Cited by 383Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

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Inflammatory Response in the Hippocampus of PS1M146L/APP751SLMouse Model of Alzheimer's Disease: Age-Dependent Switch in the Microglial Phenotype from Alternative to Classic

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Jimenez, Sebastian, Baglietto-Vargas, David, Caballero, Cristina, Moreno-Gonzalez, Ines, Torres, Manuel, Sanchez-Varo, Raquel, Ruano, Diego, Vizuete, Marisa, Gutierrez, Antonia, Vitorica, Javier·2008·The Journal of Neuroscience

DOI 10.1523/jneurosci.3024-08.2008PMC PMC6671312

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Abstract

Although the microglial activation is concomitant to the Alzheimer's disease, its precise role (neuroprotection vs neurodegeneration) has not yet been resolved. Here, we show the existence of an age-dependent phenotypic change of microglial activation in the hippocampus of PS1xAPP model, from an alternative activation state with Aβ phagocytic capabilities (at 6 months) to a classic cytotoxic phenotype (expressing TNF-α and related factors) at 18 months of age. This switch was coincident with high levels of soluble Aβ oligomers and a significant pyramidal neurodegeneration.In vitro assays, using astromicroglial cultures, demonstrated that oligomeric Aβ42 and soluble extracts from 18-month-old PS1xAPP hippocampus produced a potent TNF-α induction whereas monomeric Aβ42 and soluble extract from 6- or 18-month-old control and 6-month-old PS1xAPP hippocampi produced no stimulation. This stimulatory effect was avoided by immunodepletion using 6E10 or A11. In conclusion, our results show evidence of a switch in the activated microglia phenotype from alternative, at the beginning of Aβ pathology, to a classical at advanced stage of the disease in this model. This change was induced, at least in part, by the age-dependent accumulation of extracellular soluble Aβ oligomers. Finally, these cytotoxic activated microglial cells could participate in the neuronal lost observed in AD.

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1 retracted

RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
Lesné, S., Koh, M. T., Kotilinek, L., Kayed, R., Glabe, C. G., Yang, A., Gallagher, M., & Ashe, K. H. (2006) · Nature · doi:10.1038/nature04533 · Cited by 2,769 · cited 2×
“The observed 6E10-positive bands corresponded with the reported Mr for the oligomeric A forms, detected by Western blots (see Lambert et al., 2007), and also similar to soluble oligomers identified in other aged tg models (Lesné et al., 2006).”
Background
Retracted
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
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Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis
Kayed, R., Head, E., Thompson, J. L., McIntire, T. M., Milton, S. C., Cotman, C. W., & Glabe, C. G. (2003) · Science · doi:10.1126/science.1079469 · Cited by 4,064 · cited 1×
“The soluble fractions (S1) were obtained by ultracentrifugation of the homogenates as described previously (Kayed et al., 2003).”
Method
Unbiased stereological estimation of the total number of neurons in the subdivisions of the rat hippocampus using the optical fractionator
West, M. J., Slomianka, L., & Gundersen, H. J. G. (1991) · The Anatomical Record · doi:10.1002/ar.1092310411 · Cited by 2,994 · cited 2×
“The software calculated the estimated total number of cresyl-violet stained nuclei in the CA1 region using the optical fractionator formula (West et al., 1991; Schmitz and Hof, 2005), N 1/bsf.1/ssf.1/asf.1/hsf.”
Method
IL-17 family cytokines and the expanding diversity of effector T cell lineages
Weaver, C. T., Hatton, R. D., Mangan, P. R., & Harrington, L. E. (2007) · Annual Review of Immunology · doi:10.1146/annurev.immunol.25.022106.141557 · Cited by 1,842 · cited 1×
“The recruitment of CD4 Th1-cells in experimental autoimmune encephalomyelitis (EAE; a disease similar to human multiple sclerosis) induced the production of, among other cytotoxic factors, TNF- (Dhib-Jalbut et al., 2006; Weaver et al., 2007).”
Background
Control of microglial neurotoxicity by the fractalkine receptor
Cardona, A. E., Pioro, E. P., Sasse, M. E., Kostenko, V., Cardona, S. M., Dijkstra, I. M., Huang, D., Kidd, G., Dombrowski, S., Dutta, R., et al. (2006) · Nature Neuroscience · doi:10.1038/nn1715 · Cited by 1,531 · cited 1×
“…reported that aging and/or A could decrease the neuronal expression of microglial inhibitory factors, such as CD200, fractalkine or neurotransmitters (Acetylcholine or noradrenaline) (Cardona et al., 2006; Chitnis et al., 2007; Heneka and O’Banion, 2007; Lyons et al., 2007a; Duan et al., 2008).”
Background
The efficiency of systematic sampling in stereology—reconsidered
GUNDERSEN, H. J. G., JENSEN, E. B. V., KIÊU, K., & NIELSEN, J. (1999) · Journal of Microscopy · doi:10.1046/j.1365-2818.1999.00457.x · Cited by 1,317 · cited 1×
“The precision of the individual estimations is expressed by the coefficient of error (CE) (Gundersen et al., 1999) and here we have estimated the total CE (CE group value) that was calculated using the CEs in each individual animal.”
Method
Untitled work
Wyss-Coray (2006) · doi:10.1038/nm1484 · Cited by 1,284 · cited 1×
“As proposed by the inflammation hypothesis of Alzheimer’s disease (AD), the neurodegenerative process could be exacerbated by a chronic inflammatory response to -amyloid (A ) peptides (for review, see Griffin et al., 1998; Wyss-Coray, 2006; Heneka and O’Banion, 2007).”
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Bone Marrow-Derived Microglia Play a Critical Role in Restricting Senile Plaque Formation in Alzheimer's Disease
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“We observed a close spatial and temporal parallelism between A deposits and microglial activation (Simard et al., 2006).”
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Background
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“Additionally, studies have found that gut microbiota alterations in AD affect cognitive function by altering the status of the microglia [15].”
Background
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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
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The Molecular Genetics of Autism Spectrum Disorders: Genomic Mechanisms, Neuroimmunopathology, and Clinical Implications
Guerra, D. J. (2011) · Autism Research and Treatment · doi:10.1155/2011/398636 · Cited by 23
Catalytic Immunoglobulin Gene Delivery in a Mouse Model of Alzheimer’s Disease: Prophylactic and Therapeutic Applications
Kou, J., Yang, J., Lim, J.-E., Pattanayak, A., Song, M., Planque, S. A., Paul, S., & Fukuchi, K.-I. (2014) · Molecular Neurobiology · doi:10.1007/s12035-014-8691-z · Cited by 22
“Indeed, microglia isolated from 6-month-old AD mouse models (TgPS1M146L/APP751SL) show an alternative activation state with Aβ phagocytic capabilities and those from 18-month-old AD mouse models display a classic cytotoxic phenotype [53].”
Background
Therapeutic versus neuroinflammatory effects of passive immunization is dependent on Aβ/amyloid burden in a transgenic mouse model of Alzheimer's disease
Minami, S., Sidahmed, E., Aïd, S., Shimoji, M., Niikura, T., Mocchetti, I., Rebeck, G. W., Prendergast, J., Dealwis, C. G., Wetzel, R. B., et al. (2010) · Journal of Neuroinflammation · doi:10.1186/1742-2094-7-57 · Cited by 26
“The effects of microglial activation may be pathology-dependent, as TNFa induction in younger PS1xAPP mice results in microglial phagocytosis while activation at older ages results in cytotoxic effects [29].”
Background
Microglia-Synapse Pathways: Promising Therapeutic Strategy for Alzheimer’s Disease
Xie, J., Wang, H., Lin, T., & Bi, B. (2017) · BioMed Research International · doi:10.1155/2017/2986460 · Cited by 22
“M2 microglia with Aβ phagocytic capability inAPP/PS1 transgenicmice at 6months of age can switch to M1 phenotypes at 18 months of age, in accordance with the levels of soluble Aβ oligomers [31].”
Gene Expression Profiling in the APP/PS1KI Mouse Model of Familial Alzheimer’s Disease
Weißmann, R., Hüttenrauch, M., Kacprowski, T., Bouter, Y., Pradier, L., Bayer, T. A., Kuss, A. W., & Wirths, O. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-150745 · Cited by 21
Curcumin Ameliorates the Reduction Effect of PGE2 on Fibrillar β-Amyloid Peptide (1-42)-Induced Microglial Phagocytosis through the Inhibition of EP2-PKA Signaling in N9 Microglial Cells
He, G., Luo, Z., Yang, J., Shen, T., Chen, Y., & Yang, X. (2016) · PLoS ONE · doi:10.1371/journal.pone.0147721 · Cited by 21
“microglia transform to a pro-inflammatory phenotype, lose their ability to clear Aβ, and produce pro-inflammatory cytokines which in turn reduce Aβ uptake and degradation [25].”
Background
Expression of Phenotypic Astrocyte Marker Is Increased in a Transgenic Mouse Model of Alzheimer’s Disease versus Age-Matched Controls: A Presymptomatic Stage Study
Doméné, A., Cavanagh, C., Page, G., Bodard, S., Klein, C., Delarasse, C., Chalon, S., & Krantic, S. M. (2016) · International Journal of Alzheimer s Disease · doi:10.1155/2016/5696241 · Cited by 21
Effects of collagen-induced rheumatoid arthritis on amyloidosis and microvascular pathology in APP/PS1 mice
Park, S. M., Shin, J. H., Moon, G. J., Cho, S. I., Lee, Y. B., & Gwag, B. J. (2011) · BMC Neuroscience · doi:10.1186/1471-2202-12-106 · Cited by 19
“to wild-type as previously reported [25-27].”
Ambivalent effects of compound C (dorsomorphin) on inflammatory response in LPS-stimulated rat primary microglial cultures
Łabuzek, K., Liber, S., Gabryel, B., Bułdak, Ł., & Okopień, B. (2009) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-009-0472-2 · Cited by 20
“Although microglial active participation in pathological processes affecting the brain is widely recognized, the relevance of their action has not been revealed thoroughly (Jimenez et al. 2008).”
BackgroundInfluential
Bioenergetic Impairment in the Neuro-Glia-Vascular Unit: An Emerging Physiopathology during Aging
Yuan, M., Wang, Y., Wang, S., Huang, Z., Jin, F., Zou, Q., Li, J., Pu, Y., & Cai, Z. (2021) · Aging and Disease · doi:10.14336/ad.2021.04017 · Cited by 20
The Innate and Adaptive Immune Cells in Alzheimer’s and Parkinson’s Diseases
Huang, B., Zhenxin, Y., Chen, S., Tan, Z., Zong, Z., Zhang, H., & Xiong, X. (2022) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2022/1315248 · Cited by 19
“It was demonstrated that in the early stage of AD, activated microglia can serve as neuroprotective by releasing several proteases for clearance of A β plaque [24].”
Proteome of brain glia: The molecular basis of diverse glial phenotypes
Jha, M. K., Kim, J., & Suk, K. (2013) · PROTEOMICS · doi:10.1002/pmic.201300236 · Cited by 19
“[187] Qin, H., Wilson, C. A., Roberts, K. L., Baker, B. J. et al., IL-10 inhibits lipopolysaccharide-induced CD40 gene expression through induction of suppressor of cytokine signaling-3.”
BackgroundInfluential
Alterations in intestinal microbiota and metabolites in individuals with Down syndrome and their correlation with inflammation and behavior disorders in mice
Cai, S., Lin, J., Li, Z., Liu, S., Feng, Z., Zhang, Y., Zhang, Y., Huang, J., & Chen, Q. (2023) · Frontiers in Microbiology · doi:10.3389/fmicb.2023.1016872 · Cited by 19
“This observation is consistent with clinical evidence suggesting that the alteration of intestinal microbiota in individuals with DS influences cognitive function by shifting the status of the microglia, such as through an increase in Firmicutes abundance (Jimenez et al., 2008).”
Result
Inhibition of hematopoietic cell kinase dysregulates microglial function and accelerates early stage Alzheimer's disease‐like neuropathology
Lim, S., Tran, D. N., Zumkehr, J., Chen, C., Ghiaar, S., Kieu, Z., Villanueva, E., Gallup, V., Rodríguez‐Ortiz, C. J., & Kitazawa, M. (2018) · Glia · doi:10.1002/glia.23522 · Cited by 20
“…in vivo results also suggest that Hck deficiency promotes microglia toward more proinflammatory state, which has been observed in longitudinal studies of microglial activation phenotypes in APP/PS1 AD mouse model (Jimenez et al., 2008) and in human AD patients (Fan, Brooks, Okello, & Edison, 2017).”
BackgroundResult
Encapsulated Choroid Plexus Epithelial Cells Actively Protect Against Intrahippocampal Aβ-induced Long-Term Memory Dysfunction; Upregulation of Effective Neurogenesis with the Abrogated Apoptosis and Neuroinflammation
Aliaghaei, A., Digaleh, H., Khodagholi, F., & Ahmadiani, A. (2015) · Journal of Molecular Neuroscience · doi:10.1007/s12031-015-0492-y · Cited by 18
Identifying an Optimal Neuroinflammation Treatment Using a Nanoligomer Discovery Engine
Sharma, S., Borski, C., Hanson, J. L., Garcia, M. A., Link, C. D., Hoeffer, C. A., Chatterjee, A., & Nagpal, P. (2022) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.2c00365 · Cited by 15
Circular RNA APP contributes to Alzheimer’s disease pathogenesis by modulating microglial polarization via miR-1906/CLIC1 axis
Wu, D., Wei, Y., Hou, L.-X., Du, Y., Yan, Q., Liu, L., Zhao, Y., Yan, R., Yu, C., Zhong, Z.-G., et al. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01698-7 · Cited by 17
“The imbalance of microglial polarization contributes to a vicious cycle between chronic neuroinflammation and AD pathology, which ultimately causes synaptic injury and cognitive decline [9, 10].”
The protective effect of betulinic acid on microvascular responsivity and protein expression in alzheimer disease induced by cerebral micro‐injection of beta‐amyloid and streptozotocin
Sarkaki, A., Farbood, Y., Badavi, M., Ghadiri, A., Dehcheshmeh, M. G., Mansouri, E., & Navabi, S. P. (2018) · Microcirculation · doi:10.1111/micc.12503 · Cited by 17
Genomic background-related activation of microglia and reduced β-amyloidosis in a mouse model of Alzheimer's disease
Fröhlich, C., Paarmann, K., Steffen, J., Stenzel, J., Krohn, M., Heinze, H., & Pahnke, J. (2013) · European Journal of Microbiology and Immunology · doi:10.1556/eujmi.3.2013.1.3 · Cited by 17
Region-specific distribution of β-amyloid peptide and cytokine expression in TgCRND8 mice
Ma, K., Mount, H. T. J., & McLaurin, J. (2011) · Neuroscience Letters · doi:10.1016/j.neulet.2011.01.035 · Cited by 17
The Role of Immunity in Alzheimer's Disease
McManus, R. M. (2022) · Advanced Biology · doi:10.1002/adbi.202101166 · Cited by 16
Amyloid β peptide-mediated neurotoxicity is attenuated by the proliferating microglia more potently than by the quiescent phenotype
Tsay, H.-J., Huang, Y., Huang, F.-L., Chen, C.-P., Tsai, Y.-C., Wang, Y.-H., Wu, M.-F., Chiang, F.-Y., & Shiao, Y. (2013) · Journal of Biomedical Science · doi:10.1186/1423-0127-20-78 · Cited by 16
“An age-dependent switch of microglial phenotype from phagocytic to classic cytotoxic was observed in APP/PS1 transgenic mice at 18 months old [46].”
Background
Gut-immune-brain interactions during neurodevelopment: from a brain-centric to a multisystem perspective
Volpedo, G., Riva, A., Nobili, L., Zara, F., Ravizza, T., & Striano, P. (2025) · BMC Medicine · doi:10.1186/s12916-025-04093-z · Cited by 21
“Interestingly, in Alzheimer’s disease (AD) [48, 49] and amyotrophic lateral sclerosis [50, 51] the opposite occurs, where microglia start out with an anti-inflammatory phenotype, followed by a pro-inflammatory phenotype during the advanced stage.”
Structural analysis of the microglia–interneuron interactions in the CA1 hippocampal area of the APP/PS1 mouse model of Alzheimer's disease
Gervais, É., Iloun, P., Martianova, E., Bessa, A. C. G., Rivest, S., & Topolnik, L. (2021) · The Journal of Comparative Neurology · doi:10.1002/cne.25289 · Cited by 15
“…hippocampal microglia surrounding the Aβ aggregations aremorphologically activated, displaying thicker and shorter processes, while the majority of microglial cells not in the vicinity of Aβ plaques demonstrate resting characteristics, with many branched thin processes (Jimenez et al., 2008).”
Background
Salidroside attenuates lipopolysaccharide-induced neuroinflammation and cognitive impairment in septic encephalopathy mice
Xiao, L., Li, L., Huang, J., Luan, Y., Pan, J., Gai, Y., & Xu, Z. (2023) · International Immunopharmacology · doi:10.1016/j.intimp.2023.109975 · Cited by 15
Should We Open Fire on Microglia? Depletion Models as Tools to Elucidate Microglial Role in Health and Alzheimer’s Disease
Romero‐Molina, C., Navarro, V., Jiménez, S., Muñoz‐Castro, C., Sanchez-Mico, M. V., Gutiérrez, A., Vitórica, J., & Vizuete, M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22189734 · Cited by 14
“Nevertheless, our results and others show that microglial activation increases with age in animals models with amyloid or Tau pathologies [20,26].”
ResultSelf-citation
Lactylation and Central Nervous System Diseases
Chen, Y., Xiao, D., & Li, X. (2025) · Brain Sciences · doi:10.3390/brainsci15030294 · Cited by 15
“When the CNS is damaged, microglia quickly activate and trigger a series of adaptive changes, including metabolic reprogramming [92].”
Mutant presenilin-1 deregulated peripheral immunity exacerbates Alzheimer-like pathology
Zhu, Y., Obregon, D. F., Hou, H., Giunta, B. N., Ehrhart, J. C., Fernandez, F., Mori, T., Nikolic, W. V., Zhao, Y., Morgan, D., et al. (2009) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2009.00962.x · Cited by 14
“Additionally, PS1 dysfunction profoundly inhibits A phagocytosis and clearance from the brain [8, 9].”
Background
Does the Interplay Between Aging and Neuroinflammation Modulate Alzheimer’s Disease Clinical Phenotypes? A Clinico-Pathological Perspective
Taipa, R. J. F., Sousa, A. L., Pires, M. M., & Sousa, N. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160121 · Cited by 15
Nitrosylation of Vesicular Transporters in Brain of Amyloid Precursor Protein/Presenilin 1 Double Transgenic Mice
Wang, Y., Zhou, Z., Tan, H. T., Zhu, S., Wang, Y., Sun, Y., Li, X., & Wang, J. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160700 · Cited by 14
“In addition, expression of iNOS was found to be increased in hippocampus of APP/PS1 mice [33, 34].”
Background
Impact of Aβ40 and Aβ42 Fibrils on the Transcriptome of Primary Astrocytes and Microglia
Zhu, X. A., Schrader, J. M., Irizarry, B. A., Smith, S. O., & Nostrand, W. E. V. (2022) · Biomedicines · doi:10.3390/biomedicines10112982 · Cited by 14
An insight into the TAM system in Alzheimer’s disease
Zhou, S., Li, Y., Zhang, Z., & Yuan, Y. (2023) · International Immunopharmacology · doi:10.1016/j.intimp.2023.109791 · Cited by 14
CD200‐CD200R1 signaling pathway regulates neuroinflammation after stroke
Zhao, S., Xu, H., Ya‐ping, W., Di, L., Wen‐qian, W., Ling‐song, M., Chu, Z., & Xu, Y. (2020) · Brain and Behavior · doi:10.1002/brb3.1882 · Cited by 13
“However, the switch depends on the alteration of inflammatory signals with the evolution of the disease (Jimenez et al., 2008).”
Background
Evolution of Alzheimer’s Disease Therapeutics: From Conventional Drugs to Medicinal Plants, Immunotherapy, Microbiotherapy and Nanotherapy
Ortiz-Islas, E., Montes, P., Rodríguez-Pérez, C. E., Ruiz-Sánchez, E., Sánchez-Barbosa, T., Pichardo-Rojas, D., Zavala‐Tecuapetla, C., Carvajal, K., & Campos‐Peña, V. (2025) · Pharmaceutics · doi:10.3390/pharmaceutics17010128 · Cited by 14
Global trends and prospects about synaptic plasticity in Alzheimer’s disease: a bibliometric analysis
Zhang, Y., Zhang, J., Wang, Y., & Yao, J. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1234719 · Cited by 12
Molecular imaging of neuroinflammation in Alzheimer’s disease
Varrone, A., & Nordberg, A. K. (2015) · Clinical and Translational Imaging · doi:10.1007/s40336-015-0137-8 · Cited by 13
Brain Lipids in the Pathophysiology and Treatment of Alzheimer’s Disease
Torres, M., Busquets, X., & Escribá, P. V. (2016) · InTech eBooks · doi:10.5772/64757 · Cited by 14
“However, this putative role for AD-associated neuroin‐ flammation is not supported by evidence showing that the inflammatory response is not neurotoxic and, indeed, it is even neuroprotective in a transgenic mouse model of AD [28].”
BackgroundSelf-citation
Somatostatin: Linking Cognition and Alzheimer Disease to Therapeutic Targeting
Sandoval, K. E., & WITT, K. A. (2024) · Pharmacological Reviews · doi:10.1124/pharmrev.124.001117 · Cited by 14
“An age-dependent accumulation of soluble A b Os in APP/PS1 mice showed to be a primary factor in the microglia switch to the cytotoxic M1 form (Jimenez et al., 2008), consistent with other preclinical studies (Sondag et al., 2009; Maezawa et al., 2011; Ferretti et al., 2012).”
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
“In lateonset AD (LOAD), microglia have been deprived of their beneficiary function due to a tenacious production of proinflammatory mediators [174].”
Background
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
Cudrania cochinchinensis attenuates amyloid β protein-mediated microglial activation and promotes glia-related clearance of amyloid β protein
Wang, C.-J., Chen, C.-C., Tsay, H.-J., Chiang, F.-Y., Wu, M.-F., & Shiao, Y. (2013) · Journal of Biomedical Science · doi:10.1186/1423-0127-20-55 · Cited by 12
“In neurodegenerative diseases, the number of activated microglia increase was observed near the foci of lesions [6,7].”
Background
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
“They can decrease Aβ toxicity to neurons via alternative activation states(Jimenez et al. 2008; Condello et al. 2015; Hickman et al. 2018).”
Inactivation of the PHD3-FOXO3 axis blunts the type I interferon response in microglia and ameliorates Alzheimer’s disease progression
Sánchez-García, M. A., Lara-Ureña, N., March‐Díaz, R., Luis, C. O. S., Quiñones-Cañete, S., Mora-Romero, B., Cabello-Rivera, D., Cabello-Rivera, D., Romero‐Molina, C., Romero‐Molina, C., et al. (2025) · Science Advances · doi:10.1126/sciadv.adu2244 · Cited by 10
“To understand the role of PHD3 induction in microglia, we exposed primary neonatal microglial cell cultures to oligomeric A ß (oA ß ), which activates microglia in contrast to monomeric A ß treatment ( 47 ).”
Self-citation
Age-Related Decrease in Glucagon-Like Peptide-1 in Mouse Prefrontal Cortex but Not in Hippocampus Despite the Preservation of Its Receptor
Ohshima, R. (2015) · American Journal of BioScience · doi:10.11648/j.ajbio.20150301.13 · Cited by 10
“Therefore, because the GLP-1R expression level is preserved even in aged mPFC, treatment with GLP-1 analogues and GLP-1R stimulation may enhance GLP-1 expression and could rescue from the accumulation of Aβ and microglial activation which are observed in AD patients [63, 64].”
Background
Association of CSF CD40 levels and synaptic degeneration across the Alzheimer’s disease spectrum
Ye, X., Zhou, W., & Zhang, J. (2018) · Neuroscience Letters · doi:10.1016/j.neulet.2018.11.019 · Cited by 9
Anti-Aβ antibodies bound to neuritic plaques enhance microglia activity and mitigate tau pathology
Laversenne, V., Nazeeruddin, S., Källstig, E., Colin, P., Voize, C., & Schneider, B. L. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-01069-3 · Cited by 11
A Novel Synthetic Compound 4-Acetyl-3-methyl-6-(2-bromophenyl)pyrano[3,4-c]pyran-1,8-dione Inhibits the Production of Nitric Oxide and Proinflammatory Cytokines Via the NF-κB Pathway in Lipopolysaccharide-Activated Microglia Cells
Chung, H.-S., Kim, S.-N., Jeong, J.-H., & Bae, H. (2013) · Neurochemical Research · doi:10.1007/s11064-013-0983-6 · Cited by 10
Type I Interferon Signaling Drives Microglial Dysfunction and Senescence in Human iPSC Models of Down Syndrome and Alzheimer's DiseasePreprint
Jin, M., Xu, R., Alam, M. M., Ma, Z., Zhu, S., Wang, L., Martini, A. C., Bernabucci, M., Xie, P., Kwan, K. Y., et al. (2021) · SSRN Electronic Journal · doi:10.2139/ssrn.3985173 · Cited by 10
Traumatic Brain Injury Accelerates the Onset of Cognitive Dysfunction and Aggravates Alzheimer's-Like Pathology in the Hippocampus by Altering the Phenotype of Microglia in the APP/PS1 Mouse Model
Wu, D., Kumal, J. P. P., Lu, X., Li, Y., Mao, D., Tang, X., Nie, M., Liu, X., Sun, L., Liu, B., et al. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.666430 · Cited by 11

Authors: Jimenez, S., Baglietto-Vargas, D., Caballero, C., Moreno-Gonzalez, I., Torres, M., Sanchez-Varo, R., Ruano, D., Vizuete, M., Gutierrez, A., & Vitorica, J.
Affiliations: Universidad de Sevilla (ES)
Universidad de Málaga (ES)
ORCID: Torres, Manuel
Sanchez-Varo, Raquel
Ruano, Diego
Vizuete, Marisa
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2008-11-05
Volume: 28
Issue: 45
Pages: 11650-11661
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.3024-08.2008
PMC: PMC6671312
OpenAlex: W2001334299
Cited by: 383
References: 70
Citations by year: 2026: 7 · 2025: 19 · 2024: 19 · 2023: 14 · 2022: 19 · 2021: 30 · 2020: 22 · 2019: 21 · 2018: 19 · 2017: 20 · 2016: 19 · 2015: 26 · 2014: 28 · 2013: 37 · 2012: 25
FWCI: 12.75
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 181 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion, cc-by-nc-nd)
DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, other-oa)
Repositorio Institucional de la Universidad de Málaga (University of Málaga) (submittedVersion, cc-by)
Funders: Ministerio de Economía y Competitividad
Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas
Instituto de Salud Carlos III
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords: Alzheimer's disease, microglial activation, alternative activation, hippocampus, amyloid-beta oligomers, soluble amyloid-beta, TNF-α, neurodegeneration, age-dependent disease progression, 6E10 antibody
MeSH terms: Aging, Alzheimer Disease, Analysis of Variance, Animals, Disease Models, Animal, Gene Expression Regulation, Glial Fibrillary Acidic Protein, Inflammation, Mice, Transgenic, Mutation, Phenotype, Tumor Necrosis Factor-alpha, Amyloid beta-Protein Precursor, CD3 Complex, Microglia, Lectins, CD11b Antigen, Mice, Nitric Oxide Synthase Type II, Presenilin-1

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Inflammatory Response in the Hippocampus of PS1M146L/APP751SLMouse Model of Alzheimer's Disease: Age-Dependent Switch in the Microglial Phenotype from Alternative to Classic

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