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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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“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]
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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]
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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).”
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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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“…hypothesis, we developed a method to isolate fresh adult mouse microglia from the bigenic APPswe/PSEN1dE9 (PS1-APP) mice (Borchelt et al., 1997; Jankowsky et al., 2001), a robust mouse model of AD, and from their nontransgenic littermates at various ages and stages of AD-like pathology, and…”
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“Interestingly, the Aβ- clearing capacity of microglia in APP/PS1 mice is impaired with aging, as indicated by the reduced expression of Aβ- binding receptors and Aβ- degrading enzymes (Hickman & Allison, 2008), but the exact mechanism is unclear.”
BackgroundProprotein convertase subtilisin/kexin type 9 (PCSK9) in the central nervous system
Bell, A. S., Wagner, J., Rosoff, D. B., & Lohoff, F. W. (2023) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2023.105155 · Cited by 36
Dendrimers and Derivatives as Multifunctional Nanotherapeutics for Alzheimer’s Disease
Moreira, D. A., Santos, S. D., Leiro, V., & Pêgo, A. P. (2023) · Pharmaceutics · doi:10.3390/pharmaceutics15041054 · Cited by 39
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“Studies showing activated microglia and astrocytes surrounding A β plaques suggest significant involvement of inflammatory pathways in the disease (6, 7, 10, 11).”
Passive immunotherapy for Alzheimer’s disease: challenges & future directions
Yi, L., Tan, E. K., & Zhou, Z. (2024) · Journal of Translational Medicine · doi:10.1186/s12967-024-05248-x · Cited by 41
“In PS1-APP mice the phagocytosis capacity of microglia was significantly reduced with down-regulated expression of scavenger receptors and pathogenic protein degrading enzymes [40].”
BackgroundLloyd, A. F., Martínez‐Muriana, A., Davis, E., Daniels, M. J. D., Hou, P., Mancuso, R., Brenes, A. J., Sinclair, L. V., Geric, I., Snellinx, A., et al. (2024) · Cell Reports · doi:10.1016/j.celrep.2024.114908 · Cited by 47
Bittencourt, L. D. S., Zeidán‐Chuliá, F., Yatsu, F. K. J., Schnorr, C. E., Moresco, K. S., Kolling, E. A., Gelain, D. P., Bassani, V. L., & Moreira, J. C. F. (2014) · Phytotherapy Research · doi:10.1002/ptr.5173 · Cited by 37
“In fact, several reports showed the presence of activated microglial cells, Aβ deposition, and increased AGEs levels in the brains of AD individuals, suggesting their pathological role in this context of neurodegeneration (Hickman et al., 2008; Krautwald et al., 2011).”
BackgroundLi, X., Melief, E. J., Postupna, N. O., Montine, K. S., Keene, C. D., & Montine, T. J. (2014) · American Journal Of Pathology · doi:10.1016/j.ajpath.2014.09.016 · Cited by 37
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“In support of this hypothesis, Hickman and colleagues [38] found that, in the PS1-APP [B6C3-Tg(APPswe, PSEN1dE9)85Dbo/J] mouse model, the phenotype of accumulating microglia changes as pathology progresses.”
BackgroundAmniotic Mesenchymal Stem Cells Decrease Aβ Deposition and Improve Memory in APP/PS1 Transgenic Mice
Zheng, X., Wan, Q.-Q., Zheng, C.-Y., Zhou, H., Dong, X., Deng, Q., Yao, H., Fu, Q., Gao, M., Yan, Z., et al. (2017) · Neurochemical Research · doi:10.1007/s11064-017-2226-8 · Cited by 37
“These proinflammatory cytokines have been shown to promote Aβ production and reduce Aβ removal in an AD mouse model [45].”
BackgroundMolecular and cellular mechanisms of sporadic Alzheimer’s disease: Studies on rodent models in vivo
Gulyaeva, N. V., Bobkova, N. V., Kolosova, N. G., Samokhin, A. N., Stepanichev, M. Y., & Stefanova, N. A. (2017) · Biochemistry (Moscow) · doi:10.1134/s0006297917100029 · Cited by 39
Chuang, K., Li, M., Lin, N., Chang, C.-H., Lu, I.-H., Pan, I.-H., Takahashi, T., Perng, M., & Wen, S. (2017) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2017/5414297 · Cited by 40
“Binding of Aβ to, for example, RAGE results in the production of inflammatory cytokines and reduces Aβ uptake in cultured microglia [82, 83] and in transgenic mice expressing human mutant APP [84].”
BackgroundModelling Sporadic Alzheimer’s Disease Using Induced Pluripotent Stem Cells
Rowland, H. A., Hooper, N. M., & Kellett, K. A. B. (2018) · Neurochemical Research · doi:10.1007/s11064-018-2663-z · Cited by 38
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Stromal cell-derived factor 1α decreases β-amyloid deposition in Alzheimer's disease mouse model
Wang, Q., Xu, Y., Chen, J., Qin, Y., Liu, M., Liu, Y., Xie, M.-J., Yu, Z., Zhu, Z., & Wang, W. (2012) · Brain Research · doi:10.1016/j.brainres.2012.04.011 · Cited by 39
Cimino, P. J., Yang, Y., Li, X., Hemingway, J. F., Cherne, M. K., Khademi, S. B., Fukui, Y., Montine, K. S., Montine, T. J., & Keene, C. D. (2013) · Experimental and Molecular Pathology · doi:10.1016/j.yexmp.2013.01.002 · Cited by 36
Vargas-Restrepo, F., Sabogal-Guáqueta, A. M., & Cardona‐Gómez, G. P. (2017) · Biomédica · doi:10.7705/biomedica.v38i0.3761 · Cited by 36
“Human Alzheimer’s disease and models are characterized by a high microglial hyperreactivity (1,3), which increases the release of proinflammatory cytokines and decreases βA clearance (4,22).”
BackgroundMicroglia in Alzheimer's Disease: A Role for Ion Channels
Thei, L., Imm, J. L., Kaisis, E., Dallas, M. L., & Kerrigan, T. L. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00676 · Cited by 37
“…in microglial function, documented by several lines of investigation, such as altered responses to Aβ aggregates or downregulation of “sensome” genes (Hickman et al., 2008; Cameron et al., 2012; Heneka et al., 2013; Hickman and El Khoury, 2013; Johansson et al., 2015) ever, this downregulation is…”
BackgroundFu, H., Liu, B., Li, L., & Lemere, C. A. (2020) · Neuroscience · doi:10.1016/j.neuroscience.2020.07.020 · Cited by 36
“Microglia cell culture N9 microglial cells were cultured as described (Hickman et al., 2008).”
BackgroundMethodComplex role of chemokine mediators in animal models of Alzheimer's Disease
Martin, E., & Delarasse, C. (2018) · Biomedical Journal · doi:10.1016/j.bj.2018.01.002 · Cited by 40
“[8] Hickman SE, Allison EK, El Khoury J.”
BackgroundFang, Y., Wang, J., Yao, L., Li, C., Wang, J., Liu, Y., Tao, X., Sun, H., & Liao, H. (2018) · Journal of Neuroinflammation · doi:10.1186/s12974-018-1250-1 · Cited by 35
“Moreover, in line with progression of AD pathology, proinflammatory cytokines reduce expressions of Aβ-binding receptors and Aβ-degrading enzymes and further decrease ability of microglial Aβ clearance [11].”
BackgroundPCSK9 and the nervous system: a no-brainer?
Jaafar, A. K., Techer, R., Chemello, K., Lambert, G., & Bourane, S. (2023) · Journal of Lipid Research · doi:10.1016/j.jlr.2023.100426 · Cited by 35
“(2023) 64(9) 100426 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).”
BackgroundLi, Q., Peng, J., Luo, Y., Zhou, J., Li, T., Cao, L. S., Peng, S., Zuo, Z., & Wang, Z. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02521-y · Cited by 36
“Nevertheless, the phagocytic ability of microglia decreases with aging, leading to the reduction of Aβ clearance during AD development [22].”
BackgroundGu, X., Zhou, Y., Zhang, Y., Wang, L., Gao, W., Luo, K., Sun, B., Li, T., Wang, H., Si, N., et al. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01587-5 · Cited by 39
“Additionally, cytokines such as IL-1α, MCP-1, IL-6 and TNF-α, were found to impair microglial clearance functions [20, 21].”
BackgroundEugenín, J. L., Vecchiola, A., Murgas, P., Arroyo, P., Cornejo, F., & Rommy von Bernhardi, M. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160083 · Cited by 35
“Reduction of microglial cells results in an increased accumulation of A (cid:2) in a murine AD model [47] and impairment of glia function by inflammatory conditions appears to contribute to AD pathogenesis by decreasing A (cid:2) clearance [37, 44, 54–56] and increasing neurotox-icity [57].”
Altered Processing of β-Amyloid in SH-SY5Y Cells Induced by Model Senescent Microglia
Angelova, D. M., & Brown, D. R. (2018) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.8b00334 · Cited by 36
Analysis of the Microglial Sensome
Hickman, S. E., & Khoury, J. B. E. (2019) · Methods in molecular biology · doi:10.1007/978-1-4939-9658-2_23 · Cited by 35
Self-citationMicroglial heterogeneity in aging and Alzheimer's disease: Is sex relevant?
Delage, C. I., Šimončičová, E., & Tremblay, M. (2021) · Journal of Pharmacological Sciences · doi:10.1016/j.jphs.2021.03.006 · Cited by 36
New insights in drug development for Alzheimer's disease based on microglia function
Qiao, O., Ji, H., Zhang, Y., Zhang, X., Zhang, X., Liu, N., Huang, L., Liu, C., & Gao, W. (2021) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2021.111703 · Cited by 35
Yanguas‐Casás, N., Torres‐Fuentes, C., Crespo‐Castrillo, A., Díaz-Pacheco, S., Healy, K., Stanton, C., Chowen, J. A., García‐Segura, L. M., Arévalo, M., Cryan, J. F., et al. (2021) · Neurobiology of Disease · doi:10.1016/j.nbd.2021.105495 · Cited by 36
“Thus, we analyzed different genes involved in inflammation-induced phagocytosis, such as CD36, IRAK4, MHCII, and P2RY6 (Fu et al., 2014; Hickman et al., 2008; Husemann et al., 2002; Xu et al., 2015).”
Animal models in the study of Alzheimer's disease and Parkinson's disease: A historical perspective
Banerjee, R., Rai, A., Iyer, S., Narwal, S., & Tare, M. (2022) · Animal Models and Experimental Medicine · doi:10.1002/ame2.12209 · Cited by 37
Lecordier, S., Pons, V., Rivest, S., & ElAli, A. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2021.813536 · Cited by 34
“Microglia Are Activated After Multifocal Microinfarcts Dependently Upon Biological Sex At the early stages of AD, microglial cell activation slows disease progression via elimination of Ab through phagocytosis (65, 68).”
BackgroundButyrylcholinesterase genotype and gender influence Alzheimer's disease phenotype
Lane, R. M., & He, Y. (2012) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2010.12.005 · Cited by 35
“The conflicting roles of microglia may have important implications for the treatment of AD pathology [153] (Figs.”
BackgroundResultInfluentialMercan, D., & Heneka, M. T. (2022) · Biology · doi:10.3390/biology11121822 · Cited by 34
“However, after prolonged duration of activation, they lose their ability to clear Aβ deposits [61,62] as a consequence of continued inflammatory activation [63].”
BackgroundGebril, H. M., Aryasomayajula, A., de Lima, M. R. N., Uhrich, K. E., & Moghe, P. V. (2024) · Translational Neurodegeneration · doi:10.1186/s40035-023-00393-7 · Cited by 37
“However, lysosomal degradation of fAβ has been shown to be interrupted in AD [77, 85, 110].”
BackgroundHe, S., Li, X., Mittra, N., Bhattacharjee, A., Wang, H., Song, S., Zhao, S., Liu, F., & Han, X. (2025) · Advanced Science · doi:10.1002/advs.202410910 · Cited by 34
Neuroimmune Biomarkers in Mental Illness
Herron, J. W., Nerurkar, L., & Cavanagh, J. (2018) · Current topics in behavioral neurosciences · doi:10.1007/7854_2018_45 · Cited by 35
Stem Cells as Potential Targets of Polyphenols in Multiple Sclerosis and Alzheimer’s Disease
Tandon, A., Singh, S. J., & Chaturvedi, R. K. (2018) · BioMed Research International · doi:10.1155/2018/1483791 · Cited by 36
Microglia changes associated to Alzheimer's disease pathology in aged chimpanzees
Edler, M. K., Sherwood, C. C., Meindl, R. S., Munger, E. L., Hopkins, W. D., Ely, J. J., ERWIN, J. M., Perl, D. P., Mufson, E. J., Hof, P. R., et al. (2018) · The Journal of Comparative Neurology · doi:10.1002/cne.24484 · Cited by 37
French, T., Düsedau, H. P., Steffen, J., Biswas, A., Ahmed, N., Hartmann, S., Schüler, T., Schott, B. H., & Dunay, I. R. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1539-8 · Cited by 33
Guo, E., Hu, Y.-W., Du, T., Zhu, H., Chen, L., Qu, W., Zhang, J., Xie, N., Liu, W., Feng, F., et al. (2019) · Bioorganic Chemistry · doi:10.1016/j.bioorg.2019.103258 · Cited by 34
Bellozi, P. M. Q., Gomes, G. F., da Silva, M. C. M., Lima, I. V. D. A., Batista, C. R. Á., Carneiro, W. D. O., Doria, J. G., Vieira, É. L. M., Vieira, R. P., de Freitas, R. P., et al. (2019) · Neuropharmacology · doi:10.1016/j.neuropharm.2019.107785 · Cited by 34
Cisbani, G., Koppel, A., Knezevic, D., Suridjan, I., Mizrahi, R., & Bazinet, R. P. (2020) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2020.02.014 · Cited by 37
Wan, T., Fu, M., Jiang, Y., Jiang, W., Li, P., & Zhou, S. (2021) · Neurochemical Research · doi:10.1007/s11064-021-03448-1 · Cited by 38
Godoy, B., Murgas, P., Tichauer, J. E., & Rommy von Bernhardi, M. (2012) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2012.06.004 · Cited by 34
“The presence of SR-A on astrocytes is especially relevant because SR-A is involved in inflammatory diseases (Sun et al., 2007; Hickman et al., 2008; Manning-Tobin et al., 2009) and astrocytes are key regulator of the inflammatory response in the CNS.”
BackgroundMethodInfluentialSenescent Microglia Represent a Subset of Disease-Associated Microglia in P301S Mice
Ng, P. Y., Zhang, C., Li, H., & Baker, D. J. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230109 · Cited by 38
Hickey, J. P., Collins, A. E., Nelson, M. L., Chen, H., & Kalisch, B. E. (2024) · Current Issues in Molecular Biology · doi:10.3390/cimb46050266 · Cited by 39
“…3 (GSK3) pathway, the decreased clearance of A β , the reduced clearance of tau through increased competitive binding and the internalization of CX3CL1, the production of proinflammatory molecules and ROS, the structural and functional dysregulation of the BBB, and cognitive decline [49,64–70].”
BackgroundPositron Emission Tomography Imaging of Neuroinflammation
Kannan, S., Balakrishnan, B., Muzik, O., Romero, R. J., & Chugani, D. C. (2009) · Journal of Child Neurology · doi:10.1177/0883073809338063 · Cited by 33
“Microglia isolated from aged transgenic mice models of Alzheimer disease exhibit marked reduction of Ab binding scavenger receptors and Ab-degrading enzymes along with an increase in the proinflammatory cytokines interleukin-1b and tumor necrosis factor-a, thereby setting the stage for disease progression.(21) Similar…”
BackgroundRole of amyloid-β CSF levels in cognitive deficit in MS
Gentile, A., Mori, F., Bernardini, S., & Centonze, D. (2015) · Clinica Chimica Acta · doi:10.1016/j.cca.2015.01.035 · Cited by 32
Immunology meets neuroscience – Opportunities for immune intervention in neurodegenerative diseases
Lynch, M. A., & Mills, K. H. G. (2011) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2011.05.013 · Cited by 34
Severini, C., Barbato, C., Certo, M. G. D., Gabanella, F., Petrella, C., Stadio, A. D., VINCENTIIS, M. D., Polimeni, A., Ralli, M., & Greco, A. (2020) · Current Neuropharmacology · doi:10.2174/1570159x18666200621204546 · Cited by 34
“Indeed, protracted activation of the immune response induces a reactive microgliosis with a persistent secretion of pro-inflammatory molecules and the recruitment of peripheral macrophages into the brain, which in turn aggravate AD pathology [43, 47-49].”
BackgroundMaresin 1 attenuates pro‐inflammatory activation induced by β‐amyloid and stimulates its uptake
Wang, Y., Leppert, A., Tan, S., van der Gaag, B., Li, N., Schultzberg, M., & Hjorth, E. (2021) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.16098 · Cited by 33
Ernest James Phillips, T., & Maguire, E. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.652593 · Cited by 33
The Potential Role of Protein Kinase R as a Regulator of Age-Related Neurodegeneration
Martínez, N. W., Gómez, F. E., & Matus, S. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.638208 · Cited by 31
“Notably, the increase in glial proinflammatory cytokines has also been correlated with a significant decrease in hippocampal LTP on several models of AD (Hickman et al., 2008; Ojala et al., 2008; Chakrabarty et al., 2010; Park and Bowers, 2010; Kitazawa et al., 2011; Spooren et al., 2011; Zhao et al., 2011; Sutinen et…”
BackgroundMicroglial cell response to experimental periodontal disease
Almarhoumi, R., Álvarez, C., Harris, T., Tognoni, C. M., Paster, B. J., Carreras, I., Dedeoglu, A., & Kantarcı, A. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02821-x · Cited by 36
“It is critical to note that our in vitro microglial activation with PD-associated microbiomes was done for 24 h, considered an acute model of microglial activation as previously suggested [38], and may not fully represent the chronic or evolving microglial activation that happens in AD [39].”
BackgroundElAli, A., Bordeleau, M., Thériault, P., Filali, M., Lampron, A., & Rivest, S. (2015) · Neuropsychopharmacology · doi:10.1038/npp.2015.279 · Cited by 32
Dual impact of neuroinflammation on cognitive and motor impairments in Alzheimer's disease
Fakorede, S., Lateef, O. M., Garuba, W. A., Akosile, P. O., Okon, D. A., & Aborode, A. T. (2025) · Journal of Alzheimer s Disease Reports · doi:10.1177/25424823251341870 · Cited by 40
“39 – 41 Astrocytes, essential for maintaining neuronal health and synaptic support, also become reactive in response to A β and tau pathology.”
Xue, F., Tian, J., Yu, C., Du, H., & Guo, L. (2021) · Neurobiology of Disease · doi:10.1016/j.nbd.2021.105272 · Cited by 32
Xie, Z., Meng, J., Kong, W., Wu, Z., Lan, F., Narengaowa, Hayashi, Y., Yang, Q., Bai, Z., Nakanishi, H., et al. (2022) · Aging Cell · doi:10.1111/acel.13565 · Cited by 33
“Microglial cells secrete several enzymes capable of degrading extracellular Aβ (Hickman et al., 2008).”
BackgroundCircular RNAs in Alzheimer’s Disease: A New Perspective of Diagnostic and Therapeutic Targets
Vakili, O., Asili, P., Babaei, Z., Mirahmad, M., Keshavarzmotamed, A., Asemi, Z., & Mafi, A. (2022) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1871527321666220829164211 · Cited by 34
Mannix, R., Zhang, J., Park, J., Lee, C., & Whalen, M. J. (2011) · Journal of Neurotrauma · doi:10.1089/neu.2011.1759 · Cited by 32
“, 2001), and agedependent differences in Ab clearance (Hickman et al., 2008) may modify the efficacy of strategies targeting Ab-induced secondary injury after TBI.”
Influential
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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