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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]
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).”
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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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“The efficacy of microglia in eliminating Aβ decreases over time in AD due to the formation of a stressful microenvironment [36].”
BackgroundInfluentialZeng, X., Cheung, S. K. K., Shi, M., Or, P. M. Y., Li, Z., Liu, J. Y. H., Ho, W. L.-H., Liu, T., Lu, K., Rudd, J. A., et al. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02970-z · Cited by 28
“Indeed, the ability of microglia cells to clear Aβ is still controversial and appears to be stage-specific [44–46].”
BackgroundMcKinsey, G. L., Santander, N. G., Zhang, X., Kleemann, K. L., Tran, L. T., Katewa, A., Conant, K., Barraza, M., Waddell, K., Lizama, C. O., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-57684-y · Cited by 32
“Please clarify which sex each data point is in each figure and discuss this as a limitation in the discussion.”
The age-related microglial transformation in Alzheimer's disease pathogenesis
Yuan, C., Aierken, A., Xie, Z., Li, N., Zhao, J., & Qing, H. (2020) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2020.03.024 · Cited by 27
Glycoengineering artificial receptors for microglia to phagocytose Aβ aggregates
Yu, D., Liu, C., Zhang, H., Ren, J., & Qu, X. (2021) · Chemical Science · doi:10.1039/d0sc07067j · Cited by 28
Microglial crosstalk with astrocytes and immune cells in amyotrophic lateral sclerosis
Calafatti, M., Cocozza, G., Limatola, C., & Garofalo, S. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1223096 · Cited by 29
Immunotherapy in Alzheimer's Disease: Where Do We Stand? Where Should We Go?
Rommy von Bernhardi, M. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-1248 · Cited by 28
TDP-43: A new player on the AD field?
Youmans, K. L., & Wolozin, B. L. (2012) · Experimental Neurology · doi:10.1016/j.expneurol.2012.05.018 · Cited by 28
The mixed-lineage kinase 3 inhibitor URMC-099 facilitates microglial amyloid-β degradation
Dong, W., Embury, C. M., Lu, Y., Whitmire, S. M., Dyavarshetty, B., Gelbard, H. A., Gendelman, H. E., & Kiyota, T. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0646-z · Cited by 28
“Microglial phagocytic capacity is linked to SR expression levels [45].”
BackgroundLessons Learned about Neurodegeneration from Microglia and Monocyte Depletion Studies
Lund, H., Pieber, M., & Harris, R. A. (2017) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2017.00234 · Cited by 27
“This is supported by evidence that microglia in the vicinity of amyloid beta plaques progressively lose phagocytic capacity (Hickman et al., 2008; Krabbe et al., 2013).”
BackgroundInflammatory Cyclooxygenase Activity and PGE2 Signaling in Models of Alzheimer’s Disease
Johansson, J. U., Woodling, N. S., Shi, J., & Andreasson, K. I. (2015) · Current Immunology Reviews · doi:10.2174/1573395511666150707181414 · Cited by 28
The Microglial Response to Neurodegenerative Disease
Song, W. M., & Colonna, M. (2018) · Advances in immunology · doi:10.1016/bs.ai.2018.04.002 · Cited by 30
Martínez‐Mármol, R., Mohannak, N., Qian, L., Wang, T., Gormal, R. S., Ruitenberg, M. J., Vanhaesebroeck, B., Coulson, E. J., & Meunier, F. A. (2019) · Journal of Neuroscience · doi:10.1523/jneurosci.0674-19.2019 · Cited by 27
“However, at later stages of disease, excess TNF levels in the brain in response to amyloid aggregates and fibrils can inhibit the microglial clearance of A (Hickman et al., 2008), inducing surrounding astrocytes into a toxic “A1” state that causes neuronal death (Liddelow et al.”
BackgroundVersatile nanomaterials for Alzheimer’s disease: Pathogenesis inspired disease-modifying therapy
Xi, Y., Chen, Y., Jin, Y., Han, G., Song, M., Song, T., Shi, Y., Tao, L., Huang, Z., Zhou, J., et al. (2022) · Journal of Controlled Release · doi:10.1016/j.jconrel.2022.02.034 · Cited by 27
Alzheimer’s Disease: From Molecular Mechanisms to Promising Therapeutic Strategies
Ivanova, A. V., Kutuzova, A. D., Kuzmichev, I., & Abakumov, M. A. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26199444 · Cited by 33
He, G., Luo, Z., Shen, T., Li, P., Yang, J., Luo, X. G., Chen, C., Gao, P., & Yang, X. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0762-9 · Cited by 27
Gil, V., & del Rı́o, J. A. (2019) · Cells · doi:10.3390/cells8030206 · Cited by 25
“This Sema3A might trigger microglia cell death, as described in other neuroinflammatory models, reducing their phagocytic-promoting functions which are necessary to reduce amyloid burden in affected brains [136].”
Thomas, L., Florio, T., & Perez-Castro, C. (2020) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2020.590034 · Cited by 28
A Review of the Application of Hyperbaric Oxygen Therapy in Alzheimer’s Disease
Somaa, F. A. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210157 · Cited by 26
Microglial activation in Alzheimer's disease: The role of flavonoids and microRNAs
Medrano-Jiménez, E., Meza‐Sosa, K. F., Aragon, J. A. U., Secundino, I., Pedraza-Alva, G., & Pérez-Martínez, L. (2022) · Journal of Leukocyte Biology · doi:10.1002/jlb.3mr1021-531r · Cited by 28
Lorenzi, E. D., Franceschini, D., Contardi, C., Martino, R. M. C. D., Seghetti, F., Serra, M., Bisceglia, F., Pagetta, A., Zusso, M., & Belluti, F. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23084381 · Cited by 28
“, interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α), chemokines, complement components, and reactive oxygen and nitrogen species, resulting in neuronal cell degeneration [19,20].”
BackgroundSt‐Pierre, M., VanderZwaag, J., Loewen, S. M., & Tremblay, M. (2022) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2022.932572 · Cited by 27
“As much as microglia are able to take up Aß (Hickman et al., 2008; Sebastian Monasor et al., 2020), indicating their ability to initially inhibit plaque growth, they are ultimately not as effective at removing existing deposits later on in the disease process (Sebastian Monasor et al.”
BackgroundWang, J., Gu, Y., Liu, X., Fan, Y., Zhang, Y., Yi, C., Cheng, C., & Yang, M. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms231810885 · Cited by 28
He, Y., Cong, L., Liang, S.-L., Ma, X., Tian, J.-N., Li, H., & Wu, Y. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.1056312 · Cited by 28
“Further experimental evidence suggests that the continued activation of the immune response indicates the accumulation of more microglia, making the Aβ deposition-immune response a positive feedback loop that further exacerbates the pathological changes of neuroinflammation and AD (Hickman et al., 2008).”
BackgroundExosomes: A missing link between chronic systemic inflammation and Alzheimer’s disease?
Ozansoy, M., Mikati, H., Velioğlu, H. A., & Yuluğ, B. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2022.114161 · Cited by 30
Yi, H., Zuo, D., Yu, X., Hu, F., Manjili, M. H., Chen, Z., Subjeck, J. R., & Wang, X. (2011) · Journal of Molecular Medicine · doi:10.1007/s00109-011-0828-1 · Cited by 27
“protective role in endotoxic shock [6], Alzheimer’s disease [7], and hyperoxia-induced lung injury [8], it has been”
New Molecular Targets for PET and SPECT Imaging in Neurodegenerative Diseases
Benadiba, M., Luurtsema, G., Wichert‐Ana, L., Buchpiguel, C. A., & Busatto, G. F. (2012) · Brazilian Journal of Psychiatry · doi:10.1016/j.rbp.2012.07.002 · Cited by 29
Ge, T.-Q., Guan, P.-P., & Wang, P. (2024) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2024.105868 · Cited by 28
Microvessel occlusions alter amyloid-beta plaque morphology in a mouse model of Alzheimer’s disease
Zhang, Y., Bander, E. D., Lee, Y., Muoser, C. A., Schaffer, C. B., & Nishimura, N. (2019) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x19889092 · Cited by 28
Dyne, E. D., Prakash, P. S., Li, J., Yu, B., Schmidt, T. L., Huang, S. D., & Kim, M. (2021) · Nanomedicine Nanotechnology Biology and Medicine · doi:10.1016/j.nano.2021.102397 · Cited by 26
Ye, Y., Gao, M., Shi, W., Gao, Y., Li, Y., Yang, W., Zheng, X., & Lu, X. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1325530 · Cited by 29
Let’s make microglia great again in neurodegenerative disorders
Guillot‐Sestier, M., & Town, T. (2017) · Journal of Neural Transmission · doi:10.1007/s00702-017-1792-x · Cited by 26
“In the context of neurodegenerative diseases, microglia lose their ability to phagocytose Ab (Hickman et al. 2008; Mawuenyega et al. 2010), a-synuclein (Bliederhaeuser et al. 2016) and infectious prion proteins (Sisková et al. 2009).”
Jović, M., Lončarević‐Vasiljković, N., Ivković, S., Dinić, J., Milanović, D., Zloković, B. V., & Kanazir, S. (2019) · PLoS ONE · doi:10.1371/journal.pone.0216726 · Cited by 27
Jang, S. K., Yu, J. M., Kim, S. T., Kim, G. H., Park, D. W., Lee, D. I., & Joo, S. S. (2015) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2015.03.071 · Cited by 26
Alemán-Villa, K. M., Armienta-Rojas, D. A., Camberos-Barraza, J., Rábago-Monzón, Á. R., Camacho-Zamora, A., Osuna‐Ramos, J. F., Magaña‐Gómez, J. A., Guadrón‐Llanos, A. M., Calderón-Zamora, L., Norzagaray-Valenzuela, C. D., et al. (2025) · NeuroImmunoModulation · doi:10.1159/000548021 · Cited by 34
“Aβ, especially in its oligomeric and fibrillar conformations, binds to multiple PRRs, including TLR2, TLR4, scavenger receptors, and RAGE, thereby activating NF-κB and MAPK pathways and inducing pro-inflammatory cytokine release [54].”
Cornejo, F., & Rommy von Bernhardi, M. (2013) · Mediators of Inflammation · doi:10.1155/2013/895651 · Cited by 25
“…glial cells in Alzheimer’s disease and the role played by scavenger receptors in the development of this pathology, focusing on the relevance of class A scavenger receptor (SR-A) for A𝛽 clearance and inflammatory activation of glial cell, and as a potential target for Alzheimer’s disease therapy.”
BackgroundDrug Development in Alzheimer’s Disease: The Contribution of PET and SPECT
Declercq, L., Vandenberghe, R. R., Laere, K. V., Verbruggen, A., & Bormans, G. M. (2016) · Frontiers in Pharmacology · doi:10.3389/fphar.2016.00088 · Cited by 27
“Once a more progressed AD state has been reached, neuroinflammation turns chronic and becomes harmful (Hickman et al., 2008).”
BackgroundHanna, L., Poluyi, E., Ikwuegbuenyi, C. A., Morgan, E., & Imaguezegie, G. (2022) · The Egyptian Journal of Neurosurgery : the official publication of the Egyptian Society of Neurological Surgeons/Egyptian journal of neurosurgery · doi:10.1186/s41984-022-00150-4 · Cited by 30
“Instead, microglial activation will be sustained in a feed-forward loop, or microgliosis, resulting in further accumulation of Aβ, production of inflammatory amplifiers and subsequent sustained proinflammatory cytokine signalling, thus exacerbating AD pathology due to the uncontrollable neuronal damage [44, 45].”
BackgroundPini, L., Salvalaggio, A., Wennberg, A. M. V., Dimakou, A., Matteoli, M., & Corbetta, M. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.101867 · Cited by 26
“In the earliest disease stage, microglia phagocytose A β , suggesting a protective role against the initial stages of the amyloid cascade (Simard et al., 2006; Hickman et al., 2008).”
Zhang, T., Feng, T., Wu, K., Guo, J. D., Nana, A. L., Yang, G., Seeley, W. W., & Hu, F. (2023) · Acta Neuropathologica · doi:10.1007/s00401-023-02578-w · Cited by 27
“CD11b + microglia were isolated from adult mouse brains using magnetic-activated cell sorting (MACS) according to published protocols [32, 44].”
MethodPreventive immunization of aged and juvenile non-human primates to beta-amyloid
Kofler, J., Lopresti, B. J., Janssen, C., Trichel, A. M., Masliah, E., Finn, O. J., Salter, R. D., MURDOCH, G. H., Mathis, C. A., & Wiley, C. A. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-84 · Cited by 26
“However, there are conflicting data in the literature as to which activation state may be more beneficial for Aβ phagocytosis [75-79].”
BackgroundBeta-amyloid and phosphorylated tau metabolism changes in narcolepsy over time
Liguori, C., Placidi, F., Izzi, F., Nuccetelli, M., Bernardini, S., Sarpa, M. G., Cum, F., Marciani, M. G., Mercuri, N. B., & Romigi, A. (2016) · Sleep And Breathing · doi:10.1007/s11325-015-1305-9 · Cited by 25
“In fact, it has been demonstrated that the beta-amyloidmetabolism could be affected by inflammatory processes [20]; moreover, the activation of the immune system may alter the beta-amyloid metabolism [21].”
BackgroundCurcumin and Novel Synthetic Analogs in Cell-Based Studies of Alzheimer’s Disease
Gagliardi, S., Franco, V., Sorrentino, S., Zucca, S., Pandini, C., Rota, P., Bernuzzi, S., Costa, A. C., Sinforiani, E., Pansarasa, O., et al. (2018) · Frontiers in Pharmacology · doi:10.3389/fphar.2018.01404 · Cited by 26
“This constitutes one important step related to Aβ-plaque formation and MGAT3 may also stabilize BACE1 in oxidative stress conditions (Hickman et al., 2008; Palmigiano et al., 2016).”
BackgroundContributions of Microglia to Structural Synaptic Plasticity
Kim, K. H., Son, S. M., & Mook‐Jung, I. (2013) · Journal of Experimental Neuroscience · doi:10.4137/jen.s11269 · Cited by 25
Muth, C., Schröck, K., Madore, C., Hartmann, K., Fanek, Z., Butovsky, O., Glatzel, M., & Krasemann, S. (2017) · Brain Pathology · doi:10.1111/bpa.12441 · Cited by 23
“The role of microglia in neurodegeneration is not fully understood and although these cells are able to clear misfolded proteins, they acquire detrimental effects in the course of a neurodegenerative disease (19, 23).”
Tarale, P., & Alam, M. M. (2022) · Inflammopharmacology · doi:10.1007/s10787-022-00958-4 · Cited by 26
Back to the origins: Human brain organoids to investigate neurodegeneration
Faravelli, I., Costamagna, G., Tamanini, S., & Corti, S. (2020) · Brain Research · doi:10.1016/j.brainres.2019.146561 · Cited by 25
A multi-targeting immunotherapy ameliorates multiple facets of Alzheimer’s disease in 3xTg mice
Feng, X., Hou, Y., Liu, J., Yan, F., Dai, M., Chen, M., Wang, J., Li, J., Liu, Z., Sun, D., et al. (2024) · npj Vaccines · doi:10.1038/s41541-024-00942-9 · Cited by 28
Hassan, H., Rawlinson, C., Lan, Y., Jenkins, S. I., & Chen, R. (2025) · Biomolecules · doi:10.3390/biom15111629 · Cited by 30
“Scavenger receptors such as Scavenger receptor A (SR-A) and class A1 scavenger receptor (Scara1) also mediate A β uptake but are down-regulated in aged APP transgenic mice, correlating with diminished phagocytosis and heightened inflammation [86].”
Yin, P., Wang, S., Wei, Y., Wang, X., Zhang, J., Yin, X., Feng, J., & Zhu, M. (2020) · Journal of Alzheimer’s Disease · doi:10.3233/jad-190682 · Cited by 24
Chen, R., Zhang, Q., Yan, Y., Zhang, Y., & Zhang, T. (2020) · Molecular Neurobiology · doi:10.1007/s12035-020-02219-3 · Cited by 23
Islam, J., Cho, J., Kim, J.-Y., Park, K., Koh, Y.-J., Chung, C. Y., Lee, E., Nam, S. J., Lee, K., Kim, S.-H., et al. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.766919 · Cited by 23
“In AD patients, the phagocytic ability of microglia was insufficient to clear Ab (5).”
BackgroundInfluentialMicroglia and microglial-based receptors in the pathogenesis and treatment of Alzheimer’s disease
Wang, Z., & Weaver, D. F. (2022) · International Immunopharmacology · doi:10.1016/j.intimp.2022.109070 · Cited by 26
Innate immunity dysregulation in aging eye and therapeutic interventions
Das, S., Ahmad, Z., Suryawanshi, A. S., & Kumar, A. (2022) · Ageing Research Reviews · doi:10.1016/j.arr.2022.101768 · Cited by 24
The Role of Dietary Lipids in Cognitive Health: Implications for Neurodegenerative Disease
Hans, S., Karadimou, A., Mulvihill, J. J., Grabrucker, A. M., & Zabetakis, I. (2022) · Biomedicines · doi:10.3390/biomedicines10123250 · Cited by 23
“They play a crucial part in clearing amyloid plaques in the brain, and this phagocytic activity is impaired in AD pathology [18,19].”
BackgroundAmyloid-β in Alzheimer’s disease – front and centre after all?
Weglinski, C., & Jeans, A. F. (2022) · Neuronal Signaling · doi:10.1042/ns20220086 · Cited by 24
Li, H., Sun, J., Miao, Z., Chen, S., & Yang, G. (2023) · Heliyon · doi:10.1016/j.heliyon.2023.e13411 · Cited by 24
“AS-IV reduces the production of Aβ plaques in 5xFAD mice Senile plaques accumulate in the brain due to neuroinflammation and microglial dysfunction which is an indication of AD histopathology [13,35].”
BackgroundBiological agents and the aging brain: glial inflammation and neurotoxic signaling
Latham, A. S., Moreno, J. A., & Geer, C. E. (2023) · Frontiers in Aging · doi:10.3389/fragi.2023.1244149 · Cited by 27
“Microglia in AD models are unable to properly phagocytose and degrade amyloid β fibrils, leading to the formation of insoluble aggregates (Wegiel et al., 2001; Suzanne et al., 2008).”
BackgroundSimufilam Reverses Aberrant Receptor Interactions of Filamin A in Alzheimer’s Disease
Wang, H.-Y., Cecon, E., Dam, J., Pei, Z., Jockers, R., & Burns, L. H. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241813927 · Cited by 27
“Although early microglial recruitment promotes clearance of soluble Aβ, as the disease progresses, elevated inflammatory cytokines can lead to insufficient phagocytic clearance of soluble Aβ, resulting in greater toxic signaling via α7nAChR and TLR4/2, intraneuronal Aβ accumulation, tau hyperphosphorylation and furthe…”
BackgroundInflammation, Autoimmunity and Neurodegenerative Diseases, Therapeutics and Beyond
Garmendia, J. V., Sanctis, C. V. D., Das, V., Annadurai, N., Hajdúch, M., & Sanctis, J. B. D. (2023) · Current Neuropharmacology · doi:10.2174/1570159x22666231017141636 · Cited by 27
“Interestingly, another AD mouse model showed an inverse correlation between cytokines IL-1 and TNF α production and amyloid-β clearance [58].”
BackgroundAssessment of Retinal Function and Morphology in Aging Ccl2 Knockout Mice
Vessey, K. A., Waugh, M., Jobling, A. I., Phipps, J. A., Ho, T., Trogrlic, L., Greferath, U., & Fletcher, E. L. (2015) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.14-15334 · Cited by 26
“Ccl2 has subsequently been shown to mediate the clearance of amyloid-b in Alzheimer’s disease.(10,11) Ccl2 has been found to be upregulated in the aqueous humor of patients with exudative age-related macular degeneration (AMD), suggesting a role for this signaling pathway in this disease.”
BackgroundHow dependent is synaptic plasticity on microglial phenotype?
Jones, R. S., & Lynch, M. A. (2014) · Neuropharmacology · doi:10.1016/j.neuropharm.2014.08.012 · Cited by 25
“It has been reported that released inflammatory mediators and oxidative species from activated glia decrease phagocytic function (Hickman et al., 2008); others have similarly reported a negative impact of inflammatory mediators on microglial phagocytosis (Koenigsknecht and Landreth, 2004; Pan et al.”
BackgroundLevy‐Barazany, H., & Frenkel, D. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-120 · Cited by 23
“Furthermore, it was found that the expression of these microglial Aβ phagocytic receptors decreased significantly in transgenic AD mice and, thereby, promoted Aβ accumulation and contributed to neurodegeneration [18].”
BackgroundMicroglia in Alzheimer’s Disease
Süß, P., & Schlachetzki, J. C. M. (2020) · Current Alzheimer Research · doi:10.2174/1567205017666200212155234 · Cited by 26
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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