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Depletion of NK Cells Improves Cognitive Function in the Alzheimer Disease Mouse Model
Open accessAbstract
Despite mounting evidence suggesting the involvement of the immune system in regulating brain function, the specific role of immune and inflammatory cells in neurodegenerative diseases remain poorly understood. In this study, we report that depletion of NK cells, a type of innate lymphocytes, alleviates neuroinflammation, stimulates neurogenesis, and improves cognitive function in a triple-transgenic Alzheimer disease (AD) mouse model. NK cells in the brains of triple-transgenic AD mouse model (3xTg-AD) mice exhibited an enhanced proinflammatory profile. Depletion of NK cells by anti-NK1.1 Abs drastically improved cognitive function of 3xTg-AD mice. NK cell depletion did not affect amyloid β concentrations but enhanced neurogenesis and reduced neuroinflammation. Notably, in 3xTg-AD mice depleted of NK cells, microglia demonstrated a homeostatic-like morphology, decreased proliferative response and reduced expression of neurodestructive proinflammatory cytokines. Together, our results suggest a proinflammatory role for NK cells in 3xTg-AD mice and indicate that targeting NK cells might unlock novel strategies to combat AD.
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“Such discrepancies may stem from differences in experimental models, including differences in NK cell deficiency which could contribute to the divergent outcomes observed [111].”
From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [111]
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Cites
Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources
Huang, D. W., Sherman, B. T., & Lempicki, R. A. (2009) · Nature Protocols · doi:10.1038/nprot.2008.211 · Cited by 35,890 · cited 1×
“Gene pathway analysis was performed with the Database for Annotation, Visualization and Integrated Discovery (30, 31).”
MethodHuang, D. W., Sherman, B. T., & Lempicki, R. A. (2009) · Nucleic Acids Research · doi:10.1093/nar/gkn923 · Cited by 14,108 · cited 2×
“2009 Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources.”
MethodMorris water maze: procedures for assessing spatial and related forms of learning and memory
Vorhees, C. V., & Williams, M. T. (2006) · Nature Protocols · doi:10.1038/nprot.2006.116 · Cited by 4,629 · cited 1×
“We used a Morris Water Maze test (47) to examine the cognitive function of 3xTg-AD mice that were treated with anti-NK1.”
MethodTriple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
Oddo, S., Caccamo, A., Shepherd, J. D., Murphy, M. P., Golde, T. E., Kayed, R., Metherate, R., Mattson, M. P., Akbari, Y., & LaFerla, F. M. (2003) · Neuron · doi:10.1016/s0896-6273(03)00434-3 · Cited by 4,126
Microglia in Alzheimer’s disease
Hansen, D. V., Hanson, J. E., & Sheng, M. (2018) · Journal of Cell Biology · doi:10.1083/jcb.201709069 · Cited by 1,935
Neuroinflammation in Alzheimer's disease: current evidence and future directions
Calsolaro, V., & Edison, P. (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.02.010 · Cited by 1,726
Moreno-Jiménez, E. P., Flor-García, M., Terreros-Roncal, J., Rábano, A., Cafini, F., Pallas-Bazarra, N., Ávila, J., & Llorens-Martín, M. (2019) · Nature Medicine · doi:10.1038/s41591-019-0375-9 · Cited by 1,577 · cited 3×
“Adult neurogenesis was diminished in the inflamed brains of AD patients and transgenic AD mouse models, which might contribute to declined cognitive function in AD (48, 62).”
BackgroundBillings, L. M., Oddo, S., Green, K. N., McGaugh, J. L., & LaFerla, F. M. (2005) · Neuron · doi:10.1016/j.neuron.2005.01.040 · Cited by 1,294
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 · cited 1×
“These microglia also exhibited intact expression of Trem2, a surface receptor that plays an essential role in promoting microglial metabolic fitness (63).”
BackgroundRole of Pro-Inflammatory Cytokines Released from Microglia in Neurodegenerative Diseases
Smith, J. A., Das, A., Ray, S. K., & Banik, N. L. (2012) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2011.10.004 · Cited by 1,165
Natural Killer Cells: Development, Maturation, and Clinical Utilization
Abel, A. M., Yang, C., Thakar, M. S., & Malarkannan, S. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.01869 · Cited by 1,150 · cited 2×
“NK cells are innate cytotoxic lymphocytes that can be rapidly induced to secrete cytotoxic molecules and inflammatory cytokines such as granzymes, cathepsins, perforins, IFNγ and TNFα (20).”
BackgroundThe Alzheimer's Disease-Associated Amyloid β-Protein Is an Antimicrobial Peptide
Soscia, S. J., Kirby, J. E., Washicosky, K. J., Tucker, S. M., Ingelsson, M., Hyman, B., Burton, M. A., Goldstein, L. E., Duong, S., Tanzi, R. E., et al. (2010) · PLoS ONE · doi:10.1371/journal.pone.0009505 · Cited by 1,060
Shen, Q., Wang, Y., Kokovay, E., Lin, G., Chuang, S.-M., Goderie, S. K., Roysam, B., & Temple, S. (2008) · Cell stem cell · doi:10.1016/j.stem.2008.07.026 · Cited by 1,027 · cited 1×
“Neurogenesis remains active in the SVZ, and to a less degree, in the hippocampus regions of healthy adult humans and mice (48, 61).”
Kumar, D. K. V., Choi, S. H., Washicosky, K. J., Eimer, W. A., Tucker, S., Ghofrani, J., Lefkowitz, A., McColl, G., Goldstein, L. E., Tanzi, R. E., et al. (2016) · Science Translational Medicine · doi:10.1126/scitranslmed.aaf1059 · Cited by 971
A critical appraisal of amyloid-β-targeting therapies for Alzheimer disease
Panza, F., Lozupone, M., Logroscino, G., & Imbimbo, B. P. (2019) · Nature Reviews Neurology · doi:10.1038/s41582-018-0116-6 · Cited by 965
Neutrophils promote Alzheimer's disease–like pathology and cognitive decline via LFA-1 integrin
Zenaro, E., Pietronigro, E., Bianca, V. D., Piacentino, G., Marongiu, L., Budui, S., Turano, E., Rossi, B., Angiari, S., Dusi, S., et al. (2015) · Nature Medicine · doi:10.1038/nm.3913 · Cited by 865 · cited 3×
“In addition, depletion of neutrophils reduces Aβ burdens in mouse models of Alzheimer’s disease (14); whereas depletion of NK cells improves cognitive function without affecting Aβ burdens (Fig.”
BackgroundInfluentialCrinier, A., Milpied, P., Escalière, B., Piperoglou, C., Galluso, J., Balsamo, A., Spinelli, L., Cervera-Marzal, I., Ebbo, M., Girard-Madoux, M., et al. (2018) · Immunity · doi:10.1016/j.immuni.2018.09.009 · Cited by 470
Marsh, S. E., Abud, E. M., Lakatos, A., Karimzadeh, A., Yeung, S. T., Davtyan, H., Fote, G. M., Lau, L., Weinger, J. G., Lane, T. E., et al. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1525466113 · Cited by 411 · cited 1×
“Genetic deletion of lymphocytes in 5xFAD mice resulted in accelerated amyloid pathology and exacerbated neuroinflammation (15).”
BackgroundCysteine Cathepsins and Their Extracellular Roles: Shaping the Microenvironment
Vidak, E., Javoršek, U., Vizovišek, M., & Turk, B. (2019) · Cells · doi:10.3390/cells8030264 · Cited by 408
Human CD56bright NK Cells: An Update
Michel, T., Poli, A., Cuapio, A., Briquemont, B., Iserentant, G., Ollert, M. W., & Zimmer, J. (2016) · The Journal of Immunology · doi:10.4049/jimmunol.1502570 · Cited by 395 · cited 1×
“Certain subsets of NK cells may produce multiple inflammatory cytokines and chemokines (21).”
BackgroundRodríguez, J. J., Jones, V. C., Tabuchi, M., Allan, S. M., Knight, E. M., LaFerla, F. M., Oddo, S., & Verkhratsky, A. (2008) · PLoS ONE · doi:10.1371/journal.pone.0002935 · Cited by 377 · cited 1×
“Adult neurogenesis was diminished in the inflamed brains of AD patients and transgenic AD mouse models, which might contribute to declined cognitive function in AD (47, 61).”
BackgroundRegulatory T cells delay disease progression in Alzheimer-like pathology
Dansokho, C., Ahmed, D. A., Aïd, S., Toly‐Ndour, C., Chaigneau, T., Calle, V., Cagnard, N., Holzenberger, M., Piaggio, E., Aucouturier, P., et al. (2016) · Brain · doi:10.1093/brain/awv408 · Cited by 375
The identity and function of microglia in neurodegeneration
Song, W. M., & Colonna, M. (2018) · Nature Immunology · doi:10.1038/s41590-018-0212-1 · Cited by 308
Human and Mouse Granzyme A Induce a Proinflammatory Cytokine Response
Metkar, S. S., Menaa, C., Pardo, J., Wang, B., Wallich, R., Freudenberg, M. A., Kim, S. H., Raja, S. M., Shi, L. F., Simon, M. M., et al. (2008) · Immunity · doi:10.1016/j.immuni.2008.08.014 · Cited by 304
Neuroinflammation in mild cognitive impairment and Alzheimer’s disease: A meta-analysis
Bradburn, S., Murgatroyd, C., & Ray, N. J. (2019) · Ageing Research Reviews · doi:10.1016/j.arr.2019.01.002 · Cited by 277
Granzyme B-Dependent Proteolysis Acts as a Switch to Enhance the Proinflammatory Activity of IL-1α
Afonina, I. S., Tynan, G. A., Logue, S. E., Cullen, S. P., Bots, M. L., Lüthi, A. U., Reeves, E. P., McElvaney, N. G., Medema, J. P., Lavelle, E. C., et al. (2011) · Molecular Cell · doi:10.1016/j.molcel.2011.07.037 · Cited by 275
Microglia in Alzheimer's Disease: Exploring How Genetics and Phenotype Influence Risk
McQuade, A., & Blurton-Jones, M. (2019) · Journal of Molecular Biology · doi:10.1016/j.jmb.2019.01.045 · Cited by 244
Microglia in Alzheimer’s Disease: Activated, Dysfunctional or Degenerative
Navarro, V., Sanchez-Mejias, E., Jimenez, S., Muñoz-Castro, C., Sanchez-Varo, R., Davila, J. C., Vizuete, M., Gutierrez, A., & Vitorica, J. (2018) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00140 · Cited by 229 · cited 1×
“Chronic microglial activation in AD is demonstrated by multiple dynamic changes including altered morphology, abnormal proliferation, and increased secretion of neurotoxic pro-inflammatory mediators (8, 9).”
BackgroundGranzyme A is an interleukin 1 beta-converting enzyme.
Irmler, M., Hertig, S., MacDonald, H. R., Sadoul, R., Becherer, J. D., Proudfoot, A. E. I., Solari, R. C. E., & Tschopp, J. (1995) · The Journal of Experimental Medicine · doi:10.1084/jem.181.5.1917 · Cited by 227
Ion Channel Formation by Amyloid-β42 Oligomers but Not Amyloid-β40 in Cellular Membranes
Bode, D. C., Baker, M. D., & Viles, J. H. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.m116.762526 · Cited by 210
Bourgade, K., Garneau, H., Giroux, G., Le Page, A. Y., Bocti, C., Dupuis, G., Frost, E. H., & Fülöp, T. (2015) · Biogerontology · doi:10.1007/s10522-014-9538-8 · Cited by 208
Neuroinflammation and Alzheimer's Disease: Implications for Microglial Activation
Regen, F., Hellmann-Regen, J., Costantini, E., & Reale, M. (2017) · Current Alzheimer Research · doi:10.2174/1567205014666170203141717 · Cited by 204
Early detection of cognitive deficits in the 3xTg-AD mouse model of Alzheimer's disease
Stover, K. R., Campbell, M. A., Winssen, C. M. V., & Brown, R. E. (2015) · Behavioural Brain Research · doi:10.1016/j.bbr.2015.04.012 · Cited by 203 · cited 1×
“3xTg-AD mice exhibit progressive loss of cognitive function as early as 3–6 months, and impairment in cognitive function is very obvious in 7–8 months old (44).”
BackgroundNeuroprotective effects of CD4+CD25+Foxp3+ regulatory T cells in a 3xTg-AD Alzheimer's disease model
Baek, H., Ye, M., Kang, G., Lee, C., Lee, G., Choi, D. B., Jung, J., Kim, H., Lee, S., Kim, J. S., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.12469 · Cited by 174
A modified α-galactosyl ceramide for staining and stimulating natural killer T cells
Liu, Y., Goff, R. D., Zhou, D., Mattner, J., Sullivan, B. A., Khurana, A., Cantu, C., Ravkov, E. V., Ibegbu, C., Altman, J. D., et al. (2006) · Journal of Immunological Methods · doi:10.1016/j.jim.2006.02.009 · Cited by 170
The Characterization of Regulatory T-Cell Profiles in Alzheimer’s Disease and Multiple Sclerosis
Ciccocioppo, F., Lanuti, P., Pierdomenico, L., Simeone, P., Bologna, G., Ercolino, E., Buttari, F., Fantozzi, R., Thomas, A., ONOFRJ, M. C., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-45433-3 · Cited by 142
Cysteine cathepsins in the immune response
Zavašnik‐Bergant, T., & Turk, B. (2006) · Tissue Antigens · doi:10.1111/j.1399-0039.2006.00585.x · Cited by 135
Granzyme B is a novel interleukin-18 converting enzyme
Omoto, Y., Yamanaka, K., Tokime, K., Kitano, S., Kakeda, M., Akeda, T., Kurokawa, I., Gabazza, E. C., Tsutsui, H., Katayama, N., et al. (2010) · Journal of Dermatological Science · doi:10.1016/j.jdermsci.2010.05.004 · Cited by 129
Microglial cathepsin B as a key driver of inflammatory brain diseases and brain aging
Nakanishi, H. (2019) · Neural Regeneration Research · doi:10.4103/1673-5374.264444 · Cited by 128
In vivo molecular imaging of neuroinflammation in Alzheimer's disease
Chaney, A. M., Williams, S. R., & Boutin, H. (2018) · Journal of Neurochemistry · doi:10.1111/jnc.14615 · Cited by 119
Extracellular Activities of Human Granzymes
Sower, L. E., Klimpel, G. R., Hanna, W. L., & Froelich, C. J. (1996) · Cellular Immunology · doi:10.1006/cimm.1996.0187 · Cited by 114
Extracellular activities of human granzyme A. Monocyte activation by granzyme A versus α-thrombin
Sower, L. E., Froelich, C. J., Allegretto, N. J., Rose, P. M., Hanna, W. D., & Klimpel, G. R. (1996) · The Journal of Immunology · doi:10.4049/jimmunol.156.7.2585 · Cited by 114
Spencer, C. T., Abate, G., Sakala, I. G., Xia, M., Truscott, S. M., Eickhoff, C. S., Linn, R. L., Blazevic, A., Metkar, S. S., Peng, G., et al. (2013) · PLoS Pathogens · doi:10.1371/journal.ppat.1003119 · Cited by 111
Mouse granzyme K has pro-inflammatory potential
Joeckel, L. T., Wallich, R., Martin, P., Sánchez‐Martínez, D., Weber, F. C., Martin, S. F., Borner, C., Pardo, J., Froelich, C. J., & Simon, M. M. (2011) · Cell Death and Differentiation · doi:10.1038/cdd.2011.5 · Cited by 106
Cathepsin G and Its Role in Inflammation and Autoimmune Diseases
Gao, S., Honglin, Z. H. U., Xiaoxia, Z. U. O., & Hui, L. U. O. (2018) · Archives of Rheumatology · doi:10.5606/archrheumatol.2018.6595 · Cited by 106
Solerte, S. B., Cravello, L., Ferrari, E., & Fioravanti, M. (2000) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2000.tb05399.x · Cited by 99
Activation of group 2 innate lymphoid cells alleviates aging-associated cognitive decline
Fung, I. T. H., Sankar, P., Zhang, Y., Robison, L. S., Zhao, X., D’Souza, S. S., Salinero, A. E., Wang, Y., Qian, J., Kuentzel, M. L., et al. (2019) · The Journal of Experimental Medicine · doi:10.1084/jem.20190915 · Cited by 97 · cited 1×
“Our recent work also indicates that activation of group-2 innate lymphoid cells can alleviate aging-associated cognitive decline (19).”
BackgroundSelf-citationHigh fat diet-induced diabetes in mice exacerbates cognitive deficit due to chronic hypoperfusion
Zuloaga, K. L., Johnson, L. A., Roese, N. E., Marzulla, T., Zhang, W. H., Nie, X. J., Alkayed, F. N., Hong, C., Grafe, M. R., Pike, M. M., et al. (2015) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x15616400 · Cited by 88 · cited 1×
“1 treatment as we previously described (32).”
Self-citationGranzyme K Activates Protease-Activated Receptor-1
Cooper, D., Pechkovsky, D. V., Hackett, T., Knight, D. A., & Granville, D. J. (2011) · PLoS ONE · doi:10.1371/journal.pone.0021484 · Cited by 86
Immunosenescence of Natural Killer Cells, Inflammation, and Alzheimer’s Disease
Solana, C., Tarazona, R., & Solana, R. (2018) · International Journal of Alzheimer s Disease · doi:10.1155/2018/3128758 · Cited by 79
Cathepsin G Controls Arterial But Not Venular Myeloid Cell Recruitment
Ortega‐Gómez, A., Salvermoser, M., Rossaint, J., Pick, R., Brauner, J., Lemnitzer, P., Tilgner, J., de Jong, R. J., Megens, R. T. A., Jamasbi, J., et al. (2016) · Circulation · doi:10.1161/circulationaha.116.024790 · Cited by 79
Granzyme K synergistically potentiates LPS-induced cytokine responses in human monocytes
Wensink, A. C., Kemp, V., Fermie, J., García-Laorden, M. I., van der Poll, T., Hack, C. E., & Bovenschen, N. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1317347111 · Cited by 69
Elucidating Sources and Roles of Granzymes A and B during Bacterial Infection and Sepsis
Arias, M. A., de Bagüés, M. P. J., Aguiló, N., Menao, S., Hervás‐Stubbs, S., Martino, A. D., Alcaraz, A., Simon, M. M., Froelich, C. J., & Pardo, J. (2014) · Cell Reports · doi:10.1016/j.celrep.2014.06.012 · Cited by 65
Solerte, S. B., Fioravanti, M., Pascale, A., Ferrari, E., Govoni, S. M., & Battaini, F. (1998) · Neurobiology of Aging · doi:10.1016/s0197-4580(98)00050-5 · Cited by 61
Aghdassi, A., John, D. S., Sendler, M., Weiss, F., Reinheckel, T., Mayerle, J., & Lerch, M. (2017) · Journal of Biological Chemistry · doi:10.1074/jbc.m117.814772 · Cited by 51
Hannaford, J., Guo, H., & Chen, X. (2013) · Obesity · doi:10.1002/oby.20136 · Cited by 46
Self-citationThe Role of Natural Killer Cells in Alzheimer’s Disease
Jadidi‐Niaragh, F., Shegarfi, H., Naddafi, F., & Mirshafiey, A. (2012) · Scandinavian Journal of Immunology · doi:10.1111/j.1365-3083.2012.02769.x · Cited by 40
Apoptosis of CD4+ T and Natural Killer Cells in Alzheimer's Disease
Schindowski, K., Peters, J., Gorriz, C., Schramm, U., Weinandi, T., Leutner, S., Maurer, K., Frölich, L., Müller, W. E. G., & Eckert, A. (2006) · Pharmacopsychiatry · doi:10.1055/s-2006-954591 · Cited by 39
Masera, R. G., Prolo, P., Sartori, M. L., Staurenghi, A., Griot, G., Ravizza, L., Dovio, A., Chiappelli, F., & Angeli, A. (2002) · Psychoneuroendocrinology · doi:10.1016/s0306-4530(01)00062-2 · Cited by 31
Martins, L. C., Rocha, N. P., Torres, K., dos Santos, R. R., França, G. S., de Moraes, E. N., Mukhamedyarov, M. A., Zefirov, A. L., Rizvanov, A. A., Kiyasov, A. P., et al. (2012) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2012.06.003 · Cited by 30
A novel proinflammatory role for granzyme A
van Eck, J. A., Shan, L., Meeldijk, J., Hack, C. E., & Bovenschen, N. (2017) · Cell Death and Disease · doi:10.1038/cddis.2017.56 · Cited by 25
Prolo, P., Chiappelli, F., Angeli, A., Dovio, A., Perotti, P., Pautasso, M., Sartori, M. L., Saba, L., Mussino, S., Fraccalini, T., et al. (2007) · Bioinformation · doi:10.6026/97320630001363 · Cited by 22
Enhanced Cytotoxic Response of Natural Killer Cells to lnterleukin-2 in Alzheimer's Disease
Solerte, S. B., Fioravanti, M., Severgnini, S., Locatelli, M., Renzullo, M., Pezza, N., Cerutti, N., & Ferrari, E. (1996) · Dementia and Geriatric Cognitive Disorders · doi:10.1159/000106901 · Cited by 21
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“Studies have shown that both NK1a cells, which have low levels of cytotoxic molecules, and NK1b cells, which have high levels of cytotoxic molecules, exhibit increased activity [47].”
BackgroundInfluential
Metadata
- Authors
- Zhang, Y., Fung, I. T. H., Sankar, P., Chen, X., Robison, L. S., Ye, L., D’Souza, S. S., Salinero, A. E., Kuentzel, M. L., Chittur, S. V., Zhang, W., Zuloaga, K. L., & Yang, Q.
- Affiliations
- Albany Medical College (US)
- Department of Immunology and Microbial Disease, Albany Medical College , Albany, NY 12208
- University at Albany, State University of New York (US)
- Corresponding author
- Zhang, Yuanyue
- Sankar, Poornima
- Chen, Xiangyu
- Yang, Qi
- ORCID
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2020-07
- Volume
- 205
- Issue
- 2
- Pages
- 502-510
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC7343613
- OpenAlex
- W3033144109
- Cited by
- 113
- References
- 64
- Citations by year
- 2026: 13 · 2025: 25 · 2024: 22 · 2023: 20 · 2022: 27 · 2021: 6
- FWCI
- 5.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R01HL137813, R01AG057782, R01NS110749)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- natural killer cells, Alzheimer's disease, neuroinflammation, neurogenesis, cognitive function, microglia, innate lymphoid cells, inflammatory cytokines, amyloid-beta, neurodegeneration
- MeSH terms
- Alzheimer Disease, Animals, Antibodies, Antigens, Ly, Cognition, Disease Models, Animal, Humans, Killer Cells, Natural, Lymphocyte Depletion, Mice, Transgenic, Apoptosis, Neurogenic Inflammation, Recovery of Function, Mice, Neurogenesis, NK Cell Lectin-Like Receptor Subfamily B
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