbyqxmd.com/read/29169609/microglia-mediated-neuroprotection-trem2-and-alzheimer-s-disease-evidence-from-optical%C3%A2-imaging
#20
REVIEW
Carlo Condello, Peng Yuan, Jaime Grutzendler
Recent genetic studies have provided overwhelming evidence of the involvement of microglia-related molecular networks in the pathophysiology of Alzheimer's disease (AD). However, the precise mechanisms by which microglia alter the course of AD neuropathology remain poorly understood. Here we discuss current evidence of the neuroprotective functions of microglia with a focus on optical imaging studies that have revealed a role of these cells in the encapsulation of amyloid deposits ("microglia barrier"). This barrier modulates the degree of plaque compaction, amyloid fibril surface area, and insulation from adjacent axons thereby reducing neurotoxicity...
October 14, 2017: Biological Psychiatry
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