The role of TREM2 in Alzheimer's disease and other neurodegenerative disorders
Open accessAbstract
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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Whole-genome analysis identified relatively rare mutations in the TREM2 gene that are associated with a high AD risk.
“Whole-genome analysis led to the identification of relatively rare mutations in TREM2 gene that are associated with a high AD risk.187”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [187]
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TREM2 mutations are rare in a French cohort of patients with frontotemporal dementia
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Genetic meta-analysis identifies 9 novel loci and functional pathways for Alzheimer’s disease riskPreprint
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TREM2 R47H variant and risk of essential tremor: A cross-sectional international multicenter study
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Evidence of CNS β-amyloid deposition in Nasu-Hakola disease due to the TREM2 Q33X mutation
Ghezzi, L., Carandini, T., Arighi, A., Fenoglio, C., Arcaro, M., Riz, M. A. D., Pietroboni, A. M., Fumagalli, G., Basilico, P., Calvi, A., et al. (2017) · Neurology · doi:10.1212/wnl.0000000000004747 · Cited by 31 · see citing works
The Alzheimer's disease-associated TREM2 gene is regulated by p53 tumor suppressor protein
Zajkowicz, A., Gdowicz‐Kłosok, A., Krześniak, M., Janus, P., Łasut-Szyszka, B., & Rusin, M. (2018) · Neuroscience Letters · doi:10.1016/j.neulet.2018.05.037 · Cited by 29 · see citing works
Exome array study did not identify novel variants in Alzheimer's disease
Chung, S. J., Kim, M., Kim, J., Kim, Y. J., You, S., Koh, J., Kim, S. Y., & Lee, J. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.03.007 · Cited by 25 · see citing works
Evaluating pathogenic dementia variants in posterior cortical atrophy
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Alzheimer's disease pathology in Nasu-Hakola disease brains
Satoh, J., Kino, Y., Yanaizu, M., & Saito, Y. (2018) · Intractable & Rare Diseases Research · doi:10.5582/irdr.2017.01088 · Cited by 24 · see citing works
TREM2 rare variant p.R47H is not associated with Parkinson's disease
Mengel, D., Thelen, M., Balzer‐Geldsetzer, M., Söling, C., Bach, J., Schaeffer, E., Herold, C., Becker, T., Liepelt, I., Becker, J., et al. (2015) · Parkinsonism & Related Disorders · doi:10.1016/j.parkreldis.2015.11.026 · Cited by 23 · see citing works
TREM2 p.R47H substitution is not associated with dementia with Lewy bodies
Walton, R. L., Soto‐Ortolaza, A. I., Murray, M. E., Lorenzo‐Betancor, O., Ogaki, K., Heckman, M. G., Rayaprolu, S., Rademakers, R., Ertekin‐Taner, N., Uitti, R. J., et al. (2016) · Neurology Genetics · doi:10.1212/nxg.0000000000000085 · Cited by 21 · see citing works
Frontotemporal Dementia and Chorea Associated with a Compound Heterozygous TREM2 Mutation
Redaelli, V., Salsano, E., Colleoni, L., Corbetta, P., Tringali, G., Sole, A. D., Giaccone, G., & Rossi, G. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180018 · Cited by 20 · see citing works
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Genetic analysis of TREM2 variants in Chinese Han patients with sporadic Parkinson’s disease
Tan, T., Song, Z. J., Yuan, L., Xiong, W., Deng, X., Ni, B., Chen, Y., & Deng, H. (2015) · Neuroscience Letters · doi:10.1016/j.neulet.2015.12.029 · Cited by 18 · see citing works
Genetic analysis of MC1R variants in Chinese Han patients with sporadic Parkinson’s disease
He, S., Tan, T., Song, Z. J., Yuan, L., Deng, X., Ni, B., Chen, Y., & Deng, H. (2015) · Neuroscience Letters · doi:10.1016/j.neulet.2015.11.034 · Cited by 17 · see citing works
Mutations in TYROBP are not a common cause of dementia in a Turkish cohort
Darwent, L., Carmona, S., Lohmann, E., Güven, G., Kun‐Rodrigues, C., Bılgıç, B., Hanağası, H. A., Gurvit, H. I., Erginel‐Ünaltuna, N., Pak, M., et al. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.06.019 · Cited by 16 · see citing works
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14GENETIC META-ANALYSIS IDENTIFIES 9 NOVEL LOCI AND FUNCTIONAL PATHWAYS FOR ALZHEIMER'S DISEASE RISK
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Heterozygous TYROBP deletion (PLOSLFIN) is not a strong risk factor for cognitive impairment
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The C9ORF72 expansion does not affect the phenotype in Nasu-Hakola disease with the DAP12 mutation
Solje, E., Hartikainen, P. H., Valori, M., Vanninen, R. L., Tiihonen, J., Hakola, P., Tienari, P. J., & Remes, A. M. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.01.149 · Cited by 3 · see citing works
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Research works printed but not linked: 5
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Cited by
Sorted by citations
Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes
Kwon, H. S., & Koh, S.-H. (2020) · Translational Neurodegeneration · doi:10.1186/s40035-020-00221-2 · Cited by 2,595 · see citing works
Role of neuroinflammation in neurodegeneration development
Zhang, W., Xiao, D., Mao, Q., & Xia, H. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01486-5 · Cited by 1,668 · see citing works
“TREM2: Whole-genome analysis led to the identification of relatively rare mutations in TREM2 gene that are associated with a high AD risk.(187) Given the TREM2 is exclusively expressed in immune cells,(188) and involved in the activation of immune cells by stimulating phagocytosis and reducing cytokine production, we…”
BackgroundMarschallinger, J., Iram, T., Zardeneta, M., Lee, S. E., Lehallier, B., Haney, M. S., Pluvinage, J. V., Mathur, V., Hahn, O., Morgens, D. W., et al. (2020) · Nature Neuroscience · doi:10.1038/s41593-019-0566-1 · Cited by 1,384 · see citing works
Plasma GFAP is an early marker of amyloid-β but not tau pathology in Alzheimer's disease
Pereira, J. B., Janelidze, S., Smith, R., Mattsson-Carlgren, N., Palmqvist, S., Teunissen, C. E., Zetterberg, H., Stomrud, E., Ashton, N. J., Blennow, K., et al. (2021) · Brain · doi:10.1093/brain/awab223 · Cited by 598 · see citing works
Immune Signaling in Neurodegeneration
Hammond, T. R., Marsh, S. E., & Stevens, B. (2019) · Immunity · doi:10.1016/j.immuni.2019.03.016 · Cited by 336 · see citing works
“In addition, homozygous TREM2 variants were also found to be potentially casual for a form of FTD (Carmona et al., 2018; Chouery et al., 2008; Guerreiro et al., 2013a), while other variants significantly elevated FTD risk (Carmona et al.”
BackgroundInfluentialThe <i>MS4A</i> gene cluster is a key modulator of soluble TREM2 and Alzheimer’s disease risk
Deming, Y., Filipello, F., Cignarella, F., Cantoni, C., Hsu, S., Mikesell, R., Li, Z., Del-Aguila, J. L., Dube, U., Farias, F. G., et al. (2019) · Science Translational Medicine · doi:10.1126/scitranslmed.aau2291 · Cited by 271 · see citing works
“Our findings and previous studies indicate that increasing TREM2 or activating the TREM2 signaling pathway could offer a new therapeutic approach for treating AD (45).”
GBA, Gaucher Disease, and Parkinson’s Disease: From Genetic to Clinic to New Therapeutic Approaches
Riboldi, G. M., & Di Fonzo, A. B. (2019) · Cells · doi:10.3390/cells8040364 · Cited by 274 · see citing works
“Of note, TREM2 plays a crucial role in microglia cells as part of the phagocytic scavenger pathway [116].”
BackgroundCellular senescence and Alzheimer disease: the egg and the chicken scenario
Saez-Atienzar, S., & Masliah, E. (2020) · Nature Reviews Neuroscience · doi:10.1038/s41583-020-0325-z · Cited by 257 · see citing works
Xia, X., Wang, Y., Huang, Y., Zhang, H., Lu, H., & Zheng, J. (2019) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2019.101694 · Cited by 206 · see citing works
Veitch, D. P., Weiner, M. W., Aisen, P. S., Beckett, L. A., DeCarli, C., Green, R. C., Harvey, D., Jack, C. R., Jagust, W., Landau, S. M., et al. (2022) · Alzheimer's & Dementia · doi:10.1002/alz.12422 · Cited by 184 · see citing works
Mitochondrial Dysfunction and Alzheimer’s Disease: Role of Microglia
Agrawal, I., & Jha, S. (2020) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2020.00252 · Cited by 181 · see citing works
“TREM2 is a microglial cell surface receptor central to phagocytosis, chemotaxis, survival, and proliferation ofmicroglia (Carmona et al., 2018).”
BackgroundTherapeutic approaches targeting Apolipoprotein E function in Alzheimer’s disease
Williams, T., Borchelt, D., & Chakrabarty, P. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-0358-9 · Cited by 166 · see citing works
“Recent genome wide association studies have identified several microglial genes that regulate AD risk, foremost among them being TREM2 [204].”
BackgroundInfluentialRabinovici, G. D. (2019) · Continuum · doi:10.1212/con.0000000000000700 · Cited by 170 · see citing works
Time to test antibacterial therapy in Alzheimer’s disease
Panza, F., Lozupone, M., Solfrizzi, V., Watling, M., & Imbimbo, B. P. (2019) · Brain · doi:10.1093/brain/awz244 · Cited by 161 · see citing works
Exercise suppresses neuroinflammation for alleviating Alzheimer’s disease
Wang, M., Zhang, H., Liang, J., Huang, J., & Chen, N. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02753-6 · Cited by 149 · see citing works
“In AD and other neurodegenerative diseases, the function of TREM2-mediated activation of microglia depends on the stage of disease progression and the type of microglia [74].”
BackgroundUrolithin A improves Alzheimer's disease cognition and restores mitophagy and lysosomal functions
Hou, Y., Chu, X., Park, J., Zhu, Q., Hussain, M., Li, Z., Madsen, H. B., Yang, B., Wei, Y., Wang, Y., et al. (2024) · Alzheimer's & Dementia · doi:10.1002/alz.13847 · Cited by 145 · see citing works
A unifying hypothesis for Alzheimer's disease: from plaques to neurodegeneration
Edwards, F. A. (2019) · Trends in Neurosciences · doi:10.1016/j.tins.2019.03.003 · Cited by 140 · see citing works
“The recent advances in our knowledge of genetic risk factors for Alzheimer’s disease [82], 426 and advances in early detection of it [83-85], raise the hope that it may be possible to 427 identify people who have rising amyloidβ long before cognitive deficits reach a diagnosable 428 level[5].”
BackgroundTransgenic Mouse Models of Alzheimer’s Disease: An Integrative Analysis
Sanchez-Varo, R. M., Mejias‐Ortega, M., Fernandez-Valenzuela, J. J., Nuñez‐Diaz, C., Cáceres-Palomo, L., Vegas‐Gomez, L., Sánchez‐Mejías, E., Trujillo‐Estrada, L., García‐León, J. A., Moreno‐González, I., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23105404 · Cited by 130 · see citing works
Alzheimer's disease: Updated multi-targets therapeutics are in clinical and in progress
Sang, Z., Wang, K., Dong, J., & Tang, L. (2022) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2022.114464 · Cited by 127 · see citing works
Frontotemporal Dementia, Where Do We Stand? A Narrative Review
Antonioni, A., Raho, E. M., Lopriore, P., Pace, A. P., Latino, R. R., Assogna, M., Mancuso, M., Gragnaniello, D., Granieri, E., Pugliatti, M., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241411732 · Cited by 133 · see citing works
“Protein triggering receptor expressed on myeloid cells 2 (TREM2): TREM2 is an innate immunity receptor that characterises microglial cells, and its expression increases during phagocytosis, response to neuronal damage, and chemotaxis [223].”
BackgroundRehman, M. U., Sehar, N., Dar, N. J., Khan, A., Arafah, A., Rashid, S., Rashid, S. M., & Ganaie, M. A. (2023) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2022.104961 · Cited by 130 · see citing works
Rivera, S., García‐González, L., Khrestchatisky, M., & Baranger, K. (2019) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-019-03178-2 · Cited by 112 · see citing works
“Of note, some authors have reported association between TREM2 variants and increased risk of PD, although the data are not conclusive for the moment [134].”
BackgroundSystematic Pan-Cancer Analysis Identifies TREM2 as an Immunological and Prognostic Biomarker
Cheng, X. M., Wang, X., Nie, K., Cheng, L., Zhang, Z., Hu, Y., & Peng, W. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.646523 · Cited by 111 · see citing works
“TREM2 affects the prognosis and clinical phenotype of tumors through its role in tumor-associated macrophages (TAMs) and myeloidderived suppressor cells (MDSCs) (7, 8).”
BackgroundDistinct Signaling Pathways Regulate TREM2 Phagocytic and NFκB Antagonistic Activities
Yao, H., Coppola, K., Schweig, J. E., Crawford, F., Mullan, M., & Paris, D. (2019) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2019.00457 · Cited by 110 · see citing works
Hoogmartens, J., Cacace, R., & Broeckhoven, C. V. (2021) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12155 · Cited by 101 · see citing works
Advances and considerations in AD tau-targeted immunotherapy
Bittar, A., Bhatt, N. N., & Kayed, R. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.104707 · Cited by 105 · see citing works
“Overall, PET imaging could be highly utilized in combination with CSF and blood biomarkers in clinical studies in smaller and specific populations like those with TREM2 variants (Gratuze et al., 2018; Carmona et al., 2018), APOE4 carriers (Safieh et al.”
Genomics of Alzheimer’s disease implicates the innate and adaptive immune systems
Li, Y., Laws, S. M., Miles, L. A., Wiley, J. S., Huang, X., Masters, C. L., & Gu, B. J. (2021) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-021-03986-5 · Cited by 93 · see citing works
Amyloid-beta uptake by blood monocytes is reduced with ageing and Alzheimer’s disease
Chen, S.-H., Tian, D.-Y., Shen, Y.-Y., Cheng, Y., Fan, D.-Y., Sun, H.-L., He, C.-Y., Sun, P.-Y., Bu, X.-L., Zeng, F., et al. (2020) · Translational Psychiatry · doi:10.1038/s41398-020-01113-9 · Cited by 89 · see citing works
Mesenchymal Stem Cell Therapy for Alzheimer's Disease
Hernández, A. E., & García, E. (2021) · Stem Cells International · doi:10.1155/2021/7834421 · Cited by 74 · see citing works
“This mutation affects the behavior of microglial cells, especially their response to Aβ plaques [17].”
BackgroundABC transporters: human disease and pharmacotherapeutic potential
Moore, J. M., Bell, E. L., Hughes, R. O., & Garfield, A. S. (2022) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2022.11.001 · Cited by 83 · see citing works
Microvascular Alterations in Alzheimer's Disease
Steinman, J., Sun, H., & Feng, Z. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2020.618986 · Cited by 82 · see citing works
“TREM2 mutation reduces microglial clustering around plaques in mice and humans, resulting in enhanced neuritic dystrophy (Carmona et al., 2018).”
BackgroundLista, S., Imbimbo, B. P., Grasso, M., Fidilio, A., Emanuele, E., Minoretti, P., López-Ortiz, S., Martín-Hernández, J., Gabelle, A., Caruso, G., et al. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03163-y · Cited by 81 · see citing works
“This underscores the need to investigate various ethnic populations to discover specific disease risk variants and explore potential associations between these variants and specific disease phenotypes [50].”
BackgroundInfluentialThe Ubiquitin System in Alzheimer’s Disease
Harris, L. D., Jasem, S., & Licchesi, J. D. F. (2020) · Advances in experimental medicine and biology · doi:10.1007/978-3-030-38266-7_8 · Cited by 76 · see citing works
Bayazid, A. B., & Lim, B. O. (2022) · Nutrients · doi:10.3390/nu14235132 · Cited by 78 · see citing works
“Moreover, exogenous Aβ could develop AD by triggering a receptor expressed on myeloid cells 2 (TREM2) and formi g senile plaques [103,104].”
BackgroundInfluentialTREM2: A new player in the tumor microenvironment
Molgora, M., Liu, Y. A., Colonna, M., & Cella, M. (2023) · Seminars in Immunology · doi:10.1016/j.smim.2023.101739 · Cited by 76 · see citing works
Gadhave, K., Kumar, D., Uversky, V. N., & Giri, R. (2020) · Medicinal Research Reviews · doi:10.1002/med.21719 · Cited by 70 · see citing works
“On the other hand, mutations in APOEε4 allele represent a genetic risk factor of LOAD.28 The collapse of various neurotransmitter systems, such as those found in cholinergic, glutaminergic, and serotonergic neurons, might lead to the neurochemical abnormalities in the brain that end with the AD development.29–32 Altho…”
BackgroundInfluentialRecent Advances in the Genetics of Frontotemporal Dementia
Sirkis, D. W., Geier, E. G., Bonham, L. W., Karch, C. M. M., & Yokoyama, J. S. (2019) · Current Genetic Medicine Reports · doi:10.1007/s40142-019-0160-6 · Cited by 68 · see citing works
Low-Dose Ionizing Radiation Modulates Microglia Phenotypes in the Models of Alzheimer’s Disease
Kim, S.-J., Chung, H., Mai, H. N., Nam, Y., Shin, S. J., Park, Y., Chung, M. J., Lee, J. K., Rhee, H. Y., Jahng, G., et al. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21124532 · Cited by 66 · see citing works
“Triggering receptor expressed on myeloid cells 2 (TREM2) is a type of membrane protein present on the surface of microglia and plays key roles in proliferation and survival of microglia, and secretion of inflammatory cytokines from microglia [21].”
BackgroundMetabolic Regulation of Glia and Their Neuroinflammatory Role in Alzheimer's Disease
Kumari, P., Sood, A., & Fernandes, V. (2021) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-021-01147-7 · Cited by 67 · see citing works
Passive immunotherapy for Alzheimer's disease
Guo, X., Li, Y., Zhang, D., & Zhao, Y. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102192 · Cited by 66 · see citing works
“TREM2 variants such as R47H significantly increase AD risk (Guerreiro et al., 2013; Jonsson et al., 2013), probably due to partial loss of function (Carmona et al., 2018).”
Different pattern of CSF glial markers between dementia with Lewy bodies and Alzheimer’s disease
Morenas‐Rodríguez, E., Alcolea, D. A., Suárez‐Calvet, M., Muñoz, L., Vilaplana, E., Sala, I., Subirana, A., Querol‐Vilaseca, M., Carmona‐Iragui, M., Illán‐Gala, I., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-44173-8 · Cited by 58 · see citing works
TREM2 Insufficiency Protects against Pulmonary Fibrosis by Inhibiting M2 Macrophage Polarization
Luo, Q., Deng, D., Li, Y., Shi, H., Zhao, J., Qian, Q., Wang, W., Cai, J., Yu, W., & Liu, J. (2023) · International Immunopharmacology · doi:10.1016/j.intimp.2023.110070 · Cited by 61 · see citing works
The Immune System's Role in the Consequences of Mild Traumatic Brain Injury (Concussion)
Verboon, L. N., Patel, H. C., & Greenhalgh, A. D. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.620698 · Cited by 58 · see citing works
“Moreover, homozygous Trem2 variants have been proposed to be causal for Frontotemporal Dementia (FTD) or linked to increased FTD risk (111).”
BackgroundJabbari, E., Woodside, J., Guo, T., Magdalinou, N. K., Chelban, V., Athauda, D. S., Lees, A. J., Foltynie, T., Houlden, H., Church, A., et al. (2019) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2018-320151 · Cited by 56 · see citing works
Role of TREM2 in Alzheimer’s Disease: A Long Road Ahead
Kulkarni, B., Kumar, D., Martins, N. A., & Sellamuthu, S. (2021) · Molecular Neurobiology · doi:10.1007/s12035-021-02477-9 · Cited by 52 · see citing works
“This domain binds to polyanionic ligands, such as bacterial polysaccharides, phospholipids [24], and DNA [11].”
BackgroundInfluentialGenetic Phenotypes of Alzheimer’s Disease: Mechanisms and Potential Therapy
Quan, M., Cao, S., Wang, Q., Wang, S., & Jia, J. (2023) · Phenomics · doi:10.1007/s43657-023-00098-x · Cited by 60 · see citing works
“The association of R47H with elevated LOAD risk was successfully replicated in European-American, Spanish, French-Caucasian, North American-Caucasian and AfricanAmerican populations, but failed in Han Chinese population (Carmona et al. 2018).”
BackgroundSingle-Cell Quantification of mRNA Expression in The Human Brain
Jolly, S., Lang, V., Koelzer, V. H., Frigerio, C. S., Magno, L., Salinas, P. C., Whiting, P. J., & Palomer, E. (2019) · Scientific Reports · doi:10.1038/s41598-019-48787-w · Cited by 53 · see citing works
Macrophages protect against sensory axon loss in peripheral neuropathy
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Markers of aging: Unsupervised integrated analyses of the human plasma proteome
Coenen, L., Lehallier, B., de Vries, H. E., & Middeldorp, J. (2023) · Frontiers in Aging · doi:10.3389/fragi.2023.1112109 · Cited by 50 · see citing works
“variants are a well-known risk factor for Alzheimer’s disease and other neurodegenerative diseases (Carmona et al., 2018), in individuals who deviate from their chronological age.”
BackgroundSpatiotemporal patterns of gene expression around implanted silicon electrode arrays
Thompson, C. H., Saxena, A., Heelan, N., Salatino, J. W., & Purcell, E. K. (2021) · Journal of Neural Engineering · doi:10.1088/1741-2552/abf2e6 · Cited by 47 · see citing works
The role of TREM2 in Alzheimer’s disease: from the perspective of Tau
Huang, W., Huang, J., Huang, N., & Luo, Y. (2023) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2023.1280257 · Cited by 49 · see citing works
Malvaso, A., Gatti, A., Negro, G., Calatozzolo, C., Medici, V., & Poloni, T. E. (2023) · Cells · doi:10.3390/cells12242824 · Cited by 51 · see citing works
“TREM2 mutations are infrequent but determine a neurodegenerative risk similar to that of the APOE ε 4 allele ( APOE4 ), the most important genetic risk factor for late-onset AD [97–99].”
BackgroundKnapskog, A., Henjum, K., Idland, A., Eldholm, R. S., Persson, K., Saltvedt, I. T., Watne, L. O., Engedal, K., & Nilsson, L. N. G. (2020) · Scientific Reports · doi:10.1038/s41598-020-72878-8 · Cited by 51 · see citing works
Review: Fluid biomarkers for frontotemporal dementias
Zetterberg, H., van Swieten, J. C., Boxer, A. L., & Rohrer, J. D. (2019) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12530 · Cited by 48 · see citing works
Can mouse models mimic sporadic Alzheimer’s disease?
Humpel, C., & Foidl, B. (2020) · Neural Regeneration Research · doi:10.4103/1673-5374.266046 · Cited by 56 · see citing works
“Arg47His variant of TREM2 have been tested in a mouse model of amyloidosis (Carmona et al., 2018; Song et al., 2018), which may reflect a form of late onset sporadic AD.”
BackgroundWhite matter-associated microglia: New players in brain aging and neurodegenerative diseases
Ahn, K., Lee, S., & Mook‐Jung, I. (2022) · Ageing Research Reviews · doi:10.1016/j.arr.2022.101574 · Cited by 46 · see citing works
“important genetic risk factor for diverse neurodegenerative disorders, including AD (Carmona et al., 2018).”
BackgroundTranscriptional Networks of Microglia in Alzheimer’s Disease and Insights into Pathogenesis
Chew, G., & Petretto, E. G. (2019) · Genes · doi:10.3390/genes10100798 · Cited by 45 · see citing works
Genetic architecture of common non-Alzheimer’s disease dementias
Guerreiro, R. J., Gibbons, E., Tábuas‐Pereira, M., Kun‐Rodrigues, C., Cordeiro, G., & Brás, J. (2020) · Neurobiology of Disease · doi:10.1016/j.nbd.2020.104946 · Cited by 46 · see citing works
Self-citationChallenge accepted: uncovering the role of rare genetic variants in Alzheimer’s disease
Khani, M., Gibbons, E., Bras, J., & Guerreiro, R. (2022) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00505-9 · Cited by 39 · see citing works
“After these studies, associations have been reported across different populations [28], and in a large LOAD family (n=21 affected individuals), p.”
BackgroundSelf-citationDuggan, M. R., Peng, Z., Sipilä, P. N., Lindbohm, J. V., Chen, J., Lü, Y., Davatzikos, C. A., Erus, G., Hohman, T. J., Andrews, S. J., et al. (2024) · Nature Aging · doi:10.1038/s43587-024-00682-4 · Cited by 42 · see citing works
“42)) and several proteins that we recently showed to be associated with inflammatory dietary patterns and adverse neurocognitive outcomes (CDCP1 and CCL3 (ref.”
Tajbakhsh, A., Read, M. I., Barreto, G. E., Ávila-Rodriguez, M., Hayat, S. M. G., & Sahebkar, A. (2021) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2021.173873 · Cited by 41 · see citing works
COVID-19 as a Risk Factor for Alzheimer’s Disease
Golzari-Sorkheh, M., Weaver, D. F., & Reed, M. A. (2023) · Journal of Alzheimer's Disease · doi:10.3233/jad-220800 · Cited by 39 · see citing works
Maintenance of mitochondrial homeostasis for Alzheimer's disease: Strategies and challenges
Han, Y., Liu, D., Cheng, Y. H., Ji, Q., Liu, M., Zhang, B., & Zhou, S. (2023) · Redox Biology · doi:10.1016/j.redox.2023.102734 · Cited by 40 · see citing works
“Blocking the activity of this pathway in mouse models of AD has shown to protect synapses by preventing synaptic degeneration and memory impairment [31,32].”
BackgroundFirdaus, Z., & Li, X. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25042320 · Cited by 43 · see citing works
“Within each population, these variants cause a roughly 2–4-fold increase in the risk of developing LOAD [148].”
BackgroundRoles of TREM2 in the Pathological Mechanism and the Therapeutic Strategies of Alzheimer's Disease
Lin, M., Yu, J., Zhang, W., Lao, F., & Huang, H. (2024) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2024.164 · Cited by 41 · see citing works
Therapeutic potential of ADAM10 modulation in Alzheimer’s disease: a review of the current evidence
Khezri, M. R., Mohebalizadeh, M., & Ghasemnejad‐Berenji, M. (2023) · Cell Communication and Signaling · doi:10.1186/s12964-023-01072-w · Cited by 41 · see citing works
“Some studies have also shown that alleles in the TREM2 gene are 3–5 times more likely to develop AD [12].”
BackgroundČuperlović‐Culf, M., & Badhwar, A. (2019) · Expert Opinion on Drug Discovery · doi:10.1080/17460441.2020.1674808 · Cited by 40 · see citing works
“variations in microglia’s immune receptor genes increase the risk of late-onset AD [21].”
BackgroundAbrogation of type-I interferon signalling alters the microglial response to Aβ1–42
Moore, Z., Mobilio, F., Walker, F. R., Taylor, J. M., & Crack, P. J. (2020) · Scientific Reports · doi:10.1038/s41598-020-59917-0 · Cited by 38 · see citing works
Emerging genetic complexity and rare genetic variants in neurodegenerative brain diseases
Perrone, F., Cacace, R., van der Zee, J., & Broeckhoven, C. V. (2021) · Genome Medicine · doi:10.1186/s13073-021-00878-y · Cited by 37 · see citing works
“Rare heterozygous TREM2 mutations that increase the risk for developing disease have been described in AD, FTD, ALS, and PD [51], though their role in disease pathogenesis needs further follow-up.”
BackgroundInfluentialWijesinghe, P., Whitmore, C. A., Campbell, M., Li, C. H., Tsuyuki, M., To, E. C., Haynes, J. R., Pham, W. N., & Matsubara, J. A. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1107436 · Cited by 36 · see citing works
“Moreover, dysfunction of innate immunity, mainly involving microglia and peripheral myeloid cells, has been suggested as a critical reason in the development of AD (Bradshaw et al., 2013; Vasquez et al., 2013; Carmona et al., 2018).”
BackgroundTargeting epigenetics: A novel promise for Alzheimer’s disease treatment
Jeremic, D., Jiménez‐Díaz, L., & Navarro‐López, J. D. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.102003 · Cited by 36 · see citing works
Zhao, L., Yu, S., Li, L., Zhou, C., Wang, L., Tang, S., Gu, N., Zhang, Z., Huang, Z., Chen, H., et al. (2024) · Clinical and Translational Medicine · doi:10.1002/ctm2.1665 · Cited by 34 · see citing works
The vexing complexity of the amyloidogenic pathway
Castro, M., Hadziselimovic, A., & Sanders, C. R. (2019) · Protein Science · doi:10.1002/pro.3606 · Cited by 36 · see citing works
Schwartz, M., Ramos, J. M. P., & Ben-Yehuda, H. (2020) · The Journal of Immunology · doi:10.4049/jimmunol.1900844 · Cited by 31 · see citing works
Tucker, A. E., Pauneto, C. D. M. A., Barnett, A., & Coleman, L. G. (2022) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2022.886634 · Cited by 33 · see citing works
Alzheimer's disease – Where do we go from here?
Борисович, Б. И. (2022) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2022.08.075 · Cited by 34 · see citing works
Edwin, T. H., Henjum, K., Nilsson, L. N. G., Watne, L. O., Persson, K., Eldholm, R. S., Saltvedt, I. T., Halaas, N. B., Selbæk, G., Engedal, K., et al. (2020) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12128 · Cited by 35 · see citing works
Protein and Gene Delivery Systems for Neurodegenerative Disorders: Where Do We Stand Today?
Siafaka, P. I., Okur, M. E., Dilsiz, P., Çağlar, E. Ş., Özgenç, E., Gündoğdu, E., Köprülü, R. E. P., Karantas, I. D., & Okur, N. Ü. (2022) · Pharmaceutics · doi:10.3390/pharmaceutics14112425 · Cited by 34 · see citing works
“AD seems to deactivate APP, presenilin-1 (PSEN1), and presenilin-2, presenting a complex genetic architecture with rare, highly penetrating mutations in the genes coding for (PSEN2) [61].”
BackgroundRusty Microglia: Trainers of Innate Immunity in Alzheimer's Disease
Sfera, A., Gradini, R., Cummings, M., Diaz, E. L., Price, A. I., & Osorio, C. P. (2018) · Frontiers in Neurology · doi:10.3389/fneur.2018.01062 · Cited by 32 · see citing works
Hernández, E. R., Sánchez-Maldonado, C., Chávez, M. Á. M., Hernández-Zimbrón, L. F., Patricio-Martínez, A., Zenteno, E., & Limón, I. D. (2020) · Expert Review of Neurotherapeutics · doi:10.1080/14737175.2020.1750955 · Cited by 31 · see citing works
Osteoporosis and Dementia: Establishing a Link
Lary, C. W., Rosen, C. J., & Kiel, D. P. (2021) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.4431 · Cited by 31 · see citing works
“This gene is also known to regulate osteoclastogenesis((22)) and is important in AD, especially in the microglia.((23,24)) The gene FNDC5, or Irisin, which results through cleavage of the protein precursor, has been shown to have exercise-mediated effects on bone((25-27)) and to have important effects in AD.”
BackgroundWang, Z., Zhang, Q., Lin, J.-R., Jabalameli, M. R., Mitra, J., Nguyen, N., & Zhang, Z. D. (2021) · Scientific Reports · doi:10.1038/s41598-021-99352-3 · Cited by 29 · see citing works
Thyroid dysfunction and Alzheimer's disease, a vicious circle
Li, Z., & Liu, J. (2024) · Frontiers in Endocrinology · doi:10.3389/fendo.2024.1354372 · Cited by 29 · see citing works
Mani, S., Wasnik, S., Shandilya, C., Srivastava, V., Khan, S., & Singh, K. K. (2025) · Frontiers in Aging · doi:10.3389/fragi.2025.1615764 · Cited by 28 · see citing works
Qin, Q., Wan, H., Wang, D., Li, J., Qu, Y., Zhao, J., Li, J., & Xue, Z. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.892493 · Cited by 29 · see citing works
“Previous studies had confirmed that TREM2 mutations increased the risk of Alzheimer’s disease (AD) (Carmona et al., 2018), whereas the association of TREM2 mutations with PD remains controversial (Benitez and Cruchaga, 2013; Rayaprolu et al.”
ResultNeuroinflammatory Pathways in the ALS-FTD Continuum: A Focus on Genetic Variants
Marchi, F. D., Tondo, G., Corrado, L., Menegon, F., Aprile, D., Anselmi, M., D’Alfonso, S., Comi, C., & Mazzini, L. (2023) · Genes · doi:10.3390/genes14081658 · Cited by 28 · see citing works
“However, a large amount of data suggests the involvement of TREM2 in AD and other neurodegenerative dementia [124].”
BackgroundPsilocybin for the treatment of Alzheimer’s disease
Zheng, S., Ma, R., Yang, Y., & Li, G. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1420601 · Cited by 23 · see citing works
Zhou, W., He, J., Shen, G., Liu, Y., Zhao, P., & Li, J. (2024) · Cell Death and Disease · doi:10.1038/s41419-024-07002-z · Cited by 28 · see citing works
Review: Molecular pathology of frontotemporal lobar degenerations
Borroni, B., Alberici, A., & Buratti, E. (2018) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12534 · Cited by 26 · see citing works
The Potential Roles of Redox Enzymes in Alzheimer’s Disease: Focus on Thioredoxin
Jia, J., Zeng, X., Xu, G., & Wang, Z. (2021) · ASN NEURO · doi:10.1177/1759091421994351 · Cited by 26 · see citing works
“Triggering receptor expressed in myeloid cells 2 (TREM2) is a microglial cell surface receptor central to proliferation, survival, and phagocytosis of microglia (Carmona et al., 2018).”
BackgroundNeurodegenerative phagocytes mediate synaptic stripping in Neuro-HIV
Liberto, G. D., Égervári, K., Kreutzfeldt, M., Schürch, C. M., Hewer, E., Wagner, I., Pasquier, R. D., & Merkler, D. (2022) · Brain · doi:10.1093/brain/awac102 · Cited by 26 · see citing works
“microglia, more neuritic dystrophy and increased risk of late-onset Alzheimer’s disease, suggesting a protective role of this receptor in disease development.(75) In mice, TREM2-deficient microglia do not exhibit the typical increase in expression of HLA markers or DAM markers and are locked into amore homeostatic phe…”
Lu, Y., Huang, X., Liang, W., Li, Y., Xing, M., Pan, W., Zhang, Y., Wang, Z., & Song, W. (2023) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2023.104688 · Cited by 26 · see citing works
“All of these functions of microglia are compromised in AD (4).”
BackgroundDoes the CD33 rs3865444 Polymorphism Confer Susceptibility to Alzheimer’s Disease?
Siokas, V., Aslanidou, P., Aloizou, A., Peristeri, E., Stamati, P., Liampas, I., Arseniou, S., Drakoulis, N., Aschner, M., Tsatsakis, A. M., et al. (2020) · Journal of Molecular Neuroscience · doi:10.1007/s12031-020-01507-w · Cited by 25 · see citing works
“The ε4 allele of Apolipoprotein E (APOE) is a genetic risk factor consistently implicated in AD (Carmona et al. 2018; Panegyres and Chen 2013), although it can only partially account for ADmanifestation (Jiang et al.”
BackgroundQuinoline-Pyrazole Scaffold as a Novel Ligand of Galectin-3 and Suppressor of TREM2 Signaling
Gabr, M. T., Rehman, A. U., & Chen, H. (2020) · ACS Medicinal Chemistry Letters · doi:10.1021/acsmedchemlett.0c00330 · Cited by 23 · see citing works
Chib, S., Dutta, B. J., Chalotra, R., Abubakar, M., Kumar, P., Singh, T. G., & Singh, R. (2024) · Phytotherapy Research · doi:10.1002/ptr.8406 · Cited by 24 · see citing works
“…Binding Clathrin Assembly Brotein (PICALM), (Harold et al. 2009; Lambert et al. 2009), Trigging Receptor Expressed on Myeloid Cells-2 (TREM2) (Carmona et al. 2018), Sortilin-related Receptor gene 1 (SORL1) (Yin, Yu, and Tan 2015), Phospholipase D3 PLD3 (Nackenoff et al. 2021), Presenilin 1,2…”
Huang, Y.-Y., & Fang, W. (2025) · npj Precision Oncology · doi:10.1038/s41698-025-01152-9 · Cited by 25 · see citing works
Oblak, A. L., Kotredes, K. P., Pandey, R. S., Reagan, A. M., Ingraham, C., Perkins, B., Lloyd, C., Baker, D., Lin, P. B., Soni, D. M., et al. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.886575 · Cited by 23 · see citing works
“Although the precise effects of the M28L variant have not yet been elucidated, like TREM2, PLCG2 is expressed by microglia and plays a role in amyloid clearance (Carmona et al., 2018).”
BackgroundWang, R., Zhan, Y., Zhu, W., Yang, Q., & Pei, J. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1407980 · Cited by 24 · see citing works
“Genetic variations significantly affect TREM2’s structure and function, and a GWAS has identified 46 TREM2 variants linked with AD that increase the risk of late-onset AD (Carmona et al., 2018).”
BackgroundThe double-edged role and therapeutic potential of TREM2 in atherosclerosis
Zhu, B., Liu, Y., & Peng, D. (2024) · Biomarker Research · doi:10.1186/s40364-024-00675-w · Cited by 26 · see citing works
TREM2 in Neurodegenerative Disorders: Mutation Spectrum, Pathophysiology, and Therapeutic Targeting
Yang, H.-W., Kim, D., Yang, Y., Bagyinszky, E., & An, S. S. A. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26157057 · Cited by 25 · see citing works
“These selective binding differences may help to explain how Arg62His could affect microglial activity and offer valuable insights into AD pathogenesis [17,107,137].”
- 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
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2018-08
- Volume
- 17
- Issue
- 8
- Pages
- 721-730
- ISSN
- 1474-4422 (ISSN-L)
- 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 · 2012: 1
- FWCI
- 2.18
- Type
- journal article
- Language
- en
- Open access
- green
- discovery.ucl.ac.uk
- Licence
- 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
- Health Sciences › Medicine › Physiology › 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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