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Microglial Dysfunction and Defective β-Amyloid Clearance Pathways in Aging Alzheimer's Disease Mice
Open accessAbstract
Early microglial accumulation in Alzheimer's disease (AD) delays disease progression by promoting clearance of β-amyloid (Aβ) before formation of senile plaques. However, persistent Aβ accumulation despite increasing microglial numbers suggests that the ability of microglia to clear Aβ may decrease with age and progression of AD pathology. To determine the effects of aging and Aβ deposition on microglial ability to clear Aβ, we used quantitative PCR to analyze gene expression in freshly isolated adult microglia from 1.5-, 3-, 8-, and 14-month-old transgenic PS1-APP mice, an established mouse model of AD, and from their nontransgenic littermates. We found that microglia from old PS1-APP mice, but not from younger mice, have a twofold to fivefold decrease in expression of the Aβ-binding scavenger receptors scavenger receptor A (SRA), CD36, and RAGE (receptor for advanced-glycosylation endproducts), and the Aβ-degrading enzymes insulysin, neprilysin, and MMP9, compared with their littermate controls. In contrast, PS1-APP microglia had a 2.5-fold increase in the proinflammatory cytokines IL-1β (interleukin-1β) and tumor necrosis factor α (TNFα), suggesting that there is an inverse correlation between cytokine production and Aβ clearance. In support of this possibility, we found that incubation of cultured N9 mouse microglia with TNFα decreased the expression of SRA and CD36 and reduced Aβ uptake. Our data indicate that, although early microglial recruitment promotes Aβ clearance and is neuroprotective in AD, as disease progresses, proinflammatory cytokines produced in response to Aβ deposition downregulate genes involved in Aβ clearance and promote Aβ accumulation, therefore contributing to neurodegeneration. Antiinflammatory therapy for AD should take this dichotomous microglial role into consideration.
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“their phagocytic capacity declines with aging, chronic exposure to Αβ, and during sustained inflammation in the AD brain76,16,17.”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [16]
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.
In the citing paper
“However, as AD progresses, microglia acquire a chronically activated phenotype through unremitting stimulation by cytokines and A itself, which compromises their clearance function (Bamberger et al., 2003;Hickman et al., 2008;Heneka et al., 2010a) .”
From PPARγ/RXRα-Induced and CD36-Mediated Microglial Amyloid-β Phagocytosis Results in Cognitive Improvement in Amyloid Precursor Protein/Presenilin 1 Mice (2012) · cites this paper as Hickman et al., 2008
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.
In the citing paper
“Progression of Alzheimer's disease is associated with reduced Aβ-clearing pathways resulting in Aβ accumulation (4–6).”
From Heterozygous CX3CR1 Deficiency in Microglia Restores Neuronal β-Amyloid Clearance Pathways and Slows Progression of Alzheimer's Like-Disease in PS1-APP Mice (2019) · cites this paper as [5]
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.
In the citing paper
“Progression of Alzheimer's disease in humans and mouse models of the disease is associated with reduced expression of these Aβ-clearing enzymes resulting in decreased Aβ clearance and increased Aβ accumulation (5, 24).”
From Heterozygous CX3CR1 Deficiency in Microglia Restores Neuronal β-Amyloid Clearance Pathways and Slows Progression of Alzheimer's Like-Disease in PS1-APP Mice (2019) · cites this paper as [5]
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.
In the citing paper
“This impairment has been shown to correlate with increased production of proinflammatory cytokines and overwhelming accumulation of Aβ plaques in the AD brain [20–22].”
From IL-1β-driven amyloid plaque clearance is associated with an expansion of transcriptionally reprogrammed microglia (2019) · cites this paper as [22]
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In the citing paper
“Notably, previous studies have shown that microglial function may be adversely affected by Aβ, particularly as a result of chronic exposure to pro-inflammatory cytokines, resulting in increased Aβ accumulation and potentially underpinning the contradiction between our in vitro and in vivo results.39,40”
From Microglial INPP5D limits plaque formation and glial reactivity in the PSAPP mouse model of Alzheimer's disease (2023) · cites this paper as [40]
The cited source says what the claim attributes to it.
In the citing paper
“Thus, endothelial expression of LRP1 promotes the clearance of Aβ across the BBB in vivo, a process directly modulated by PCSK9 inhibitor treatment (93, 94), and the expression of CD36 parallels the ability of microglia to perform Aβ clearance (95).”
From PCSK9 and the nervous system: a no-brainer? (2023) · cites this paper as [95]
The cited source says what the claim attributes to it.
In the citing paper
“Increased pro-inflammatory gene expression in response to accumulating Αβ in older AD mice leads to decreased microglial Αβ clearance receptors or Αβ-degrading enzymes, thereby promoting further Αβ accumulation16.”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [16]
The cited source says what the claim attributes to it.
In the citing paper
“the ability of microglia to remove Αβ declines over time”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [16]
The cited source says what the claim attributes to it.
In the citing paper
“supporting that the progression of amyloid pathology correlates with impaired capacity of microglia to phagocytose Αβ17,16.”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [16]
The cited source says what the claim attributes to it.
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“As one of the most relevant consequences, the loss of microglial phagocytic capacity leads to further Aβ accumulation and aggregation, accelerating the progression of AD [17].”
From Emerging Role of miR-21-5p in Neuron–Glia Dysregulation and Exosome Transfer Using Multiple Models of Alzheimer’s Disease (2022) · cites this paper as [17]
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In the citing paper
“We have previously shown that expression of IDE in microglia from PS1-APP mice decreases with age and progression of AD-like pathology (5).”
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Finally, Inpp5d was identified as a target of miR155, and constitutive deletion of miR155, which should increase SHIP1, led to an increase in amyloid plaques.40,41”
From Microglial INPP5D limits plaque formation and glial reactivity in the PSAPP mouse model of Alzheimer's disease (2023) · cites this paper as [40]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Finally, Inpp5d was identified as a target of miR155, and constitutive deletion of miR155, which should increase SHIP1, led to an increase in amyloid plaques.40,41”
From Microglial INPP5D limits plaque formation and glial reactivity in the PSAPP mouse model of Alzheimer's disease (2023) · cites this paper as [40]
Experimental — accuracy not yet measuredIn the citing paper
“Aged glial cells respond less efficiently to antigens, including amyloid-β (Aβ) and α-synuclein, and have reduced phagocytic and antiinflammatory capacity (161–163).”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [161]
In the citing paper
“AD is accompanied by activation of microglia and astrocytes1,2 that affects the clearance and production of Aβ42,3,4 development and propagation of tau pathology,5 exacerbates neurodegeneration, and influences disease progression and severity.6,7”
From CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early Alzheimer disease (2018) · cites this paper as [3]
In the citing paper
“microglia from a mouse model of Aβ deposition (Aβ-mice) have reduced expression of Aβ-phagocytic receptors and Aβ-degrading enzymes, but their ability to produce proinflammatory cytokines was maintained6.”
From Microglia in neurodegeneration (2018) · cites this paper as [6]
In the citing paper
“In response to such stimuli, microglia can initiate a neuroinflammatory response which, like peripheral inflammation, includes production of cytokines such as TNF and IL-16,27, and possibly chemokines such as Ccl228, to recruit additional cells and induce them to clear injurious agents and maintain brain homeostasis.”
From Microglia in neurodegeneration (2018) · cites this paper as [6]
In the citing paper
“Aβ clearance involves, in part36, phagocytosis and endocytosis via microglial scavenger receptors (SRs)37,38 and extracellular degradation by Aβ-degrading enzymes6,36.”
From Microglia in neurodegeneration (2018) · cites this paper as [6]
In the citing paper
“Despite effective uptake, Aβ clearance by microglia in AD may be ineffective despite phagocytic uptake [55].”
From Identification and therapeutic modulation of a pro-inflammatory subset of disease-associated-microglia in Alzheimer’s disease (2018) · cites this paper as [55]
In the citing paper
“In AD, microglia cluster around beta-amyloid plaques highlighting their inability to clear beta-amyloid (Hickman et al., 2008; Liu et al., 2010).”
From iPSC-derived human microglia-like cells to study neurological diseases (2017) · cites this paper as Hickman et al., 2008
In the citing paper
“Immune involvement in neurodegenerative disease centres on findings that pro-inflammatory microglia are closely associated with protein aggregate pathologies characteristic of most dementias.”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [13]
In the citing paper
“In Alzheimer’s disease (AD), the most common form of dementia, microglia surround amyloid plaques and respond to amyloid-β with a pro-inflammatory phenotype characterised by cytokine expression (e.g., interleukins (IL) 1β and 6 and tumour necrosis factor α (TNFα)) that may initially limit amyloidosis but likely becomes overzealous and neurotoxic [12,13,14].”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [13]
In the citing paper
“For example, PS1-APP mice (a model of Alzheimer's Disease) showed an age-dependent reduction in receptors and enzymes involved in beta amyloid degradation, although still maintaining elevated levels of cytokine (Hickman et al, 2008).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Hickman et al, 2008
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Citations
Cites
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“However, Aβ clearance pathways are lost in microglia from aging AD model mice (Hickman et al. 2008; Mawuenyega et al. 2010; Sole-Domenech et al. 2016).”
BackgroundA review of autophagy mechanism of statins in the potential therapy of Alzheimer’s disease
Liu, L., Dai, W.-Z., Zhu, X., & Ma, T. (2022) · Journal of Integrative Neuroscience · doi:10.31083/j.jin2102046 · Cited by 20
Novel Anti-Neuroinflammatory Properties of a Thiosemicarbazone–Pyridylhydrazone Copper(II) Complex
Choo, X. Y., McInnes, L. E., Grubman, A., Wasielewska, J. M., Belaya, I., Burrows, E. L., Quek, H., Cañas-Martín, J., Loppi, S. H., Sorvari, A., et al. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms231810722 · Cited by 19
“In AD, microglia are a primary source of inflammatory cytokines (reviewed in [16]), involved in mediating neurotoxic effects [58], but also participate in the clearance of Aβ plaques through phagocytosis [17,59].”
BackgroundInfluentialNordengen, K., Kirsebom, B., Richter, G., Pålhaugen, L., Gísladóttir, B., Siafarikas, N., Nakling, A. E., Rongve, A., Bråthen, G., Grøntvedt, G. R., et al. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02973-w · Cited by 21
“These findings are in line with in vivo observations that point to associations between microglial activation and tau pathology, and with recent large GWAS studies under-scoring the interaction between microglial, Aβ and tau-linked pathways [62, 63].”
ResultPiezo1: the key regulators in central nervous system diseases
Xu, Y., Wang, Y., Yang, Y., Fang, X., Wu, L., Hu, J., Jin, L., & Mei, S. (2024) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2024.1441806 · Cited by 20
“Early-onset AD is associated with increased A β production by neurons (Beutner et al., 2013; Hickman et al., 2008; Jantti et al., 2022).”
Pan, Y., Xiaotao, J., Song, E., & Xiaozhong, P. (2018) · Chinese Medical Sciences Journal · doi:10.24920/11802 · Cited by 19
Benefits of aged garlic extract on Alzheimer's disease: Possible mechanisms of action (Review)
Sripanidkulchai, B. (2019) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2019.8390 · Cited by 19
“Moreover, the activation of the microglia has been reported to promote the neurodegenerative process through the release of a number of pro-inflammatory cytokines that may lead to neuronal cell damage and eventual cell death (48-50).”
BackgroundEvaluating the Effect of Interleukin-4 in the 3xTg Mouse Model of Alzheimer’s Disease
Dionisio-Santos, D. A., Behrouzi, A., Olschowka, J. A., & O’Banion, M. K. (2020) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.00441 · Cited by 20
Vidal, C., & Li, Z. (2021) · Cells · doi:10.3390/cells10030546 · Cited by 20
Tsay, H.-J., Liu, H., Kuo, Y., Chiu, C.-S., Liang, C.-C., Chung, C.-W., Chen, C., Chen, Y.-P., & Shiao, Y. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms221910413 · Cited by 19
Brain interleukins and Alzheimer’s disease
Abdelhamed, H. G., Hassan, A. A., Sakraan, A., Al-Deeb, R. T., Mousa, D. M., Ezz, H. S. A., Noor, N. A., Khadrawy, Y. A., & Radwan, N. M. (2025) · Metabolic Brain Disease · doi:10.1007/s11011-025-01538-5 · Cited by 20
“It has been suggested that microglia lose their ability to phagocytoze Aβ during AD progression (Hickman et al. 2008).”
Shi, J., Song, C., Zhang, P., Wang, J., Huang, W., Yu, T., Wei, Z., Wang, L., Zhao, L., Zhang, R., et al. (2025) · Theranostics · doi:10.7150/thno.104709 · Cited by 18
“Amyloid uptake activity of microglia directly affects Aβ clearance in plaque pathology [33, 34].”
Tau and Amyloid beta causes microglial activation in Alzheimer’s disease
Chinnathambi, S., Adithyan, A., Chandrashekar, M., & Rangappa, N. (2025) · Advances in clinical chemistry · doi:10.1016/bs.acc.2025.06.002 · Cited by 19
Kays, J. S., & Yamamoto, B. K. (2019) · Brain Sciences · doi:10.3390/brainsci9120340 · Cited by 18
Hypoxia/ischemia impairs CD33 (Siglec-3)/TREM2 signaling: Potential role in Alzheimer's pathogenesis
Salminen, A., Kaarniranta, K., & Kauppinen, A. (2021) · Neurochemistry International · doi:10.1016/j.neuint.2021.105186 · Cited by 20
“There is substantial evidence that in AD, microglial cells are hyporesponsive in promoting the phagocytosis of β-amyloid peptides (Monsonego et al., 2001; Hickman et al., 2008; Krabbe et al., 2013).”
Berberine: Is it a Promising Agent for Mental Disorders Treatment?
Shayganfard, M. (2022) · Current Molecular Pharmacology · doi:10.2174/1874467215666220509213122 · Cited by 18
Marsool, M. D. M., Prajjwal, P., Reddy, Y. B., Marsool, A. D. M., Lam, J. R., & Nandwana, V. (2023) · Disease-a-Month · doi:10.1016/j.disamonth.2023.101547 · Cited by 18
Vicente, M. C., Paneghini, J. D. L., Stabile, A. M., Amorim, M. R., Silva, C. E. A., Patrone, L. G. A., Cunha, T. M., Bícego, K. C., Almeida, M. C., Carrettiero, D. C., et al. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230151 · Cited by 21
Age-dependent changes on fractalkine forms and their contribution to neurodegenerative diseases
Eugenín, J. L., Bernhardi, L. E.-V., & Rommy von Bernhardi, M. (2023) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2023.1249320 · Cited by 19
“, 2014), as well as, in various pathologies, including cerebrovascular disease and AD (Hickman et al., 2008; Murgas et al., 2012; von Bernhardi and Eugenin, 2012; Trougakos, 2019).”
Farnsworth, B., Peuckert, C., Zimmermann, B., JAZIN, E. E., Kettunen, P., & Emilsson, L. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160160 · Cited by 18
Evaluating the Role of Microglial Cells in Clearance of Aβ from Alzheimer’s Brain
Manchikalapudi, A. L., Chilakala, R. R., Kalia, K., & Sunkaria, A. (2019) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.8b00627 · Cited by 18
Therapeutic Potential of Direct Clearance of the Amyloid-β in Alzheimer’s Disease
Kim, D., & Priefer, R. (2020) · Brain Sciences · doi:10.3390/brainsci10020093 · Cited by 18
Anwar, M. M., Badawi, A. M., & Eltablawy, N. A. (2020) · eNeurologicalSci · doi:10.1016/j.ensci.2020.100290 · Cited by 20
Microglial Potassium Channels: From Homeostasis to Neurodegeneration
Cocozza, G., Garofalo, S., Capitani, R., D’Alessandro, G., & Limatola, C. (2021) · Biomolecules · doi:10.3390/biom11121774 · Cited by 19
Alzheimer’s disease basics: we all should know
Das, S. K. (2025) · Neurological Research · doi:10.1080/01616412.2025.2529560 · Cited by 19
“Moreover, the release of many proteases involved in Aβ breakdown stimulates Aβ clearance [34].”
Tsai, Y., Kao, S.-T., & Cheng, C.-Y. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms231911311 · Cited by 20
“Large amounts of inflammatory cytokines can activate BACE-1 and γsecretase to suppress Aβ clearance, thereby increasing Aβ accumulation [71].”
BackgroundExperimental approaches for altering the expression of Abeta‐degrading enzymes
Loeffler, D. A. (2023) · Journal of Neurochemistry · doi:10.1111/jnc.15762 · Cited by 18
“Microglial expression of IDE was reported to decrease in old APP/PS1 mice (Hickman et al., 2008) and IDE brain concentration also decreased in a mouse model of AD in which the expression of human mutant PS2 was controlled by neuron- specific enolase (Hwang et al., 2005).”
BackgroundGalron, R., Gruber, R., Lifshitz, V., Lu, H., Kirshner, M., Ziv, N., Wang, Z., Shiloh, Y., Barzilai, A., & Frenkel, D. (2011) · Journal of Molecular Neuroscience · doi:10.1007/s12031-011-9494-6 · Cited by 17
Levistolide A Attenuates Alzheimer's Pathology Through Activation of the PPARγ Pathway
Qu, X., Guan, P., Han, L., Wang, Z., & Huang, X. (2020) · Neurotherapeutics · doi:10.1007/s13311-020-00943-1 · Cited by 18
Hemonnot-Girard, A.-L., Valverde, A., Hua, J., Delaygue, C., Linck, N., Maurice, T., Rassendren, F., & Hirbec, H. (2020) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2020.10.021 · Cited by 17
Mo, Y., Wang, L., Ren, M., Xie, W., Ye, X., Zhou, B., Zhang, A., Dai, Q., & Wang, J. (2021) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2021.10.010 · Cited by 17
Huang, Y., Hsu, S.-M., Shie, F., Shiao, Y., Chao, L.-J., Chen, H., Yao, H.-H., Chien, M. A., Lin, C., & Tsay, H.-J. (2022) · PLoS ONE · doi:10.1371/journal.pone.0260966 · Cited by 17
“Insufficient Aβ clearance correlates highly with the pathogenesis of AD, and glia play critical roles in Aβ clearance [47].”
BackgroundRegion-specific distribution of β-amyloid peptide and cytokine expression in TgCRND8 mice
Ma, K., Mount, H. T. J., & McLaurin, J. (2011) · Neuroscience Letters · doi:10.1016/j.neulet.2011.01.035 · Cited by 17
Scavenger Receptor A Deficiency Accelerates Cerebrovascular Amyloidosis in an Animal Model
Lifshitz, V., Weiss, R., Levy‐Barazany, H., & Frenkel, D. (2012) · Journal of Molecular Neuroscience · doi:10.1007/s12031-012-9909-z · Cited by 17
A New Use for an Old Treatment: Radiation Therapy and Alzheimer's Disease
Wilson, G. D., & Marples, B. (2016) · Radiation Research · doi:10.1667/rr14367.1 · Cited by 17
“disease progresses, pro-inflammatory cytokines produced in response to Ab deposition downregulate genes involved in Ab clearance and promote Ab accumulation, therefore contributing to neurodegeneration (59).”
BackgroundThe role of inhibitory immune checkpoint receptors in the pathogenesis of Alzheimer’s disease
Salminen, A. (2024) · Journal of Molecular Medicine · doi:10.1007/s00109-024-02504-x · Cited by 16
Pathogenesis and therapeutic applications of microglia receptors in Alzheimer’s disease
Fu, J., Wang, R., He, J., Liu, X., Wang, X., Yao, J., Liu, Y., Ran, C., Ye, Q., & He, Y. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1508023 · Cited by 17
Gu, X., Zhao, H., Zhou, J., Zhou, Y., Wei, X., Wang, H., Bian, B., Yang, J. T., Ren, W., & Si, N. (2020) · Evidence-based Complementary and Alternative Medicine · doi:10.1155/2020/6212907 · Cited by 16
“Plenty of evidences show that, in AD, a key factor in the accumulation of Aβ throughout the brain is the failure of neuroprotective microglia to remove extracellular amyloid [34, 35].”
BackgroundRecent insights into viral infections as a trigger and accelerator in alzheimer's disease
Vlieger, L. D., Vandenbroucke, R. E., & Hoecke, L. V. (2022) · Drug Discovery Today · doi:10.1016/j.drudis.2022.103340 · Cited by 16
“If the proinflammatory status persists and Ab keeps accumulating, altered microglial function and astrocytic dysfunction occur leading to a decreased expression of phagocytosis receptors on microglial cells.(63,68) Potentially, this will be further enhanced by the altered function of the astrocytes.”
Interferons: A molecular switch between damage and repair in ageing and Alzheimer’s disease
Gorlé, N., & Vandenbroucke, R. E. (2019) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2019.111148 · Cited by 18
A unified model of dementias and age‐related neurodegeneration
Fossel, M. (2020) · Alzheimer s & Dementia · doi:10.1002/alz.12012 · Cited by 16
Amyloids in Site-Specific Autoimmune Reactions and Inflammatory Responses
Huang, Y., Hong, X., Shen, J. X., Geng, L.-J., Pan, Y.-H., Ling, W., & Zhao, H. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2019.02980 · Cited by 16
Rosenblum, S. L., & Kosman, D. J. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.855751 · Cited by 19
Türker, F., Bharadwaj, R. A., Kleinman, J. E., Weinberger, D. R., Hyde, T. M., White, C. J., Williams, D. W., & Margolis, S. S. (2023) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2023.104811 · Cited by 16
“Other reports showed increased immunoproteasome abundance (135, 153, 154) and activity (155, 156) in AD mouse models due to enhanced neuroinflammation in the diseased brain.”
BackgroundLana, D., Ugolini, F., & Giovannini, M. G. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21249441 · Cited by 17
Nairuz, T., Heo, J.-C., & Lee, J. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252212156 · Cited by 16
“It is apparent that A β plaques trigger neurons and astrocytes to produce and release proinflammatory cytokines [78,79].”
Chakraborty, A., Sami, S. A., & Marma, K. K. S. (2021) · The Egyptian Journal of Internal Medicine · doi:10.1186/s43162-021-00081-w · Cited by 18
Gervais, É., Iloun, P., Martianova, E., Bessa, A. C. G., Rivest, S., & Topolnik, L. (2021) · The Journal of Comparative Neurology · doi:10.1002/cne.25289 · Cited by 15
“…effects of microglia to a neurotoxic environment, in which the clearance of amyloid deposits by microglia is reduced, and high levels of pro-inflammatory cytokines are released microglia activation can lead to neurodegeneration and cognitive deficits (Hickman et al., 2008; Morgan et al., 2005).”
BackgroundMiron, J., Picard, C., Labonté, A., Auld, D. S., & Poirier, J. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-215410 · Cited by 16
Kim, A., Lee, J., Moon, H., Kim, C., Yoo, M. Y., Park, W., Kim, W. D., & Seo, Y.-S. (2023) · Radiation Oncology Journal · doi:10.3857/roj.2023.00052 · Cited by 15
Vasileva, L. A., Gaynanova, G. A., Romanova, E. A., Petrov, K. A., Feng, C., Zakharova, L. Y., & Sinyashin, O. G. (2024) · Russian Chemical Reviews · doi:10.59761/rcr5150 · Cited by 15
Microglial Modulation in Alzheimer’s Disease: Central Players in Neuroinflammation and Pathogenesis
Hussain, M. S., Khan, Y., Fatima, R., Maqbool, M., Ramalingam, P. S., Khan, M. G., & Bisht, A. S. (2025) · Current Alzheimer Research · doi:10.2174/0115672050364292250113063513 · Cited by 15
Sun, P., Hu, Y., Xing, Q., Deng, W., Ou, Y., Pan, G., Zhong, X., & Hu, W. (2020) · ACS Pharmacology & Translational Science · doi:10.1021/acsptsci.0c00073 · Cited by 15
Löffler, T., Flunkert, S., Havas, D., Schweinzer, C., Uger, M. D., Windisch, M., Steyrer, E., & Hutter‐Paier, B. (2014) · Journal of Neuroinflammation · doi:10.1186/1742-2094-11-84 · Cited by 15
“The importance of neuroinflammation for the development of AD pathology is still under debate since neuroinflammatory events are shown to promote Aβ clearance, whereas chronic neuroinflammatory events seem to promote Aβ accumulation [6-11].”
Richman, M., Perelman, A., Gertler, A. A., & Rahimipour, S. (2012) · Biomacromolecules · doi:10.1021/bm301401b · Cited by 15
Du, E., Fan, R., Rong, L.-L., Xie, Z., & Xu, C. (2020) · Journal of Zhejiang University SCIENCE B · doi:10.1631/jzus.b1900425 · Cited by 14
Cho, E. J., Kim, H. Y., & Lee, A. Y. (2020) · Nutrition Research and Practice · doi:10.4162/nrp.2020.14.6.593 · Cited by 14
“In turn, Aβ-induced dysfunction of glial cells causes the downregulation of Aβ-degrading enzymes, and this decline in enzymatic activity is typically observed in the brain of AD patients [7].”
BackgroundAbdel‐Aal, R. A., Hussein, O. A., Elsaady, R. G., & Abdelzaher, L. A. (2021) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2021.174695 · Cited by 17
Streptozotocin mechanisms and its role in rodent models for Alzheimer’s disease
Chik, M. W., Ramli, N. A., Hazalin, N. A. M. N., & Singh, G. K. S. (2022) · Toxin Reviews · doi:10.1080/15569543.2022.2150646 · Cited by 14
“…neuroinflammation because the clearance of Ab by microglia will release proinflammatory cytokines tumor necrosis factor (TNF), interleukin 6 (IL-6) and interleukin 1B (IL-1B) and ROS and promote an accumulation of Ab that contributes to neurodegeneration (Hickman et al. 2008) as shown in Figure 3.”
BackgroundDanziger, R., Fuchs, D.-T., Koronyo, Y., Rentsendorj, A., Sheyn, J., Hayden, E. Y., Teplow, D. B., Black, K. L., Fuchs, S., Bernstein, K. E., et al. (2023) · Frontiers in Physiology · doi:10.3389/fphys.2023.1179315 · Cited by 16
“In previous studies, these receptors have been associated with increased Aβ uptake (Hickman et al., 2008; Frenkel et al., 2013; Kim et al., 2017).”
BackgroundZhang, W., Uyemura, R., Zhong, K., Guo, R., & Zhong, L. (2023) · Aging and Disease · doi:10.14336/ad.2023.1206 · Cited by 14
“These cells play an important role in AD by participating in the phagocytosis of Aβ plaques and are involved in the inflammatory response [7, 8].”
BackgroundYassaghi, Y., Nazerian, Y., Ghasemi, M., Nazerian, A., Sayehmiri, F., Perry, G. L., & Pourbadie, H. G. (2024) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.18554 · Cited by 15
“58,59 Impaired microglial phagocytosis due to astrocytic protection, 56 prolonged microglia activation, and aberrant inflammation are detrimental at later stages.”
BackgroundThe intricate interplay between microglia and adult neurogenesis in Alzheimer’s disease
Früholz, I., & Meyer‐Luehmann, M. (2024) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2024.1456253 · Cited by 16
“One of the primary microglial functions in AD is A β clearance through phagocytosis (Hickman et al., 2008).”
Background
Metadata
- Authors
- Hickman, S. E., Allison, E. K., & El Khoury, J.
- Affiliations
- Harvard University (US)
- ORCID
- Hickman, Suzanne E.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-08-13
- Volume
- 28
- Issue
- 33
- Pages
- 8354-8360
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2597474
- OpenAlex
- W2018708829
- Cited by
- 1,329
- References
- 28
- Citations by year
- 2026: 49 · 2025: 85 · 2024: 85 · 2023: 96 · 2022: 125 · 2021: 98 · 2020: 113 · 2019: 91 · 2018: 78 · 2017: 63 · 2016: 67 · 2015: 73 · 2014: 64 · 2013: 49 · 2012: 65
- FWCI
- 27.71
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Dana Foundation
- National Institute of Neurological Disorders and Stroke (R01NS059005)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- Alzheimer's disease, microglia, amyloid-beta clearance, aging, scavenger receptor A, CD36, RAGE, neprilysin, MMP-9, inflammatory cytokines, TNF-α, IL-1β, neuroinflammation, anti-inflammatory therapy, neurodegeneration
- MeSH terms
- Aging, Alzheimer Disease, Animals, Mice, Transgenic, Signal Transduction, Amyloid beta-Peptides, Microglia, Mice
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