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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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“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]
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
“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]
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“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]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
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.
In the citing paper
“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
“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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Items 901–1,000 of 1,003
Wang, X., Zhang, S., Li, Y., & Zhang, Y. (2024) · Human Molecular Genetics · doi:10.1093/hmg/ddae154 · Cited by 14
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“Thereby, the presence of amyloid deposits activates mononuclear cells and, at the same time, prevents them from an effective phagocytosis.(18) Furthermore, IL-1 stimulates the expression of the amyloid precursor protein, thus increasing the amyloid turnover.”
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Neuroinflammation drives APOE genotype-dependent differential expression of neprilysin
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How Microglia Manages Non-cell Autonomous Vicious Cycling of Aβ Toxicity in the Pathogenesis of AD
Seol, Y., Ki, S., Ryu, H. L., Chung, S., Lee, J.-H., & Ryu, H. (2020) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2020.593724 · Cited by 12
“the phagocytosis of fibrils and plaques with an overflow of Aβ in the brain (Figure 3; Hickman et al., 2008; O’Brien and Wong, 2011; Keren-Shaul et al., 2017; Anwar and Rivest, 2020; Webers et al., 2020).”
BackgroundPihlaja, R., Haaparanta‐Solin, M., & Rinne, J. O. (2017) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00299 · Cited by 13
“One of the many negative and detrimental effects is the impairment of the crucial Aβ degradation capacity of these cells, e.g., by impairing the function of receptors phagocytosing Aβ (Hickman et al., 2008; Mawuenyega et al., 2010; Heneka et al., 2015).”
BackgroundMicroglial cGAS deletion protects against amyloid-β induced Alzheimer’s disease pathogenesisPreprint
He, S., Li, X., Mittra, N., Bhattacharjee, A., Wang, H., Zhao, S., Liu, F., & Han, X. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.08.07.552300 · Cited by 12
“In late stages of AD, overactivated microglia 288 contributes to elevated proinflammatory cytokine production and has reduced Aβ clearance 289 capacity (59).”
Efficacy of exercise rehabilitation for managing patients with Alzheimer’s disease
Li, D., Jia, J., Zeng, H., Zhong, X., Chen, H., & Yi, C. (2023) · Neural Regeneration Research · doi:10.4103/1673-5374.391308 · Cited by 15
Xiong, W., She, W., Liu, Y., Zhou, H., Wang, X., Fang, L., Li, R., Wang, J., Qin, D., Jing, S., et al. (2024) · Theranostics · doi:10.7150/thno.102315 · Cited by 11
Asraf, K., Torika, N., Roasso, E., & Fleisher‐Berkovich, S. (2015) · Biological Chemistry · doi:10.1515/hsz-2015-0219 · Cited by 11
Owens, L., Benedetto, A., Dawson, N., Gaffney, C. J., & Parkin, E. T. (2021) · Brain Research · doi:10.1016/j.brainres.2020.147264 · Cited by 11
Liang, F., Sun, F., He, B., & Wang, J. (2022) · Neuroscience · doi:10.1016/j.neuroscience.2022.03.043 · Cited by 12
Microglia in Alzheimer’s Disease: A Favorable Cellular Target to Ameliorate Alzheimer’s Pathogenesis
Sumsuzzman, D. M., Uddin, M. S., Kabir, M. T., Hasana, S., Perveen, A., Alanazi, I. S., Albadrani, G. M., Abdel‐Daim, M. M., & Ashraf, G. M. (2022) · Mediators of Inflammation · doi:10.1155/2022/6052932 · Cited by 12
“Furthermore, both the SRAI expression levels and Aβ clearance have been attenuated by prolonged preservation of microglia activation [106].”
BackgroundNeishaboori, A. M., Eshraghi, A., Asl, A. T., Shariatpanahi, M., Yousefifard, M., & Gorji, A. (2022) · Pharmacology Research & Perspectives · doi:10.1002/prp2.977 · Cited by 10
Zhai, Z., Xie, D., Qin, T., Zhong, Y., Xu, Y., & Sun, T. (2022) · Neuroscience · doi:10.1016/j.neuroscience.2022.09.012 · Cited by 11
Ban, Y.-H., Park, D., Choi, E., Kim, T. M., Joo, S. S., & Kim, Y.-B. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24119561 · Cited by 11
“Functional change in microglial cells was observed in transgenic AD mice [39].”
BackgroundJónsdóttir, G., Ingólfsdóttir, I. E., Thormodsson, F. R., & Petersen, P. H. (2012) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2012.11.012 · Cited by 11
Temporal-logic analysis of microglial phenotypic conversion with exposure to amyloid-β
Anastasio, T. J. (2014) · Molecular BioSystems · doi:10.1039/c4mb00457d · Cited by 11
Viable mouse gene ablations that robustly alter brain Aβ levels are rare
Toyn, J. H., Lin, X.-A., Thompson, M. W., Guss, V. L., Meredith, J. E., Sankaranarayanan, S., Barrezueta, N. X., Corradi, J., Majumdar, A., Small, D. L., et al. (2010) · BMC Neuroscience · doi:10.1186/1471-2202-11-143 · Cited by 11
“[50] and microglial uptake of Ab [51,52].”
Jin, W., Dai, Y., Li, F., Zhu, L., Huang, Z., Liu, W., Li, J., Zhang, M., Du, J., Zhang, W., et al. (2019) · iScience · doi:10.1016/j.isci.2019.02.031 · Cited by 10
“On the other hand, several studies have indicated that microglia play a beneficial role during the onset and the progression of Alzheimer disease by removing the amyloid b plaques accumulated in the CNS (Herz et al., 2017; Hickman et al., 2008).”
BackgroundPromising molecular targets for pharmacological therapy of neurodegenerative pathologies
Неганова, М. Е., Aleksandrova, Y. R., Nebogatikov, V. O., Klochkov, S. G., & Ustyugov, A. A. (2020) · Acta Naturae · doi:10.32607/actanaturae.10925 · Cited by 11
Condition-Dependent Coordination and Peroxidase Activity of Hemin-Aβ Complexes
Bacchella, C., Brewster, J. T., Bähring, S., Dell’Acqua, S., Root, H. D., Thiabaud, G., Reuther, J. F., Monzani, E., Sessler, J. L., & Casella, L. (2020) · Molecules · doi:10.3390/molecules25215044 · Cited by 13
Research Progress of Lipid Metabolism-Mediated Neuroinflammation in Alzheimer’s Disease
Shen, Y., Wang, X., Liu, X., Wang, G., Hou, X., & Zhou, X. (2025) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-025-01648-9 · Cited by 12
“ApoE also participates in neuronal growth and ApoE synaptic plasticity, membrane repair, and remodeling processes, and is closely associated with tau-mediated neurodegeneration, glucose metabolism, and other processes(Hickman et al. 2008).”
Xu, P., Cui, D., Jin, M., & Sun, L. (2024) · Journal of Neurorestoratology · doi:10.1016/j.jnrt.2024.100094 · Cited by 12
Liu, H., Li, J., Wang, X., Luo, S., Luo, D., Ge, W., & Ma, C. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03083-x · Cited by 9
“In this inflammatory state, microglia exhibit heightened phagocytosis and release neurotoxic cytokines, which may paradoxically contribute to AD [21].”
BackgroundPotential Alzheimer’s disease drug targets identified through microglial biology research
Lepiarz‐Raba, I., Hidayat, T., Hannan, A. J., & Jawaid, A. (2024) · Expert Opinion on Drug Discovery · doi:10.1080/17460441.2024.2335210 · Cited by 9
“However, over time, microglia may become dysfunctional and exacerbate the disease process by excessive release of pro-inflammatory cytokines and exaggerated removal of healthy synapses [4].”
BackgroundCounil, H., Silva, R. O., Rabanel, J., Zaouter, C., Haddad, M., Khedher, M. R. B., Brambilla, D., Fülöp, T., Patten, S. A., & Ramassamy, C. (2025) · Journal of Extracellular Biology · doi:10.1002/jex2.70027 · Cited by 12
Wu, L., Zhao, Y., Gong, X., Liang, Z., Yu, J., Wang, J., Zhang, Y., Wang, X., Shu, X., & Bao, J. (2025) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.202400660 · Cited by 12
The role of microglia in the prion-like transmission of protein aggregates in neurodegeneration
Öztürk, M. M., Emgård, J., García‐Revilla, J., Fernández‐Calle, R., Yang, Y., Deierborg, T., & Roos, T. T. (2025) · Brain Communications · doi:10.1093/braincomms/fcaf087 · Cited by 14
“50 51-53 Activated microglia cluster around A β plaques 54 and adapt a unique gene expression profile, namely disease-associated microglia.”
Kaniuk, J. K., Kumar, D., Mazurek, C. Y., Khavari, S., Sollenberger, C. H., Ahuja, A., Mossner, J. M., & Ahuja, C. S. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26157191 · Cited by 11
“The Aß plaques themselves elicit an inflammatory response from microglia and astrocytes, driving a positive feedback loop of chronic inflammation [3,69].”
Ahmed, M. E., Selvakumar, G. P., Thangavel, R., Kempuraj, D., Raikwar, S. P., Zaheer, S. A., Iyer, S. S., & Zaheer, A. (2020) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-020-09929-4 · Cited by 10
Mahdavi, M., Karima, S., Rajaei, S., Aghamolaii, V., Ghahremani, H., Ataeia, R., Tehrani, H. S., Baram, S. M., Tafakhori, A., Lima, B. S., et al. (2021) · Galen Medical Journal · doi:10.31661/gmj.v10i0.1974 · Cited by 10
“In vivo studies on mice have demonstrated that TNF-α and Interferon-gamma (INF-γ) increase Aβ peptide production and lead to a decline in the microglial clearance of Aβ aggregates [10].”
BackgroundSrinivasan, G. R., & Brafman, D. A. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.813544 · Cited by 10
“Studies indicate that microglia phagocytose Aβ at the earlier stages of the disease contributing to its clearance but remain chronically activated marked by a decrease in their phagocytic capacity (Hickman et al., 2008; Yang et al., 2011).”
BackgroundDo Sleep Disturbances have a Dual Effect on Alzheimer’s Disease?
Arjmandi-Rad, S., Ebrahimnejad, M., Zarrindast, M., & Vaseghi, S. (2022) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-022-01228-1 · Cited by 11
Roles of Microglia in AD Pathology
Gao, R., Wu, H., Li, Q., & Zhao, J. (2023) · Current Alzheimer Research · doi:10.2174/1567205020666230203112351 · Cited by 10
Headmasters: Microglial regulation of learning and memory in health and disease
Weinhard, L., d’Errico, P., & Tay, T. L. (2018) · AIMS molecular science · doi:10.3934/molsci.2018.1.63 · Cited by 11
“The capacity for microglia to phagocytose Aβ efficiently is compromised in aging and AD, as demonstrated by less microglial clearance of Aβ fibrils in older mice [158] and downregulation of microglial genes encoding Aβ receptors and Aβ-degrading enzymes [159].”
Gamma radiation improves AD pathogenesis in APP/PS1 mouse model by potentiating insulin sensitivity
Khandelwal, M., Manglani, K., Gupta, S., & Tiku, A. B. (2020) · Heliyon · doi:10.1016/j.heliyon.2020.e04499 · Cited by 10
Tissue-specific features of microglial innate immune responses
Timmerman, R., Burm, S. M., & Bajramovic, J. J. (2020) · Neurochemistry International · doi:10.1016/j.neuint.2020.104924 · Cited by 10
Kim, M., Park, M., Nam, G., Lee, M., Kang, J., Song, I., Choi, M., Jin, H. K., Bae, J., & Lim, M. H. (2020) · Molecular Pharmaceutics · doi:10.1021/acs.molpharmaceut.0c00677 · Cited by 10
Wickstead, E. S., Irving, M. A., Getting, S. J., & McArthur, S. (2021) · FEBS Journal · doi:10.1111/febs.15861 · Cited by 10
Chronic PPARγ Stimulation Shifts Amyloidosis to Higher Fibrillarity but Improves Cognition
Blume, T., Deussing, M., Biechele, G., Peters, F., Zott, B., Schmidt, C., Franzmeier, N., Wind, K., Eckenweber, F., Sacher, C., et al. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.854031 · Cited by 10
“their chronic activation has a detrimental impact on disease progression (12; 7).”
BackgroundFour-dimensional microglia response to anti-Aβ treatment in APP/PS1xCX3CR1/GFP mice
Garcı́a-Alloza, M., Borrelli, L. A., Thyssen, D. H., Hickman, S. E., Khoury, J. B. E., & Bacskai, B. J. (2013) · IntraVital · doi:10.4161/intv.25693 · Cited by 10
Self-citationBid regulates the immunological profile of murine microglia and macrophages
Mayo, L., Levy, A., Jacob‐Hirsch, J., Amariglio, N., Rechavi, G., & Stein, R. (2010) · Glia · doi:10.1002/glia.21109 · Cited by 10
“Isolation of microglia from adult mice Microglia from adult mice were isolated as previously described (Cardona et al., 2006; Hickman et al., 2008), with minor modifications.”
MethodLoss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microgliaPreprint
Colombo, A. V., Dinkel, L., Müller, S. A., Monasor, L. S., Schifferer, M., Cantuti‐Castelvetri, L., König, J., Vidatic, L., Brémovà-Ertl, T., Hecimovic, S. K., et al. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/789511 · Cited by 10
Savchenko, E., Malm, T., Konttinen, H., Hämäläinen, R. H., Guerrero-Toro, C., Wojciechowski, S., Giniatullin, R. A., Koıstınaho, J., & Magga, J. M. (2016) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2016.00279 · Cited by 8
“Moreover, increased intracellular calcium level has been reported to be accompanied with decreased responsiveness to external purinergic stimulation (Hoffmann et al., 2003).”
BackgroundBasile, S., Parisi, C., Bellia, F., Zimbone, S., Arrabito, G., Gulli, D., Pignataro, B., Giuffrida, M. L., Sortino, S., & Copani, A. (2024) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.4c00284 · Cited by 9
Almalki, W. H., & Almujri, S. S. (2024) · Pathology - Research and Practice · doi:10.1016/j.prp.2024.155614 · Cited by 9
Rodríguez-López, A., Esteban, D., Domínguez‐Romero, A. N., & Gevorkian, G. (2025) · Experimental Neurology · doi:10.1016/j.expneurol.2025.115189 · Cited by 9
Abbott, V., Housden, B. E., & Houldsworth, A. (2025) · Brain Communications · doi:10.1093/braincomms/fcaf092 · Cited by 9
“91-93 These microglia increase A β plagues and tau proliferation, which then activate more microglia, creating a self-proliferating pathology.”
Lyamtsev, A. S., Sentyabreva, A. V., & Kosyreva, A. M. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26189250 · Cited by 9
“Microglia are able to play a protective role by phagocytizing α -syn aggregates at an early stage, but as PD progresses, the ability of microglia to phagocytose it becomes impaired due to prolonged activation, pathological conformations of α -syn, and aging itself [195].”
Stem Cells in Alzheimer’s Disease: Current Standing and Future Challenges
Salem, H., Colpo, G. D., & Teixeira, A. L. (2018) · Advances in experimental medicine and biology · doi:10.1007/5584_2018_214 · Cited by 9
Sivasaravanaparan, M., Olesen, L. Ø., Severino, M., von Linstow, C. U., Lambertsen, K. L., Gramsbergen, J. B., Hasselstrøm, J. B., Metaxas, A., Wiborg, O., & Finsen, B. R. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220019 · Cited by 10
Izumi, M., Seki, T., Iwasaki, K., & Sakamoto, K. (2009) · The Tohoku Journal of Experimental Medicine · doi:10.1620/tjem.219.53 · Cited by 9
“Expression of the mRNAs of PGC-1α (peroxisome proliferator-activated receptor-γ coactivator-α ), UCP2 (uncoupling proteins-2) (Kakuma et al. 2000; Arumugam et al. 2008), PPAR-γ (peroxisome proliferator-activated receptor-γ ) (Tjokroprawiro 2006; Escribano et al. 2009), adiponectin (Migrenne et al. 2009), adipsin (Drev…”
InfluentialChitotriosidase enhances TGFβ-Smad signaling and uptake of β-amyloid in N9 microglia
Wang, X., Yu, W., Fu, X. L., Ke, M., Xiao, Q., & Lü, Y. (2018) · Neuroscience Letters · doi:10.1016/j.neulet.2018.09.037 · Cited by 9
Cysteine-rich granulin-3 rapidly promotes amyloid-β fibrils in both redox states
Bhopatkar, A. A., Ghag, G., Wolf, L. M., Dean, D. N., Moss, M. A., & Rangachari, V. (2019) · Biochemical Journal · doi:10.1042/bcj20180916 · Cited by 10
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Kunze, L. H., Ruch, F., Biechele, G., Eckenweber, F., Wind-Mark, K., Dinkel, L., Feyen, P., Bartenstein, P., Ziegler, S. I., Paeger, L., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241210106 · Cited by 9
“Microglia form a distinct population among myeloid immune cells of the organism [4] and they are critical to maintaining the physiological state of the brain by releasing neurotrophic factors and removing possibly neurotoxic debris such as pathological protein aggregates [2,3,5,6].”
BackgroundMalm, T., Magga, J. M., & Koıstınaho, J. (2012) · Current Translational Geriatrics and Experimental Gerontology Reports · doi:10.1007/s13670-011-0004-z · Cited by 9
“Aged animals also have reduced expression of Aβ-binding receptors and Aβ-degrading enzymes [17].”
BackgroundThe ageing immune system and its clinical implications
Wordsworth, D., & Dunn‐Walters, D. K. (2010) · Reviews in Clinical Gerontology · doi:10.1017/s0959259810000407 · Cited by 9
Lloyd, A. F., Martínez‐Muriana, A., Davis, E., Daniels, M. J. D., Hou, P., Mancuso, R., Brenes, A. J., Geric, I., Snellinx, A., Craessaerts, K., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.07.07.498804 · Cited by 9
“Fundamental differences between ex vivo and in vitro microglia associated with protein synthesis, metabolism, and inflammatory marker expression are highlighted, and dynamic reprogramming of microglia proteomes is shown to be induced by changes in environment.”
Negah, S. S., Moradi, H. R., Forouzanfar, F., Sahraian, M. A., & Faraji, M. (2025) · Neurochemical Research · doi:10.1007/s11064-025-04344-8 · Cited by 8
The role of macrophage scavenger receptor 1 (Msr1) in prion pathogenesis
Li, B., Chen, M., Aguzzi, A., & Zhu, C. (2021) · Journal of Molecular Medicine · doi:10.1007/s00109-021-02061-7 · Cited by 7
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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