Cited by 246Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsDementia and Cognitive Impairment Research

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The role of TREM2 in Alzheimer's disease and other neurodegenerative disorders

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Carmona, Susana, Zahs, Kathleen, Wu, Elizabeth, Dakin, Kelly, Bras, Jose, Guerreiro, Rita·2018·The Lancet Neurology

DOI 10.1016/s1474-4422(18)30232-1

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Abstract

Alzheimer's disease is a genetically complex disorder; rare variants in the triggering receptor expressed on myeloid cells 2 (TREM2) gene have been shown to as much as triple an individual's risk of developing Alzheimer's disease. TREM2 is a transmembrane receptor expressed in cells of the myeloid lineage, and its association with Alzheimer's disease supports the involvement of immune and inflammatory pathways in the cause of the disease, rather than as a consequence of the disease. TREM2 variants associated with Alzheimer's disease induce partial loss of function of the TREM2 protein and alter the behaviour of microglial cells, including their response to amyloid plaques. TREM2 variants have also been shown to cause polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy and frontotemporal dementia. Although the low frequency of TREM2 variants makes it difficult to establish robust genotype-phenotype correlations, such studies are essential to enable a comprehensive understanding of the role of TREM2 in different neurological diseases, with the ultimate goal of developing novel therapeutic approaches.

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A Unique Microglia Type Associated with Restricting Development of Alzheimer’s Disease
Keren-Shaul, H., Spinrad, A., Weiner, A., Matcovitch-Natan, O., Dvir-Szternfeld, R., Ulland, T. K., David, E., Baruch, K., Lara-Astaiso, D., Toth, B., et al. (2017) · Cell · doi:10.1016/j.cell.2017.05.018 · Cited by 5,493
Meta-Analysis of 74,046 Individuals Identifies 11 New Susceptibility Loci for Alzheimer’s Disease
(EADI), E. A. D. I., Lambert, J.-C., (GERAD), G. A. E. R. I. A. D., Alzheimer's Disease Genetic Consortium (ADGC), (CHARGE), C. F. H. A. A. R. I. G. E., Ibrahim-Verbaas, C. A., Harold, D., Naj, A. C., Sims, R., Bellenguez, C., et al. (2013) · Nature Genetics · doi:10.1038/ng.2802 · Cited by 4,336
TREM2 Variants in Alzheimer's Disease
Guerreiro, R., Wojtas, A., Bras, J., Carrasquillo, M., Rogaeva, E., Majounie, E., Cruchaga, C., Sassi, C., Kauwe, J. S. K., Younkin, S., et al. (2013) · New England Journal of Medicine · doi:10.1056/nejmoa1211851 · Cited by 3,020
Self-citation
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Krasemann, S., Madore, C., Cialic, R., Baufeld, C., Calcagno, N., El Fatimy, R., Beckers, L., O’Loughlin, E., Xu, Y., Fanek, Z., et al. (2017) · Immunity · doi:10.1016/j.immuni.2017.08.008 · Cited by 2,979
Variant of TREM2 Associated with the Risk of Alzheimer's Disease
Jonsson, T., Stefansson, H., Steinberg, S., Jonsdottir, I., Jonsson, P. V., Snaedal, J., Bjornsson, S., Huttenlocher, J., Levey, A. I., Lah, J. J., et al. (2013) · New England Journal of Medicine · doi:10.1056/nejmoa1211103 · Cited by 2,558
Genome-wide meta-analysis identifies new loci and functional pathways influencing Alzheimer’s disease risk
Jansen, I. E., Savage, J. E., Watanabe, K., Bryois, J., Williams, D. M., Steinberg, S., Sealock, J., Karlsson, I. K., Hägg, S., Athanasiu, L., et al. (2019) · Nature Genetics · doi:10.1038/s41588-018-0311-9 · Cited by 2,277
TREM2 Lipid Sensing Sustains the Microglial Response in an Alzheimer’s Disease Model
Wang, Y., Cella, M., Mallinson, K., Ulrich, J. D., Young, K. L., Robinette, M. L., Gilfillan, S., Krishnan, G. M., Sudhakar, S., Zinselmeyer, B. H., et al. (2015) · Cell · doi:10.1016/j.cell.2015.01.049 · Cited by 1,736
TREM2 Maintains Microglial Metabolic Fitness in Alzheimer’s Disease
Ulland, T. K., Song, W. M., Huang, S. C.-C., Ulrich, J. D., Sergushichev, A., Beatty, W. L., Loboda, A. A., Zhou, Y., Cairns, N. J., Kambal, A., et al. (2017) · Cell · doi:10.1016/j.cell.2017.07.023 · Cited by 1,263
Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease
ARUK Consortium, Sims, R., GERAD/PERADES, C., van der Lee, S. J., Naj, A. C., Bellenguez, C., Badarinarayan, N., Jakobsdottir, J., Kunkle, B. W., Boland, A., et al. (2017) · Nature Genetics · doi:10.1038/ng.3916 · Cited by 1,012
TREM2 Binds to Apolipoproteins, Including APOE and CLU/APOJ, and Thereby Facilitates Uptake of Amyloid-Beta by Microglia
Yeh, F. L., Wang, Y., Tom, I., Gonzalez, L. C., & Sheng, M. (2016) · Neuron · doi:10.1016/j.neuron.2016.06.015 · Cited by 943

Show all 107 references

Research works printed but not linked: 5

Bertram, 2013, TREM2 and neurodegenerative disease, N Engl J Med, 369, 1565
Rajagopalan, 2013, TREM2 and neurodegenerative disease, N Engl J Med, 369, 1565
Guerreiro, 2013, Using exome sequencing to reveal mutations in TREM2 presenting as a frontotemporal dementia-like syndrome without bone involvement, JAMA Neurol, 70, 78, 10.1001/jamaneurol.2013.579 · DOI · Paper page
Benitez, 2013, TREM2 and neurodegenerative disease, N Engl J Med, 369, 1567
Guerreiro, 2013, TREM2 and neurodegenerative disease, N Engl J Med, 369, 1569

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Background
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Ogonowski, N. S., Santamaría‐García, H. A., Báez, S., López, A., Laserna, A., Garcia-Cifuentes, E. R., Ayala‐Ramírez, P., Zarante, I., Suárez‐Obando, F., Reyes, P. A., et al. (2023) · Journal of Medical Genetics · doi:10.1136/jmg-2022-108627 · Cited by 11
Investigation of Potential Drug Targets for Cholesterol Regulation to Treat Alzheimer’s Disease
Passero, M., Zhai, T., & Huang, Z. J. (2023) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph20136217 · Cited by 10
Unraveling the Molecular Dance: Insights into TREM2/DAP12 Complex Formation in Alzheimer’s Disease through Molecular Dynamics Simulations
Zhong, Z., Ulmschneider, M. B., & Lorenz, C. D. (2024) · ACS Omega · doi:10.1021/acsomega.4c03060 · Cited by 8
Transethnic analysis identifies SORL1 variants and haplotypes protective against Alzheimer's disease
Zhou, X., Cao, H., Jiang, Y., Chen, Y., Zhong, H., Fu, W. Y., Lo, R. M. N., Wong, B. W. Y., Cheng, E. Y. L., Mok, K. Y., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14214 · Cited by 9
Serotonin-mediated regulation of mitophagy in Alzheimer's disease: Mechanistic insights and therapeutic potential
Sultana, O. F., Bandaru, M., Bushra, M. A., Reddy, P. H., & Reddy, A. P. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102957 · Cited by 11
Association of rs2062323 in the TREM1 gene with Alzheimer's disease and cerebrospinal fluid‐soluble TREM2
Wang, Z.-T., Fu, Y., Chen, S., Huang, Y., Ma, Y., Wang, Y., Tan, L., & Yu, J. (2023) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14129 · Cited by 8
“, Parkinson's disease), (3) major psychological disorders, (4) severe systemic diseases (e.”
The Other Side of Alzheimer’s Disease: Influence of Metabolic Disorder Features for Novel Diagnostic Biomarkers
Argentati, C., Tortorella, I., Bazzucchi, M., Emiliani, C., Morena, F., & Martino, S. (2020) · Journal of Personalized Medicine · doi:10.3390/jpm10030115 · Cited by 10
A Comprehensive Machine Learning Framework for the Exact Prediction of the Age of Onset in Familial and Sporadic Alzheimer’s Disease
Velez, J. I., Samper, L. A., Arcos-Holzinger, M., Espinosa, L. G., Isaza-Ruget, M. A., Lopera, F. J., & Arcos‐Burgos, M. (2021) · Diagnostics · doi:10.3390/diagnostics11050887 · Cited by 9
The role of triggering receptor expressed on myeloid cells 2 in Parkinson’s disease and other neurodegenerative disorders
Schwarz, H., Bässler, S., Balta, D., Socher, E., Zunke, F., & Arnold, P. (2022) · Behavioural Brain Research · doi:10.1016/j.bbr.2022.113977 · Cited by 8
Neurodegenerative Disease Risk in Carriers of Autosomal Recessive Disease
Vieira, S. R. L., & Morris, H. R. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.679927 · Cited by 10
“To date, over 60 coding TREM2 variants have been identified, displaying various degrees of population frequency (117).”
Background
Biofluid biomarkers for Alzheimer’s disease
Wang, S., Xie, S., Zheng, Q., Zhang, Z., Wang, T., & Zhang, G. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1380237 · Cited by 9
Elucidating the Role of Trem2 in Lipid Metabolism and Neuroinflammation
Zhao, C., Qi, W., Lv, X., Gao, X.-L., Liu, C.-N., & Zheng, S.-M. (2025) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.70338 · Cited by 7
Role of TREM2 in neuroinflammation regulation: mechanisms, disease associations, and therapeutic translation advances
Liao, Y., Mu, G., Deng, S., Lu, B. F., & Zheng, M. (2025) · Journal of Translational Medicine · doi:10.1186/s12967-025-07604-x · Cited by 8
“…have demonstrated that TREM2 exerts critical effects on the pathogenesis of neurological disorders: pathogenic mutations in TREM2 impair its normal function, while reactive upregulation of TREM2 modulates its protective capacities—both scenarios ultimately shaping disease progression [8, 9].”
TREM2 gene induces differentiation of induced pluripotent stem cells into dopaminergic neurons and promotes neuronal repair via TGF ‐β activation in 6‐OHDA ‐lesioned mouse model of Parkinson's disease
Liang, H., Liu, P., Wang, Z., Xiong, H., Yin, C., Dongdong, Z., Wu, C., & Chen, L. (2024) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14630 · Cited by 8
“10 Variants of TREM2 have been largely reported to be associated with a variety of neurodegenerative disorders, including PD. 11,12 A recent study has verified that inhibition of TREM2 contributes to the occurrence and development of PD. 13 Meanwhile, published data have suggested the important…”
Background
Comprehensive genetic screening of early-onset dementia patients in an Austrian cohort-suggesting new disease-contributing genes
Silvaieh, S., König, T., Wurm, R., Parvizi, T., Berger–Sieczkowski, E., Goeschl, S., Hotzy, C., Wagner, M., Berutti, R., Sammler, E. M., et al. (2023) · Human Genomics · doi:10.1186/s40246-023-00499-z · Cited by 8
“Two patients (EOD-2 and EOD-36) carried the well-established TREM2 risk variants p.(R47H) and p.(R62C), respectively, [12, 13].”
Background
Increased microglia activation in late non‐central nervous system cancer survivors links to chronic systemic symptomatology
Schoenberg, P. L. A., Song, A. K., Mohr, E., Rogers, B. P., Peterson, T. E., & Murphy, B. A. (2023) · Human Brain Mapping · doi:10.1002/hbm.26491 · Cited by 8
“The TREM2 receptor has been connected to various pathophysiology in brain diseases such as dementia (Carmona et al., 2018; Edwin & Henjum, 2020; Gratuze et al., 2018; Ulland & Colonna, 2018; Wang et al., 2020; Zhao et al., 2022), and TREM2 signaling is involved in the regulation of critical…”
Background
Investigation of Novel Aronia Bioactive Fraction-Alginic Acid Nanocomplex on the Enhanced Modulation of Neuroinflammation and Inhibition of Aβ Aggregation
Jang, B.-K., Shin, S. J., Park, H. H., Kumar, V., Park, Y., Kim, J. Y., Kang, H., Park, S. Y., Kwon, Y., Shin, S.-E., et al. (2024) · Pharmaceutics · doi:10.3390/pharmaceutics17010013 · Cited by 7
Temporal biphasic regulation of photoreceptor degeneration by microglial TREM2: A metabolic-immune nexus in retinitis pigmentosa
Li, R., Zhang, J., Wu, J., Fan, J.-Q., & Lin, B. (2025) · Science Advances · doi:10.1126/sciadv.adw9299 · Cited by 11
Atypical findings: Atypical parkinsonian syndromes or Atypical parkinsonian syndromes look-alikes
Çalıkuşu, F. Z., Akkuş, S., Kızılkılıç, E. K., Poyraz, B. Ç., Altunç, A. T., Kızıltan, G., & Gündüz, A. (2023) · Clinical Neurology and Neurosurgery · doi:10.1016/j.clineuro.2023.107975 · Cited by 8
Integrative Analysis of the Age-Related Dysregulated Genes Reveals an Inflammation and Immunity-Associated Regulatory Network in Alzheimer’s Disease
Wu, Z., Dong, L., Tian, Z., Yu, C., Shu, Q., Chen, W., & Li, H. (2024) · Molecular Neurobiology · doi:10.1007/s12035-023-03900-z · Cited by 7
“For example, TREM2 was proved involved in the immune and inflammatory pathways in the cause of AD [34], and microglia CST7-mediated impairment in the lysosomal pathway was essential in AD [35].”
The Unveiling of Therapeutic Targets for Alzheimer’s Disease: An Integrative Review
Madar, P. R., Nagalapur, P. P., Chaudhari, S. Y., Sharma, D., Koparde, A. A., Buchade, R. S., Kshirsagar, S. S., Uttekar, P. S., Jadhav, S. B., & Chaudhari, P. (2024) · Current Topics in Medicinal Chemistry · doi:10.2174/0115680266282492240220101049 · Cited by 7
Primary microgliopathy presenting as degenerative dementias: A case series of novel gene mutations from India
Ramakrishnan, S., Arshad, F., Bs, K., Pon, A. G., Bosco, S., Kumar, S., Chidambaram, H., Chinnathambi, S. C. B., Kulanthaivelu, K., Arunachal, G., et al. (2024) · Dementia and Geriatric Cognitive Disorders Extra · doi:10.1159/000538145 · Cited by 8
“Heterozygous variants including R47H and R62H are risk factors for Alzheimer ’ s disease, whereas homozygous loss of function was found in families with the rare recessive NHD [33 – 35].”
Background
Differential Neuropathology, Genetics, and Transcriptomics in Two Kindred Cases with Alzheimer’s Disease and Lewy Body Dementia
Palmieri, I., Poloni, T. E., Medici, V., Zucca, S., Davin, A., Pansarasa, O., Ceroni, M., Tronconi, L., Guaita, A., Gagliardi, S., et al. (2022) · Biomedicines · doi:10.3390/biomedicines10071687 · Cited by 7
MXenes for neurodegenerative disorders
Sachdeva, B., & Sachdeva, P. (2022) · Materials Today Proceedings · doi:10.1016/j.matpr.2022.10.085 · Cited by 7
Do anti‐Aβ monoclonal antibodies lower brain plaques in Alzheimer patients through microglia activation?
Pomara, N., & Imbimbo, B. P. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.13684 · Cited by 6
Advances in neuroRehabilitation of TREM2-related dementia
Luca, R. D., Marra, A., Pollicino, P., Buda, M., Mucari, M., Bonanno, M., Torregrossa, W., Caminiti, A., Rifici, C., & Calabrò, R. S. (2022) · Medicine · doi:10.1097/md.0000000000029470 · Cited by 6
Inflammatory expression profile in peripheral blood mononuclear cells from patients with Nasu-Hakola Disease
Galimberti, D., Fenoglio, C., Ghezzi, L., Serpente, M., Arcaro, M., D’Anca, M., Riz, M. A. D., Arighi, A., Fumagalli, G., Pietroboni, A. M., et al. (2019) · Cytokine · doi:10.1016/j.cyto.2018.12.024 · Cited by 6
Understanding recent advances in non‐amyloid/non‐tau (NANT) biomarkers and therapeutic targets in Alzheimer's disease
Eldik, L. J. V., Siemers, E., Collins, E. C., Gold, M., Henley, D. B., Johannsen, P., Möbius, H. J., Shulman, M. B., Zhou, J., Carrillo, M. C., et al. (2024) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.70014 · Cited by 5
“50 Recently,itwasdemonstratedthatelevated soluble TREM2 in CSF is associated with reduced cognitive decline in AD, 51 highlighting that TREM2 activation may represent a viable NANT treatment strategy to impact multiple underlying microglia-driven pathologies.”
Resilience mechanisms underlying Alzheimer’s disease
Chew, C. S., Jy, L., Ng, K. Y., Koh, R. Y., & Chye, S. M. (2025) · Metabolic Brain Disease · doi:10.1007/s11011-024-01507-4 · Cited by 6
“In sporadic AD, TREM2 with an arginine-to-histidine mutation at position 47 (R47H) or position 62 (R62H) may lead to the deposition of Aβ plaque and induce neuronal injury (Carmona et al. 2018; Hou et al. 2022; Qin et al. 2021; Ulland et al. 2017).”
Molecular and Therapeutic Targets for Amyloid-beta Plaques in Alzheimer's Disease: A Review Study
Thomas, J., & WILSON, S. K. (2021) · Basic and Clinical Neuroscience Journal · doi:10.32598/bcn.2021.3522.1 · Cited by 6
“Microglia have been shown to surround and limit Aβ plaques in the AD brain in the absence of microglial scavenging receptors and resulted in decreased clearance of Aβ by microglia (Carmona et al., 2018; Jay et al., 2017; Zheng et al., 2018).”
Background
Surgery-induced cognitive dysfunction is alleviated through triggering receptor expressed on myeloid cells 2
Niu, W., Ma, L., Tao, T., Tian, F., He, T., Qiao, M., He, H., Liu, X., & Zhao, X. (2020) · Acta Histochemica · doi:10.1016/j.acthis.2020.151553 · Cited by 5
The TREM2 H157Y Variant Influences Microglial Phagocytosis, Polarization, and Inflammatory Cytokine Release
Fu, X., Chen, S., Lian, H.-W., Deng, Y., Duan, R., Zhang, Y., & Jiang, T. (2023) · Brain Sciences · doi:10.3390/brainsci13040642 · Cited by 5
“TREM2 is located on human chromosome 6p21, a hot zone linked with AD susceptibility [12,13].”
Background
Dietary polyphenols and gut–brain axis modulation: the neuroprotective role of quercetin, allicin, and ferulic acid in traumatic brain injury and neurodegeneration
Chelliah, R., Ghimeray, S., Mettu, S., Barathikannan, K., Wei, S., Sanyal, S., Pabba, M., BANAT, F. A., & Oh, D. (2025) · Journal of Functional Foods · doi:10.1016/j.jff.2025.107091 · Cited by 5
A computational framework for identifying chemical compounds to bind Apolipoprotein E4 for Alzheimer’s disease intervention
Zhai, T., Krass, E., Zhang, F., & Huang, Z. J. (2023) · Frontiers in Systems Biology · doi:10.3389/fsysb.2023.1188430 · Cited by 6
“, Triggering receptor expressed on myeloid cells 2) induces microglial anti-inflammatory activation in ADrelated conditions, and it is regarded as a potential target for the prevention and treatment of Alzheimer’s disease (Carmona et al., 2018), (Ulrich et al.”
Background
The promising role of bioactive congeners present in Cassytha filiformis in Alzheimer's disease: An explicative review
Khabiya, R., Karati, D., Dwivedi, S., Dwivedi, A., & Mukherjee, S. (2024) · Brain Disorders · doi:10.1016/j.dscb.2024.100125 · Cited by 4
Maternal-fetal type I interferon signaling drives TREM2 dysregulation and synaptic dysfunction in neurodevelopmental disorders
Bizzotto, M., You, S. F., Tamborini, M., Faggiani, E., Morini, R., Borreca, A., Zhang, R., Aladyeva, E., Nallapu, A., Ferrari, C., et al. (2026) · Neuron · doi:10.1016/j.neuron.2026.04.043 · Cited by 4
Familial cerebral amyloid disorders with prominent white matter involvement
Banerjee, G., Schott, J. M., & Ryan, N. S. (2024) · Handbook of clinical neurology · doi:10.1016/b978-0-323-99209-1.00010-7 · Cited by 3
TREX1 p.A129fs and p.Y305C variants in a large multi-ethnic cohort of CADASIL-like unrelated patients
Foddis, M., Blumenau, S., Holtgrewe, M., Paquette, K., Westra, K., Alonso, I. D. C. M. P., Macário, C., Morgadinho, A., Velon, A. G., Santo, G., et al. (2022) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2022.11.013 · Cited by 3
Self-citation
The Radiogenomics of Late-onset Alzheimer Disease
Bonham, L. W., Sirkis, D. W., Hess, C. P., Sugrue, L. P., & Yokoyama, J. S. (2019) · Topics in Magnetic Resonance Imaging · doi:10.1097/rmr.0000000000000222 · Cited by 3
Salvianolic acid B (SalB) improves high-fat diet (HFD)-caused cognitive impairment in mice by modulating the Trem2/Dap12 pathway in vivo and in vitro
Li, H., Zheng, J., Tan, K.-W., Su, J., Chen, W., Pang, R.-K., Wu, G., Qiu, Y.-H., Li, X., Cai, Y., et al. (2025) · International Immunopharmacology · doi:10.1016/j.intimp.2025.114461 · Cited by 2
Exploiting acylaminopyrazole scaffold for polypharmacology approach in Alzheimer's disease
Orioli, R., Sarno, G., Seghetti, F., Gobbi, S., Belluti, F., Feoli, A., Massenzio, F., Monti, B., Spagnuolo, R., Bartolini, M., et al. (2025) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2025.117799 · Cited by 2
Biophysical characterization of TREM2 missense variants implicated in neurodegenerative disease
Pillai, J. P., Sung, K., Shi, L. Z., & Wu, C. (2025) · Computational and Structural Biotechnology Journal · doi:10.1016/j.csbj.2025.07.003 · Cited by 2
“Similarly to AD, the Y38C, W50C, T66M, and V126G variants have been found and validated in numerous studies as causal factors for NHD [13 – 17].”
Plasma soluble TREM2 is associated with plasma pTau-181 and pTau-231 in cognitively normal older adults at risk of Alzheimer's disease
Asih, P. R., Morris, C. W., Wang, H., Pedrini, S., Goozee, K. G., Laws, S. M., Chatterjee, P., Taddei, K., Sohrabi, H. R., Rainey‐Smith, S. R., et al. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251400780 · Cited by 2
Comparison of Cerebral Cortex Transcriptome Profiles in Ischemic Stroke and Alzheimer’s Disease Models
Song, J. (2022) · Clinical Nutrition Research · doi:10.7762/cnr.2022.11.3.159 · Cited by 2
“The Trem2 gene, which is related to microglia activation under amyloid beta toxicity in AD brain [50] was increased in the MCAO and AD mouse brain cortex in this study.”
Background
Different Splice Isoforms of Peripheral Triggering Receptor Expressed on Myeloid Cells 2 mRNA Expressions are Associated With Cognitive Decline in Mild Dementia Due to Alzheimer’s Disease and Reflect Central Neuroinflammation
Chiang, Y.-K., Lin, Y., Chen, C., Lirng, J.-F., Yang, Y., Lee, W., & Fuh, J. (2024) · American Journal of Alzheimer s Disease & Other Dementias® · doi:10.1177/15333175241243183 · Cited by 2
“39,40 While many studies demonstrate an elevation of CSF sTREM2 along the AD continuum, inconsistencies exist regarding disease stages, 41 thereby reducing the discriminative power necessary for diagnostic purposes.”
Background
A Risk Variant rs6922617 in TREM Is Discrepantly Associated With Defining Neuropathological Hallmarks in the Alzheimer’s Continuum
Qian, S., Zheng, Y., Jiang, T., Hou, J., Cao, R., Cai, J., Ma, E., Wang, W., Song, W., & Xie, C. (2024) · The Journals of Gerontology Series A · doi:10.1093/gerona/glae185 · Cited by 2
Zinc Finger Protein 90 Knockdown Promotes Cisplatin Sensitivity via Nrf2/HO-1 Pathway in Ovarian Cancer Cell
Wu, C.-H., Feng, C., Wang, C., Wen, Z., Long, C., & Tang, F. (2023) · Cancers · doi:10.3390/cancers15051586 · Cited by 2
Single-cell transcriptomic atlas of Alzheimer's disease middle temporal gyrus reveals region, cell type, and sex specificity of gene expression with novel genetic risk for MERTK in female
Zhang, L., Liu, T., He, C. H., Russo, A., Coffey, S., Yin, D., Hsu, I.-U., Zhang, C., Ye, Y., Su, C., et al. (2026) · Journal of Alzheimer’s Disease · doi:10.1177/13872877261480719 · Cited by 22
“24,25 Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astro-glia, triggering an innate immune response characterized by the release of in ﬂ ammatory mediators that contribute to disease progression and severity.”

Authors: Carmona, S., Zahs, K., Wu, E., Dakin, K., Bras, J., & Guerreiro, R.
Affiliations: UK Dementia Research Institute (GB)
Alzforum (US)
Corresponding author: Guerreiro, Rita
ORCID: Carmona, Susana
Zahs, Kathleen
Wu, Elizabeth
Guerreiro, Rita
Venue: The Lancet Neurology
Publisher: Elsevier BV
Published: 2018-08
Volume: 17
Issue: 8
Pages: 721-730
ISSN: 1474-4422 (ISSN-L)
DOI: 10.1016/s1474-4422(18)30232-1
OpenAlex: W2884070953
Cited by: 244
References: 107
Citations by year: 2026: 13 · 2025: 28 · 2024: 42 · 2023: 38 · 2022: 30 · 2021: 32 · 2020: 28 · 2019: 28 · 2018: 4
FWCI: 2.18
Type: journal article
Language: en
Open access: green
discovery.ucl.ac.uk
Licence: other-oa
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: The Lancet Neurology (publishedVersion)
PubMed (publishedVersion)
UCL Discovery (University College London) (submittedVersion, other-oa)
Funders: Alzheimer's Society
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: TREM2, Alzheimer's disease, neurodegenerative diseases, myeloid cells, microglia, amyloid plaques, neuroinflammation, genetic risk variants, loss-of-function mutations, frontotemporal dementia, genotype-phenotype correlation, therapeutic target
MeSH terms: Alzheimer Disease, Humans, Membrane Glycoproteins, Receptors, Immunologic, Neurodegenerative Diseases, Genetic Predisposition to Disease

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The role of TREM2 in Alzheimer's disease and other neurodegenerative disorders

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