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Innate immune memory in the brain shapes neurological disease hallmarks
Open accessAbstract
Innate immune memory is a vital mechanism of myeloid cell plasticity that occurs in response to environmental stimuli and alters subsequent immune responses. Two types of immunological imprinting can be distinguished-training and tolerance. These are epigenetically mediated and enhance or suppress subsequent inflammation, respectively. Whether immune memory occurs in tissue-resident macrophages in vivo and how it may affect pathology remains largely unknown. Here we demonstrate that peripherally applied inflammatory stimuli induce acute immune training and tolerance in the brain and lead to differential epigenetic reprogramming of brain-resident macrophages (microglia) that persists for at least six months. Strikingly, in a mouse model of Alzheimer's pathology, immune training exacerbates cerebral β-amyloidosis and immune tolerance alleviates it; similarly, peripheral immune stimulation modifies pathological features after stroke. Our results identify immune memory in the brain as an important modifier of neuropathology.
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“Next we tested the effect of Aβ42 and LPS on oxidative stress response in microglial cells as amyloid and inflammation trigger and exacerbate pathological changes in AD brain (Wendeln et al., 2018).”
From Alzheimer's-associated PU.1 expression levels regulate microglial inflammatory response (2021) · cites this paper as Wendeln et al., 2018
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“peripheral insults that cause a systemic inflammatory response might affect ongoing inflammation in the CNS mainly by microglial activation, production of inflammatory molecules, as well as recruitment of peripheral immune cells into the brain, thus shaping a cerebral inflammatory milieu that may seriously affect neuronal function (50, 52, 53).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [53]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“However, nonspecific microglia activation induced by lipopolysaccharide does not have the same amyloid-promoting effect as myelin dysfunction, as increases, decreases or no changes in amyloid burden have been reported48–51.”
From Myelin dysfunction drives amyloid-β deposition in models of Alzheimer’s disease (2023) · cites this paper as [49]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“A Hif1a epigenetic and transcriptomic signature was recently identified in microglia following immune training by peripheral LPS administration in APP/PS1 mice65.”
From Transcriptional signature in microglia associated with Aβ plaque phagocytosis (2021) · cites this paper as [65]
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“Animal and in-vitro studies demonstrate that inflammatory stimuli may initiate long-term priming of the microglia, peripheral CD4+ and CD8+ T cells to a proinflammatory state, (352-354) potentially increasing amyloid plaque deposition.(355)”
From Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission (2024) · cites this paper as [355]
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In the citing paper
“Our data suggest that PU.1 may contribute to this mechanism of innate immune memory in the brain (Wendeln et al., 2018).”
From Alzheimer's-associated PU.1 expression levels regulate microglial inflammatory response (2021) · cites this paper as Wendeln et al., 2018
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In the citing paper
“although it is important to note that the efficiency of individual phagocytic processes can be dependent on experimental conditions65–67.”
From Transcriptional signature in microglia associated with Aβ plaque phagocytosis (2021) · cites this paper as [65]
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“We found little overlap between the Hif1a module reported in65 and the Hif1a regulon identified here (Supplementary Fig. 13d)”
From Transcriptional signature in microglia associated with Aβ plaque phagocytosis (2021) · cites this paper as [65]
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“In healthy mice, peripherally applied LPS can differentially reprogram the epigenome of microglia by inducing either acute immune training or tolerance pending upon the number of injections [102].”
From What would it take to prove that a chronic infection is a causal agent in Alzheimer’s disease? (2025) · cites this paper as [102]
In the citing paper
“and systemic endotoxin precipitates brain pathology in mice expressing prions [74], APP variants [33] or TAU variants [69] or mice with α-synuclein injected in the brain [46].”
From The endotoxin hypothesis of neurodegeneration (2019) · cites this paper as [33]
In the citing paper
“Microglial markers such as purinergic receptor P2Y G-protein coupled 12 (P2ryl2), transmembrane protein 119 (Tmem119), and Fc receptor-like S, scavenger receptor (Fcrls), are used to define microglia homeostatic state.”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [11]
In the citing paper
“Whereas, inflammatory marker Clec7a is used to define microglia in neurodegenerative state [11].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [11]
In the citing paper
“Immune memory in microglia and macrophages are shaped by epigenetically mediated alterations in the enhancer repertoire of targeted genes [11, 32].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [11]
In the citing paper
“In addition, APP mice with four-time LPS treatment showed increased H3K4me1 levels in putative enhancers related to phagocytic function [11].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [11]
In the citing paper
“Cerebral beta-amyloidosis activates HIF-1a and mTOR pathways, which leads to transcriptional and functional alterations associated with increased inflammatory and immune response genes in MGnD [11].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [11]
In the citing paper
“Peripheral immune stimulation and cerebral beta-amyloidosis can lead to epigenetic modification in microglia.”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [11]
In the citing paper
“These data suggest the differential effect of immune training versus tolerance due to multiple peripheral immune stimulation, which is reflected in the epigenetic landscape of MGnD in AD mouse models.”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [11]
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Systemic inflammation induced the delayed reduction of excitatory synapses in the CA3 during ageing
Manabe, T., Rácz, I., Schwartz, S., Oberle, L., Santarelli, F., Emmrich, J. V., Neher, J. J., & Heneka, M. T. (2021) · Journal of Neurochemistry · doi:10.1111/jnc.15491 · Cited by 44
“In addition, the extent of the inflammatory response was enhanced by repeated injection on two consecutive days in a process termed immune training (Neher & Cunningham, 2019; Wendeln et al., 2018).”
BackgroundMethodSelf-citationMicroglia Phenotypes Converge in Aging and Neurodegenerative Disease
Candlish, M., & Hefendehl, J. K. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.660720 · Cited by 49
“These findings are of particular interest as they support other reports that microglia can be influenced by stimulation of peripheral immune cells (5) and that their responsiveness can be (partially) restored even in the aged brain.”
BackgroundResultEpigenetics: An opportunity to shape innate and adaptive immune responses
Liotti, A., Ferrara, A. L., Loffredo, S., Galdiero, M. R., Varricchi, G., Rella, F. D., Maniscalco, G. T., Belardo, M., Vastano, R., Prencipe, R., et al. (2022) · Immunology · doi:10.1111/imm.13571 · Cited by 50
“Similarly, either immune activation or tolerance are induced in brain-resident macrophages via changes in H3K4me1 and H3K27ac, and HDAC1/2 function, with repercussions on cerebral inflammation and pathological grade in a mouse model of Alzheimer disease [69, 70].”
BackgroundBlossom, V., Ullal, S. D., D’Souza, M. M., Ranade, A. V., Kumar, N. A., & Rai, R. (2025) · 3 Biotech · doi:10.1007/s13205-025-04468-2 · Cited by 57
“Recent studies have revealed that peripheral insults associated with systemic inflammation when sustained for a prolonged period can lead to neuroinflammation (Perry et al 2003; Amor et al. 2014; Wendeln et al 2018; Dinan and Cryan 2017).”
Neuroimmune Activation Drives Multiple Brain States
Tchessalova, D., Posillico, C. K., & Tronson, N. C. (2018) · Frontiers in Systems Neuroscience · doi:10.3389/fnsys.2018.00039 · Cited by 52
“priming effects after immune challenge in adults, with changes in microglial and astrocytic function and behavior (Fenn et al., 2014; Norden et al., 2015; Muccigrosso et al., 2016; Liddelow and Barres, 2017; Olivieri et al., 2018; Wendeln et al., 2018).”
BackgroundInfluentialEmerging technologies to study glial cells
Hirbec, H., Déglon, N., Foo, L. C., Goshen, I., Grutzendler, J., Hangen, E., Kreisel, T., Linck, N., Muffat, J., Regio, S., et al. (2020) · Glia · doi:10.1002/glia.23780 · Cited by 51
“Epigenetic mechanisms are also likely to define the immune memory of microglia, and possibly other glial cell types, a process that is thought to be involved in the differential responses of individuals to neurodegenerative conditions (Wendeln et al., 2018).”
BackgroundMicroglia in Health and Diseases: Integrative Hubs of the Central Nervous System (CNS)
Sierra, A., Miron, V. E., Paolicelli, R. C., & Ransohoff, R. M. (2024) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a041366 · Cited by 47
Transcriptional Networks of Microglia in Alzheimer’s Disease and Insights into Pathogenesis
Chew, G., & Petretto, E. G. (2019) · Genes · doi:10.3390/genes10100798 · Cited by 46
“posited that microglia activation requires Hif1a to switch on glycolysis, while chronic neurodegeneration results in the microglia metabolic breakdown [25,147].”
BackgroundInfluentialImmune Memory in Aging: a Wide Perspective Covering Microbiota, Brain, Metabolism, and Epigenetics
Bulut, O. P., Kılıç, G., & Domínguez‐Andrés, J. (2021) · Clinical Reviews in Allergy & Immunology · doi:10.1007/s12016-021-08905-x · Cited by 50
Harnessing Immunoproteostasis to Treat Neurodegenerative Disorders
Golde, T. E. (2019) · Neuron · doi:10.1016/j.neuron.2019.02.027 · Cited by 45
Ellert‐Miklaszewska, A., Ochocka, N., Maleszewska, M., Ding, L., Laurini, E., Jiang, Y., Roura, A.-J., Giorgio, S., Gielniewski, B., Pricl, S., et al. (2019) · Nanomedicine · doi:10.2217/nnm-2019-0176 · Cited by 50
Jiang, L., Mu, H., Xu, F., Xie, D., Su, W., Xu, J., Sun, Z., Liu, S., Luo, J., Shi, Y., et al. (2020) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x20902542 · Cited by 46
“It is recently reported that a single inflammatory stimulus induces acute immune training in microglia and exaggerates immune responses, while multiple doses of inflammatory stimuli result in immune tolerance in microglia and dampened inflammatory responses after stroke.(38) This observation reveals an immune memory w…”
BackgroundTrained Immunity Confers Prolonged Protection From Listeriosis
Théroude, C., Reverte, M., Heinonen, T., Ciarlo, E., Schrijver, I. T., Antonakos, N., Maillard, N., Pralong, F. P., Roy, D. L., & Roger, T. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.723393 · Cited by 45
“Zymosan A from Saccharomyces cerevisiae and phytohemagglutinin-L (PHA) from Phaseolus vulgaris were from Sigma-Aldrich, Salmonella minnesota ultra-pure lipopolysaccharide (LPS) from List Biologicals Laboratories (Campbell, CA), and CpG ODN 1826 (CpG) from Microsynth (Balgach, Switzerland).”
BackgroundInfluentialBasak, J. M., Ferreiro, A., Cohen, L. S., Sheehan, P. W., Nadarajah, C. J., Kanan, M. F., Sukhum, K. V., Dantas, G., & Musiek, E. S. (2021) · Neurobiology of Disease · doi:10.1016/j.nbd.2021.105292 · Cited by 46
“These experiments have yielded conflicting results that seem to depend upon both the dose, timing, and frequency of LPS administration (Tejera et al., 2019; Wendeln et al., 2018).”
Function of Glia in Aging and the Brain Diseases
Vallés, S. L., Iradi, A., Aldasoro, M., Vila, J. M., Aldasoro, C., de la Torre, J., Campos-Campos, J., & Jorda, A. (2019) · International Journal of Medical Sciences · doi:10.7150/ijms.37769 · Cited by 45
“(8) recently demonstrated that peripheral stimulation of mouse microglial cells by repeated injection of LPS can cause epigenetic changes in these cells for more than six months (8).”
BackgroundMyeloid cell‐specific topoisomerase 1 inhibition using DNA origami mitigates neuroinflammation
Zhu, K., Wang, Y., Sarlus, H., Geng, K., Nutma, E., Sun, J., Kung, S., Bay, C., Han, J., Min, J., et al. (2022) · EMBO Reports · doi:10.15252/embr.202154499 · Cited by 43
Wang, B., Ma, Y., Li, S., Yao, H., Gu, M.-N., Liu, Y., Xue, Y., Ding, J., Ma, C., Yang, S., et al. (2023) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2023.04.008 · Cited by 45
Mishra, B., & Ivashkiv, L. B. (2024) · Immunological Reviews · doi:10.1111/imr.13330 · Cited by 44
“44 Initial LPS injection induces transient changes in HSPC abundance and gene expression, and C/EBP β - dependent epigenetic memory and trained immunity, in hematopoietic progenitors.”
BackgroundHistamine modulates hippocampal inflammation and neurogenesis in adult mice
Saraiva, C., Barata‐Antunes, S., Santos, T., Ferreiro, E. B., Cristóvão, A. C., Serra-Almeida, C., Ferreira, R., & Bernardino, L. I. (2019) · Scientific Reports · doi:10.1038/s41598-019-44816-w · Cited by 45
Pathology of inflammatory diseases of the nervous system: Human disease versus animal models
Lassmann, H. (2019) · Glia · doi:10.1002/glia.23726 · Cited by 44
“Whether this is due to innate immune memory (Wendeln et al., 2018) has to be determined in the future.”
BackgroundGut dysbiosis in stroke and its implications on Alzheimer’s disease‐like cognitive dysfunction
Cho, J., Park, Y. J., Gonzales‐Portillo, B., Saft, M., Cozene, B., Sadanandan, N., & Borlongan, C. V. (2021) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.13613 · Cited by 44
“Wendeln et al. (2018) Peripheral immune stimulation, training and tolerance, modulates pathology of neurological diseases.”
BackgroundWeinberg, M. S., Zafar, A., Magdamo, C., Chung, S. Y., Chou, W. H., Nayan, M., Deodhar, M., Frendl, D. M., Feldman, A. S., Faustman, D. L., et al. (2023) · JAMA Network Open · doi:10.1001/jamanetworkopen.2023.14336 · Cited by 44
Is ‘friendly fire’ in the brain provoking Alzheimer’s disease?
Abbott, A. (2018) · Nature · doi:10.1038/d41586-018-04930-7 · Cited by 43
Life and death of microglia: Mechanisms governing microglial states and fates
Matsudaira, T., & Prinz, M. (2022) · Immunology Letters · doi:10.1016/j.imlet.2022.04.001 · Cited by 47
Self-citationFungal cell wall components modulate our immune system
Briard, B., Fontaine, T., Kanneganti, T.-D., Gow, N. A. R., & Papon, N. (2021) · The Cell Surface · doi:10.1016/j.tcsw.2021.100067 · Cited by 42
Clark, I. A., & Vissel, B. (2018) · British Journal of Pharmacology · doi:10.1111/bph.14471 · Cited by 42
“Exploration of the interplay of cellular mediators, particularly cytokines allied to TNF, that binds the worlds of brain physiology, innate immunity and neurodegenerative disease into a single conceptual entity is expanding spectacularly at present (Ahmed et al., 2018; Rankin and Artis, 2018; Wendeln et al., 2018).”
BackgroundLemche, E., Killick, R., Mitchell, J., Caton, P., Choudhary, P., & Howard, J. K. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106485 · Cited by 45
Insights into rheumatic diseases from next-generation sequencing
Donlin, L. T., Park, S. H., Γιαννοπούλου, Ε., Ivovic, A., Park‐Min, K., Siegel, R. M., & Ivashkiv, L. B. (2019) · Nature Reviews Rheumatology · doi:10.1038/s41584-019-0217-7 · Cited by 42
Melbourne, J. K., Thompson, K. R., Peng, H., & Nixon, K. (2019) · Progress in molecular biology and translational science · doi:10.1016/bs.pmbts.2019.06.011 · Cited by 40
Vargas, A. M., Rivera-Rodriguez, D. E., & Martinez, L. R. (2020) · Molecular Immunology · doi:10.1016/j.molimm.2020.03.013 · Cited by 40
Memory-Like Responses of Brain Microglia Are Controlled by Developmental State and Pathogen Dose
Lajqi, T., Stojiljkovic, M. R., Williams, D. L., Hudalla, H., Bauer, M. W., Witte, O. W., Wetzker, R., Bauer, R., & Schmeer, C. W. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.546415 · Cited by 41
“Our study supports recent evidence indicating memory-like responses of brain microglia after repeated immune challenge (14, 15, 18).”
BackgroundResultInfluentialImmune Protection of Stem Cell-Derived Islet Cell Therapy for Treating Diabetes
Tahbaz, M., & Yoshihara, E. (2021) · Frontiers in Endocrinology · doi:10.3389/fendo.2021.716625 · Cited by 43
Ahmed, M. M., Johnson, N. R., Boyd, T. D., Coughlan, C. M., Chial, H. J., & Potter, H. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.718426 · Cited by 42
“Timing and Effects of Innate Immune System Activation and Neuroinflammation in DS and AD Epidemiological studies suggest that elevated immune biomarkers in the blood may be evident years prior to the manifestation of clinical symptoms of AD or AD-related dementias (ADRDs) in the typical population (Schmidt et al., 200…”
BackgroundSroor, H. M., Hassan, A. M., Zenz, G., Valadez-Cosmes, P., Farzi, A., Holzer, P. D., El-Sharif, A., Gomaa, F. A. M., Kargl, J., & Reichmann, F. (2019) · Scientific Reports · doi:10.1038/s41598-019-56859-0 · Cited by 38
Xing, Z., Zuo, Z., Hu, D., Zheng, X., Wang, X., Yuan, L., Zhou, L., Qi, F., & Yao, Z. (2020) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2020.09.015 · Cited by 38
Metabolic flexibility ensures proper neuronal network function in moderate neuroinflammation
Chausse, B., Malorny, N., Lewen, A., Poschet, G., Berndt, N., & Kann, O. (2024) · Scientific Reports · doi:10.1038/s41598-024-64872-1 · Cited by 38
“Of note, citrate and acetyl-CoA accumulation and the resulting changes in histone acetylation have been involved in inflammation progression and innate immune memory formation in myeloid cells 53–55 .”
BackgroundLiu, P., Zhang, T., Wu, Y., Chen, Q., Sun, T., & Jiang, C. (2024) · Advanced Materials · doi:10.1002/adma.202408729 · Cited by 42
Biomarkers and Associated Immune Mechanisms for Early Detection and Therapeutic Management of Sepsis
Trzeciak, A. J., Pietropaoli, A. P., & Kim, M. (2020) · Immune Network · doi:10.4110/in.2020.20.e23 · Cited by 40
“LPS-induced tolerance has also been observed in microglia, where primary exposure to TLR4 stimulation directly influences future responses to endotoxin (132).”
BackgroundhUCMSCs Mitigate LPS-Induced Trained Immunity in Ischemic Stroke
Feng, Y., Wu, C., Liang, F., Lin, T., Li, W., Jing, Y., Dai, P., Yu, H., Lan, Y., Pei, Z., et al. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.01746 · Cited by 39
“For example, peripheral injection of lipopolysaccharide (LPS) induces trained immunity in microglia, and trainedmicroglia have been found to exacerbate ischemic brain damage 1 month after LPS challenge (5).”
BackgroundInfluentialChen, H., Chen, C., Mandhani, N., Short-Miller, J. C., Smucker, M. R., Sun, Y., & Kuan, C.-Y. (2020) · Journal of Neuroscience · doi:10.1523/jneurosci.1171-20.2020 · Cited by 40
“A recent study indicates that the peripheral inflammatory stimuli in adult mice induce long-term immune memory in the microglia via epigenetic reprogramming (Wendeln et al., 2018).”
BackgroundChen, L., & Ozato, K. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.621333 · Cited by 41
“Tolerance is the opposite side of innate immune memory/ trained immunity, in which many proinflammatory cytokines, including IL-1, TNFa, and IL-6 remain uninduced after a second LPS stimulation as observed in vivo and in vitro (45, 46).”
BackgroundMockenhaupt, K., Gonsiewski, A. K., & Kordula, T. (2021) · Cells · doi:10.3390/cells10071609 · Cited by 40
“When the initial dose of LPS is low, immune cell training (also known as priming) occurs, resulting in increased response to subsequent stimulation [98].”
BackgroundInfluentialTóth, K., Lénárt, N., Berki, P., Fekete, R., Szabadits, E., Pósfai, B., Cserép, C., Alatshan, A., Benkő, S., Kiss, D. K., et al. (2022) · PLoS Biology · doi:10.1371/journal.pbio.3001526 · Cited by 40
“To unravel the effects of pharmacological inhibition of NKCC1 in the periphery and the brain, we investigated the systemic versus central effects of bumetanide in response to bacterial endotoxin (LPS) administration, which is widely used to trigger inflammatory cytokine responses [41,52].”
BackgroundSynapses, Microglia, and Lipids in Alzheimer’s Disease
Paasila, P. J., Aramideh, J. A., Sutherland, G. T., & Graeber, M. B. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.778822 · Cited by 40
Radiotherapy induces persistent innate immune reprogramming of microglia into a primed state
Voshart, D. C., Oshima, T., Jiang, Y., van der Linden, G. P., Ainslie, A. P., Nazario, L. R., van Buuren-Broek, F., Scholma, A. C., van Weering, H. R. J., Brouwer, N., et al. (2024) · Cell Reports · doi:10.1016/j.celrep.2024.113764 · Cited by 39
“…exaggerated interleukin-1 b cytokine expression in a model of murine prion disease after a systemic endotoxin lipopolysaccharide (LPS) immune challenge 18 and have been observed in several disease mouse models, including Alzheimer’s disease (AD) 19 and accelerated aging with defective DNA repair.”
BackgroundInfluential
Metadata
- Authors
- Wendeln, A.-C., Degenhardt, K., Kaurani, L., Gertig, M., Ulas, T., Jain, G., Wagner, J., Häsler, L. M., Wild, K., Skodras, A., Blank, T., Staszewski, O., Datta, M., Centeno, T. P., Capece, V., Islam, M. R., Kerimoglu, C., Staufenbiel, M., Schultze, J. L., Beyer, M., Prinz, M., Jucker, M., Fischer, A., & Neher, J. J.
- Affiliations
- German Center for Neurodegenerative Diseases (DE)
- University of Bonn (DE)
- University of Freiburg (DE)
- Corresponding author
- Neher, Jonas J.
- ORCID
- Venue
- Nature
- Published
- 2018-04
- Volume
- 556
- Issue
- 7701
- Pages
- 332-338
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC6038912
- OpenAlex
- W2796983933
- Cited by
- 956
- References
- 51
- Citations by year
- 2026: 117 · 2025: 102 · 2024: 120 · 2023: 106 · 2022: 121 · 2021: 135 · 2020: 104 · 2019: 90 · 2018: 60
- FWCI
- 43.97
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DZNE Pub (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- trained immunity, immunological imprinting, immune tolerance, microglia, epigenetic reprogramming, neuroinflammation, Alzheimer's disease, beta-amyloidosis, stroke, neuropathology
- MeSH terms
- Alzheimer Disease, Amyloidosis, Animals, Brain, Disease Models, Animal, Female, Gene Expression Regulation, Humans, Immune Tolerance, Immunity, Innate, Immunologic Memory, Inflammation, Male, Nervous System Diseases, Microglia, Stroke, Epigenesis, Genetic, Mice
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