Cited by 347Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and Treatments

The DOI matches its Crossref record; 46 of the 48 references it cites were found in a registry or an index.

Association of Microglia with Amyloid Plaques in Brains of APP23 Transgenic Mice

Open access

Stalder, Martina, Phinney, Amie, Probst, Alphonse, Sommer, Bernd, Staufenbiel, Matthias, Jucker, Mathias·1999·The American Journal of Pathology

DOI 10.1016/s0002-9440(10)65423-5PMC PMC1866618

Open this paper in CoChat — free account Open PDF

Abstract

Microglia are a key component of the inflammatory response in the brain and are associated with senile plaques in Alzheimer's disease (AD). Although there is evidence that microglial activation is important for the pathogenesis of AD, the role of microglia in cerebral amyloidosis remains obscure. The present study was undertaken to investigate the relationship between beta-amyloid deposition and microglia activation in APP23 transgenic mice which express human mutated amyloid-beta precursor protein (betaPP) under the control of a neuron-specific promoter element. Light microscopic analysis revealed that the majority of the amyloid plaques in neocortex and hippocampus of 14- to 18- month-old APP23 mice are congophilic and associated with clusters of hypertrophic microglia with intensely stained Mac-1- and phosphotyrosine-positive processes. No association of such activated microglia was observed with diffuse plaques. In young APP23 mice, early amyloid deposits were already of dense core nature and were associated with a strong microglial response. Ultrastructurally, bundles of amyloid fibrils, sometimes surrounded by an incomplete membrane, were observed within the microglial cytoplasm. However, microglia with the typical characteristics of phagocytosis were associated more frequently with dystrophic neurites than with amyloid fibrils. Although the present observations cannot unequivocally determine whether microglia are causal, contributory, or consequential to cerebral amyloidosis, our results suggest that microglia are involved in cerebral amyloidosis either by participating in the processing of neuron-derived betaPP into amyloid fibrils and/or by ingesting amyloid fibrils via an uncommon phagocytotic mechanism. In any case, our observations demonstrate that neuron-derived betaPP is sufficient to induce not only amyloid plaque formation but also amyloid-associated microglial activation similar to that reported in AD. Moreover, our results are consistent with the idea that microglia activation may be important for the amyloid-associated neuron loss previously reported in these mice.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Integrity signals

Registry

Crossref · 10.1016/s0002-9440(10)65423-5

Cites

46 of 46 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Glutamate neurotoxicity and diseases of the nervous system
Choi, D. W. (1988) · Neuron · doi:10.1016/0896-6273(88)90162-6 · Cited by 8,188
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., & Cole, G. (1996) · Science · doi:10.1126/science.274.5284.99 · Cited by 4,210
Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
Games, D., Adams, D., Alessandrini, R., Barbour, R., Borthelette, P., Blackwell, C., Carr, T., Clemens, J., Donaldson, T., Gillespie, F., et al. (1995) · Nature · doi:10.1038/373523a0 · Cited by 2,516
RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease
Yan, S. D., Chen, X., Fu, J., Chen, M., Zhu, H., Roher, A., Slattery, T., Zhao, L., Nagashima, M., Morser, J., et al. (1996) · Nature · doi:10.1038/382685a0 · Cited by 2,012
The Fine Structure of the Nervous System.
Tennyson, V. M. (1970) · Archives of Neurology · doi:10.1001/archneur.1970.00480240094019 · Cited by 1,946
Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology
Sturchler-Pierrat, C., Abramowski, D., Duke, M., Wiederhold, K.-H., Mistl, C., Rothacher, S., Ledermann, B., Bürki, K., Frey, P., Paganetti, P. A., et al. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.24.13287 · Cited by 1,507
Self-citation
Amyloid, the presenilins and Alzheimer’s disease
Hardy, J. (1997) · Trends in Neurosciences · doi:10.1016/s0166-2236(96)01030-2 · Cited by 1,370
Arthritis and anti-inflammatory agents as possible protective factors for Alzheimer's disease: A review of 17 epidemiologic studies
McGeer, P. L., Schulzer, M., & McGeer, E. G. (1996) · Neurology · doi:10.1212/wnl.47.2.425 · Cited by 1,367
Activation of microglial cells by β-amyloid protein and interferon-γ
Meda, L., Cassatella, M. A., Szendrei, G. I., Otvos, L., Baron, P., Villalba, M., Ferrari, D., & Rossi, F. (1995) · Nature · doi:10.1038/374647a0 · Cited by 1,314
The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases
MCGEER, P., & MCGEER, E. (1995) · Brain Research Reviews · doi:10.1016/0165-0173(95)00011-9 · Cited by 1,287 · cited 2×
“–10 Activation of microglia is thought to induce an inflammatory response in the central nervous system and to be a mediator of the amyloid-associated neurodegeneration in AD brain.(11,12) The involvement of inflammation in the progress of AD is underlined by clinical studies showing an attenuation of AD symptoms by n…”
Background

Show all 48 references

Research works printed but not linked: 1

Calhoun, 1998, Neuron, synaptic bouton, and cholinergic fiber loss is associated with amyloid plaque formation in APP transgenic mice, Neurobiol Aging, 19, S143

Sorted by citations

Copper-Zinc Superoxide Dismutase (SOD1) Is Released by Microglial Cells and Confers Neuroprotection against 6-OHDA Neurotoxicity
Polazzi, E., Mengoni, I., Caprini, M., Peña‐Altamira, E., Kurtys, E., & Monti, B. (2012) · Neurosignals · doi:10.1159/000337115 · Cited by 9,023
Inflammation and Alzheimer’s disease
Akiyama, H. (2000) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00124-x · Cited by 4,514
Inflammation as a central mechanism in Alzheimer's disease
Kinney, J. W., Bemiller, S. M., Murtishaw, A. S., Leisgang, A. M., Salazar, A. M., & Lamb, B. T. (2018) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1016/j.trci.2018.06.014 · Cited by 2,253
“Activated microglia respond to Ab resulting in migration to the plaques and phagocytosis of Ab [108,112,113].”
Background
TREM2 Lipid Sensing Sustains the Microglial Response in an Alzheimer’s Disease Model
Wang, Y., Cella, M., Mallinson, K., Ulrich, J. D., Young, K. L., Robinette, M. L., Gilfillan, S., Krishnan, G. M., Sudhakar, S., Zinselmeyer, B. H., et al. (2015) · Cell · doi:10.1016/j.cell.2015.01.049 · Cited by 1,736
Microglial Dysfunction and Defective β-Amyloid Clearance Pathways in Aging Alzheimer's Disease Mice
Hickman, S. E., Allison, E. K., & El Khoury, J. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.0616-08.2008 · Cited by 1,329
“Microglia, the mononuclear phagocytes of the brain (Perry and Gordon, 1988), accumulate in senile plaques in AD patients and in animal models of AD (McGeer et al., 1987; Perlmutter et al., 1990; Frautschy et al., 1998; Dickson, 1999; Stalder et al., 1999).”
The GSK3 hypothesis of Alzheimer’s disease
Hooper, C., Killick, R., & Lovestone, S. (2008) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2007.05194.x · Cited by 1,191
Innate immunity in Alzheimer's disease
Heneka, M. T., Golenbock, D. T., & Latz, E. (2015) · Nature Immunology · doi:10.1038/ni.3102 · Cited by 902
Ccr2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer-like disease
El Khoury, J., Toft, M., Hickman, S. E., Means, T. K., Terada, K., Geula, C., & Luster, A. D. (2007) · Nature Medicine · doi:10.1038/nm1555 · Cited by 915
Stress and neuroinflammation: a systematic review of the effects of stress on microglia and the implications for mental illness
Calcia, M., Bonsall, D. R., Bloomfield, P. S., Selvaraj, S., Barichello, T., & Howes, O. D. (2016) · Psychopharmacology · doi:10.1007/s00213-016-4218-9 · Cited by 748
Lipopolysaccharide-Induced Inflammation Exacerbates Tau Pathology by a Cyclin-Dependent Kinase 5-Mediated Pathway in a Transgenic Model of Alzheimer's Disease
Kitazawa, M., Oddo, S., Yamasaki, T. R., Green, K. N., & LaFerla, F. M. (2005) · The Journal of Neuroscience · doi:10.1523/jneurosci.2868-05.2005 · Cited by 697
Bidirectional relationship between sleep and Alzheimer’s disease: role of amyloid, tau, and other factors
Wang, C., & Holtzman, D. M. (2020) · Neuropsychopharmacology · doi:10.1038/s41386-019-0478-5 · Cited by 615
Acute treatment with the PPARγ agonist pioglitazone and ibuprofen reduces glial inflammation and Aβ1–42 levels in APPV717I transgenic mice
Heneka, M. T., Sastre, M., Dumitrescu-Ozimek, L., Hanke, A., Dewachter, I., Kuiperi, C., O'Banion, K., Klockgether, T., Van Leuven, F., & Landreth, G. E. (2005) · Brain · doi:10.1093/brain/awh452 · Cited by 565
Dynamics of the Microglial/Amyloid Interaction Indicate a Role in Plaque Maintenance
Bolmont, T., Haiss, F., Eicke, D., Radde, R., Mathis, C. A., Klunk, W. E., Kohsaka, S., Jucker, M., & Calhoun, M. E. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.4814-07.2008 · Cited by 526
Self-citation
Contribution of glial cells to the development of amyloid plaques in Alzheimer’s disease
Nagele, R. G., Węgiel, J., Venkataraman, V., Imaki, H., Wang, K.-C., & Wegiel, J. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2004.01.007 · Cited by 522
Anti-Inflammatory Drug Therapy Alters β-Amyloid Processing and Deposition in an Animal Model of Alzheimer's Disease
Yan, Q., Zhang, J., Liu, H., Babu-Khan, S., Vassar, R., Biere, A. L., Citron, M., & Landreth, G. (2003) · The Journal of Neuroscience · doi:10.1523/jneurosci.23-20-07504.2003 · Cited by 469
Involvement of Microglial Receptor for Advanced Glycation Endproducts (RAGE) in Alzheimer's Disease: Identification of a Cellular Activation Mechanism
Lue, L.-F., Walker, D. G., Brachova, L., Beach, T. G., Rogers, J., Schmidt, A. M., Stern, D. M., & Yan, S. D. (2001) · Experimental Neurology · doi:10.1006/exnr.2001.7732 · Cited by 439
Microglia and Inflammation in Alzheimers Disease
Mandrekar-Colucci, S., & Landreth, G. E. (2010) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/187152710791012071 · Cited by 421
Neuronal overexpression of mutant amyloid precursor protein results in prominent deposition of cerebrovascular amyloid
Calhoun, M. E., Burgermeister, P., Phinney, A. L., Stalder, M., Tolnay, M., Wiederhold, K.-H., Abramowski, D., Sturchler-Pierrat, C., Sommer, B., Staufenbiel, M., et al. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.24.14088 · Cited by 410
Self-citation
Formation and maintenance of Alzheimer's disease β-amyloid plaques in the absence of microglia
Grathwohl, S. A., Kälin, R. E., Bolmont, T., Prokop, S., Winkelmann, G., Kaeser, S. A., Odenthal, J., Radde, R., Eldh, T., Gandy, S., et al. (2009) · Nature Neuroscience · doi:10.1038/nn.2432 · Cited by 401
Self-citation
Microglia and inflammatory mechanisms in the clearance of amyloid β peptide
Rogers, J., Strohmeyer, R., Kovelowski, C. J., & Li, R. (2002) · Glia · doi:10.1002/glia.10153 · Cited by 381
Soluble TREM2 ameliorates pathological phenotypes by modulating microglial functions in an Alzheimer's disease model
Zhong, L., Xu, Y., Zhuo, R., Wang, T., Wang, K., Huang, R., Wang, D., Gao, Y., Zhu, Y., Sheng, X., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-09118-9 · Cited by 371
Absence of C1q Leads to Less Neuropathology in Transgenic Mouse Models of Alzheimer's Disease
Fonseca, M. I., Zhou, J., Botto, M., & Tenner, A. J. (2004) · The Journal of Neuroscience · doi:10.1523/jneurosci.0901-04.2004 · Cited by 345
Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases
Vegeto, E., Benedusi, V., & Maggi, A. C. (2008) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2008.04.001 · Cited by 364
Mechanisms Underlying the Rapid Peroxisome Proliferator-Activated Receptor-γ-Mediated Amyloid Clearance and Reversal of Cognitive Deficits in a Murine Model of Alzheimer's Disease
Mandrekar-Colucci, S., Karlo, J. C., & Landreth, G. E. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.5268-11.2012 · Cited by 355
“The number of glial cells surrounding a plaque directly increases in proportion to the dimensions of the deposits (Stalder et al., 1999; Sasaki et al., 2002).”
Background
Microglia-Mediated Synapse Loss in Alzheimer's Disease
Rajendran, L., & Paolicelli, R. C. (2018) · The Journal of Neuroscience · doi:10.1523/jneurosci.1136-17.2017 · Cited by 355
Microglial Activation and β-Amyloid Deposit Reduction Caused by a Nitric Oxide-Releasing Nonsteroidal Anti-Inflammatory Drug in Amyloid Precursor Protein Plus Presenilin-1 Transgenic Mice
Jantzen, P. T., Connor, K. E., DiCarlo, G., Wenk, G. L., Wallace, J. L., Rojiani, A. M., Coppola, D., Morgan, D., & Gordon, M. N. (2002) · Journal of Neuroscience · doi:10.1523/jneurosci.22-06-02246.2002 · Cited by 341
Microglia and Alzheimer's disease pathogenesis
Streit, W. J. (2004) · Journal of Neuroscience Research · doi:10.1002/jnr.20093 · Cited by 335
RAGE‐dependent signaling in microglia contributes to neuroinflammation, Aβ accumulation, and impaired learning/memory in a mouse model of Alzheimer's disease
Fang, F., Lue, L.-F., Yan, S., Xu, H., Luddy, J. S., Chen, D., Walker, D. G., Stern, D. M., Yan, S., Schmidt, A. M., et al. (2010) · The FASEB Journal · doi:10.1096/fj.09-139634 · Cited by 335
Microglial activation and amyloid‐β clearance induced by exogenous heat‐shock proteins
Kakimura, J., Kitamura, Y., Takata, K., Umeki, M., Suzuki, S., Shibagaki, K., Taniguchi, T., Nomura, Y., Gebicke‐Haerter, P. J., Smith, M. A., et al. (2002) · The FASEB Journal · doi:10.1096/fj.01-0530fje · Cited by 333
Massive gliosis induced by interleukin‐6 suppresses Aβ deposition in vivo: evidence against inflammation as a driving force for amyloid deposition
Chakrabarty, P., Jansen‐West, K., Beccard, A., Ceballos‐Diaz, C., Levites, Y., Verbeeck, C., Zubair, A. C., Dickson, D., Golde, T. E., & Das, P. (2010) · The FASEB Journal · doi:10.1096/fj.09-141754 · Cited by 328
The multifaceted profile of activated microglia
Lynch, M. A. (2009) · Molecular Neurobiology · doi:10.1007/s12035-009-8077-9 · Cited by 268
Inflammatory cytokine levels correlate with amyloid load in transgenic mouse models of Alzheimer's disease
Patel, N. S., Paris, D., Mathura, V. S., Quadros, A., Crawford, F., & MULLAN, M. J. (2005) · Journal of Neuroinflammation · doi:10.1186/1742-2094-2-9 · Cited by 335
Microglia actions in Alzheimer's disease
Prokop, S., Miller, K. R., & Heppner, F. L. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1182-x · Cited by 291
Amyloid-β: a chameleon walking in two worlds: a review of the trophic and toxic properties of amyloid-β
Atwood, C., Obrenovich, M. E., Liu, T., Chan, H., Perry, G. L., Smith, M. A., & Martins, R. N. (2003) · Brain Research Reviews · doi:10.1016/s0165-0173(03)00174-7 · Cited by 297
Hippocampal Neuron Loss Exceeds Amyloid Plaque Load in a Transgenic Mouse Model of Alzheimer's Disease
Schmitz, C., Rutten, B. P. F., Pielen, A., Schäfer, S., Wirths, O., Tremp, G., Czech, C., Blanchard, V., Multhaup, G., Rezaie, P., et al. (2004) · The American Journal of Pathology · doi:10.1016/s0002-9440(10)63235-x · Cited by 281
Induction of Tau Pathology by Intracerebral Infusion of Amyloid-β-Containing Brain Extract and by Amyloid-β Deposition in APP × Tau Transgenic Mice
Bolmont, T., Clavaguera, F., Meyer-Luehmann, M., Herzig, M. C., Radde, R., Staufenbiel, M., Lewis, J., Hutton, M., Tolnay, M., & Jucker, M. (2007) · The American Journal of Pathology · doi:10.2353/ajpath.2007.070403 · Cited by 281
Self-citation
The Role of APOE4 in Disrupting the Homeostatic Functions of Astrocytes and Microglia in Aging and Alzheimer’s Disease
Fernandez, C. G., Hamby, M. E., McReynolds, M. L., & Ray, W. J. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00014 · Cited by 277
Transgenic animal models of Alzheimer's disease and related disorders: histopathology, behavior and therapy
Götz, J., Streffer, J. R., David, D. C., Schild, A., Hoerndli, F. J., Pennanen, L., Kurosinski, P., & Chen, F. (2004) · Molecular Psychiatry · doi:10.1038/sj.mp.4001508 · Cited by 284
Amyloid β42Activates a G-Protein-Coupled Chemoattractant Receptor, FPR-Like-1
Le, Y., Gong, W., Tiffany, H. L., Tumanov, A. V., Nedospasov, S. A., Shen, W., Dunlop, N. M., Gao, J., Murphy, P. M., Oppenheim, J. J., et al. (2001) · Journal of Neuroscience · doi:10.1523/jneurosci.21-02-j0003.2001 · Cited by 278
Retinoic Acid Attenuates β-Amyloid Deposition and Rescues Memory Deficits in an Alzheimer's Disease Transgenic Mouse Model
Ding, Y., Qiao, A., Wang, Z., Goodwin, J. S., Lee, E.-S., Block, M. L., Allsbrook, M., McDonald, M. P., & Fan, G.-H. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.3153-08.2008 · Cited by 269
Microglial activation correlates in vivo with both tau and amyloid in Alzheimer’s disease
Dani, M., Wood, M., Mizoguchi, R., Fan, Z., Walker, Z., Morgan, R., Hinz, R., Biju, M., Kuruvilla, T., Brooks, D. J., et al. (2018) · Brain · doi:10.1093/brain/awy188 · Cited by 270
Activation of microglia by secreted amyloid precursor protein evokes release of glutamate by cystine exchange and attenuates synaptic function
Barger, S. W., & Basile, A. S. (2001) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2001.00075.x · Cited by 264
Microglia and neuroprotection: From in vitro studies to therapeutic applications
Polazzi, E., & Monti, B. (2010) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2010.06.009 · Cited by 269
TREM2 is upregulated in amyloid plaque-associated microglia in aged APP23 transgenic mice
Frank, S., Burbach, G. J., Bonin, M., Walter, M., Streit, W., Bechmann, I., & Deller, T. (2008) · Glia · doi:10.1002/glia.20710 · Cited by 247
Time Course of the Development of Alzheimer-like Pathology in the Doubly Transgenic PS1+APP Mouse
Gordon, M. N., Holcomb, L. A., Jantzen, P. T., DiCarlo, G., Wilcock, D., Boyett, K. W., Connor, K., Melachrino, J., O'Callaghan, J. P., & Morgan, D. (2002) · Experimental Neurology · doi:10.1006/exnr.2001.7754 · Cited by 247
Comparative Analysis of Amyloid-β Chemical Structure and Amyloid Plaque Morphology of Transgenic Mouse and Alzheimer's Disease Brains
Kuo, Y., Kokjohn, T. A., Beach, T. G., Sue, L. I., Brune, D. C., Lopez, J. C., Kalback, W. M., Abramowski, D., Sturchler, C., Staufenbiel, M., et al. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m007859200 · Cited by 247
Self-citation
Chemotactic Signaling, Microglia, and Alzheimer's Disease Senile Plaques: Is There a Connection?
Luca, M. (2003) · Bulletin of Mathematical Biology · doi:10.1016/s0092-8240(03)00030-2 · Cited by 243
Microglial chemotaxis, activation, and phagocytosis of amyloid β-peptide as linked phenomena in Alzheimer's disease
Rogers, J., & Lue, L.-F. (2001) · Neurochemistry International · doi:10.1016/s0197-0186(01)00040-7 · Cited by 236
Noradrenergic regulation of inflammatory gene expression in brain
Feinstein, D. L., Heneka, M. T., Gavrilyuk, V., Russo, C. D., Weinberg, G. L., & Galea, E. (2002) · Neurochemistry International · doi:10.1016/s0197-0186(02)00049-9 · Cited by 222
The microglial phagocytic role with specific plaque types in the Alzheimer disease brain
D’Andrea, M. R., Cole, G. M., & Ard, M. D. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2003.12.026 · Cited by 215
Amyloid-Associated Neuron Loss and Gliogenesis in the Neocortex of Amyloid Precursor Protein Transgenic Mice
Bondolfi, L., Calhoun, M., Ermini, F., Kuhn, H. G., Wiederhold, K.-H., Walker, L., Staufenbiel, M., & Jucker, M. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-02-00515.2002 · Cited by 213
Self-citation
Aβ-Induced Inflammatory Processes in Microglia Cells of APP23 Transgenic Mice
Bornemann, K. D., Wiederhold, K., Pauli, C., Ermini, F., Stalder, M., Schnell, L., Sommer, B., Jucker, M., & Staufenbiel, M. (2001) · American Journal Of Pathology · doi:10.1016/s0002-9440(10)63945-4 · Cited by 206
Self-citation
Overexpression of human S100B exacerbates cerebral amyloidosis and gliosis in the Tg2576 mouse model of Alzheimer's disease
Mori, T., Koyama, N., Arendash, G. W., Horikoshi‐Sakuraba, Y., Tan, J., & Town, T. (2009) · Glia · doi:10.1002/glia.20924 · Cited by 212
Amyloid β and Amylin Fibrils Induce Increases in Proinflammatory Cytokine and Chemokine Production by THP‐1 Cells and Murine Microglia
Yates, S. L., Burgess, L. H., Kocsis‐Angle, J., Antal, J. M., Dority, M. D., Embury, P. B., Piotrkowski, A. M., & Brunden, K. R. (2000) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2000.0741017.x · Cited by 202
Effects of fatty acid unsaturation numbers on membrane fluidity and α-secretase-dependent amyloid precursor protein processing
Yang, X., Sheng, W., Sun, G. Y., & Lee, J. C. (2010) · Neurochemistry International · doi:10.1016/j.neuint.2010.12.004 · Cited by 215
In vivo P2X7 inhibition reduces amyloid plaques in Alzheimer's disease through GSK3β and secretases
Díaz‐Hernandéz, J. I., Gómez‐Villafuertes, R., León‐Otegui, M., Hontecillas‐Prieto, L., del Puerto, A., Trejo, J. L., Lucas, J. J., Garrido, J. J., Gualix, J., Miras‐Portugal, M. T., et al. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.09.040 · Cited by 203
Ferulic Acid Is a Nutraceutical β-Secretase Modulator That Improves Behavioral Impairment and Alzheimer-like Pathology in Transgenic Mice
Mori, T., Koyama, N., Guillot‐Sestier, M., Tan, J., & Town, T. (2013) · PLoS ONE · doi:10.1371/journal.pone.0055774 · Cited by 191
Alzheimer's Disease: Redox Dysregulation As a Common Denominator for Diverse Pathogenic Mechanisms
Rommy von Bernhardi, M., & Eugenín, J. L. (2011) · Antioxidants and Redox Signaling · doi:10.1089/ars.2011.4082 · Cited by 193
Progressive age-related impairment of cognitive behavior in APP23 transgenic mice
Kelly, P. H., Bondolfi, L., Hunziker, D., Schlecht, H. P., Carver, K., Maguire, E., Abramowski, D., Wiederhold, K., Sturchler, C., Jucker, M., et al. (2002) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00098-2 · Cited by 196
Self-citation
Cerebral Amyloid Induces Aberrant Axonal Sprouting and Ectopic Terminal Formation in Amyloid Precursor Protein Transgenic Mice
Phinney, A. L., Deller, T., Stalder, M., Calhoun, M. E., Frotscher, M., Sommer, B., Staufenbiel, M., & Jucker, M. (1999) · Journal of Neuroscience · doi:10.1523/jneurosci.19-19-08552.1999 · Cited by 188
Self-citation
Invasion of Hematopoietic Cells into the Brain of Amyloid Precursor Protein Transgenic Mice
Stalder, A. K., Ermini, F., Bondolfi, L., Krenger, W., Burbach, G. J., Deller, T., Coomaraswamy, J., Staufenbiel, M., Landmann, R. M., & Jucker, M. (2005) · Journal of Neuroscience · doi:10.1523/jneurosci.2545-05.2005 · Cited by 185
Self-citation
Transgenic mouse models of alzheimer disease: Developing a better model as a tool for therapeutic interventions.
Kitazawa, M., Medeiros, R., & M. LaFerla, F. (2012) · Current Pharmaceutical Design · doi:10.2174/138161212799315786 · Cited by 178
Tannic Acid Is a Natural β-Secretase Inhibitor That Prevents Cognitive Impairment and Mitigates Alzheimer-like Pathology in Transgenic Mice
Mori, T., Rezai-Zadeh, K. P., Koyama, N., Arendash, G. W., Yamaguchi, H., Kakuda, N., Horikoshi‐Sakuraba, Y., Tan, J., & Town, T. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.294025 · Cited by 189
Dynamic Complexity of the Microglial Activation Response in Transgenic Models of Amyloid Deposition: Implications for Alzheimer Therapeutics
Morgan, D., Gordon, M. N., Tan, J., Wilcock, D. M., & Rojiani, A. M. (2005) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/01.jnen.0000178444.33972.e0 · Cited by 176
Microglia as a Potential Bridge between the Amyloid β‐Peptide and Tau
Kitazawa, M., Yamasaki, T. R., & LaFerla, F. M. (2004) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1332.006 · Cited by 187
Young microglia restore amyloid plaque clearance of aged microglia
Daria, A., Colombo, A., Llovera, G., Hampel, H., Willem, M., Liesz, A., Haass, C., & Tahirovic, S. (2017) · The EMBO Journal · doi:10.15252/embj.201694591 · Cited by 174
Ectopic Cell Cycle Events Link Human Alzheimer's Disease and Amyloid Precursor Protein Transgenic Mouse Models
Yang, Y., Varvel, N. H., Lamb, B. T., & Herrup, K. (2006) · Journal of Neuroscience · doi:10.1523/jneurosci.3707-05.2006 · Cited by 175
Alzheimer's Disease Puzzle: Delving into Pathogenesis Hypotheses
(2024) · aging and disease · doi:10.14336/ad.2023.0608 · Cited by 183
Neuroinflammation and regeneration in the early stages of Alzheimer's disease pathology
Hoozemans, J. J. M., Veerhuis, R., Rozemüller, A. J. M., & Eikelenboom, P. (2005) · International Journal of Developmental Neuroscience · doi:10.1016/j.ijdevneu.2005.11.001 · Cited by 171
The Endogenous Estrogen Status Regulates Microglia Reactivity in Animal Models of Neuroinflammation
Vegeto, E., Belcredito, S., Ghisletti, S., Meda, C., Etteri, S., & Maggi, A. C. (2006) · Endocrinology · doi:10.1210/en.2005-1330 · Cited by 178
Pathogenic Mechanisms of Alzheimer's Disease Analyzed in the APP23 Transgenic Mouse Model
Sturchler, C., & Staufenbiel, M. (2000) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2000.tb06915.x · Cited by 171
Self-citation
Glycoprotein NMB: a novel Alzheimer’s disease associated marker expressed in a subset of activated microglia
Hüttenrauch, M., Ogorek, I., Klafki, H., Otto, M., Stadelmann, C., Weggen, S., Wiltfang, J., & Wirths, O. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0612-3 · Cited by 166
GSK3: a key target for the development of novel treatments for type 2 diabetes mellitus and Alzheimer disease
Gao, C., Hölscher, C., Liu, Y., & Li, L. (2012) · revneuro · doi:10.1515/rns.2011.061 · Cited by 164
Estrogen Enhances Uptake of Amyloid β‐Protein by Microglia Derived from the Human Cortex
Li, R., Shen, Y., Yang, L., Lue, L., Finch, C. E., & Rogers, J. (2000) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2000.0751447.x · Cited by 162
Microglia Demonstrate Age-Dependent Interaction with Amyloid-β Fibrils
Floden, A. M., & Combs, C. K. (2011) · Journal of Alzheimer s Disease · doi:10.3233/jad-2011-101014 · Cited by 166
Clearance of Amyloid-β Peptides By Microglia and Macrophages: the Issue of What, When and Where
Lai, A. Y., & McLaurin, J. (2012) · Future Neurology · doi:10.2217/fnl.12.6 · Cited by 166
Cholinergic Changes in the APP23 Transgenic Mouse Model of Cerebral Amyloidosis
Boncristiano, S., Calhoun, M. E., Kelly, P. H., Pfeifer, M., Bondolfi, L., Stalder, M., Phinney, A. L., Abramowski, D., Sturchler-Pierrat, C., Enz, A., et al. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-08-03234.2002 · Cited by 160
Self-citation
The role of microglial cells and astrocytes in fibrillar plaque evolution in transgenic APPSW mice
Wegiel, J. (2001) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00181-0 · Cited by 159
Amyloid-β Induces Chemotaxis and Oxidant Stress by Acting at Formylpeptide Receptor 2, a G Protein-coupled Receptor Expressed in Phagocytes and Brain
Tiffany, H. L., Lavigne, M. C., Cui, Y., Wang, J., Leto, T. L., Gao, J., & Murphy, P. M. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m101031200 · Cited by 161
Convergence of Amyloid-β and Tau Pathologies on Mitochondria In Vivo
Eckert, A., Schulz, K. L., Rhein, V. F., & Götz, J. (2010) · Molecular Neurobiology · doi:10.1007/s12035-010-8109-5 · Cited by 160
Cell division in the CNS: Protective response or lethal event in post-mitotic neurons?
Yang, Y., & Herrup, K. (2006) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2006.10.002 · Cited by 157
Microglial degeneration in the aging brain - bad news for neurons?
Streit, W. (2008) · Frontiers in Bioscience · doi:10.2741/2937 · Cited by 150
Fast-spiking parvalbumin-positive interneurons in brain physiology and Alzheimer’s disease
Hijazi, S., Smit, A. B., & van Kesteren, R. E. (2023) · Molecular Psychiatry · doi:10.1038/s41380-023-02168-y · Cited by 157
PK11195 labels activated microglia in Alzheimer's disease and in vivo in a mouse model using PET
Venneti, S., Lopresti, B. J., Wang, G., Hamilton, R. L., Mathis, C. A., Klunk, W. E., Apte, U. M., & Wiley, C. A. (2009) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2007.11.005 · Cited by 138
Senile plaque composition and posttranslational modification of amyloid-β peptide and associated proteins
Atwood, C., Martins, R. N., Smith, M. A., & Perry, G. L. (2002) · Peptides · doi:10.1016/s0196-9781(02)00070-0 · Cited by 142
Inflammation occurs early during the Aβ deposition process in TgCRND8 mice
Dudal, S., Krzywkowski, P., Paquette, J., Morissette, C., Lacombe, D., Tremblay, P., & Gervais, F. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2003.08.008 · Cited by 138
System Xc−and Apolipoprotein E Expressed by Microglia Have Opposite Effects on the Neurotoxicity of Amyloid-β Peptide 1–40
Qin, S., Colin, C., Hinners, I., Gervais, A., Cheret, C., & Mallat, M. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.5186-05.2006 · Cited by 135
Amyloid precursor protein and amyloid β-peptide bind to ATP synthase and regulate its activity at the surface of neural cells
Schmidt, C., Lepsverdize, E., L, S., Das, A. M., Pizzo, S. V., Dityatev, A. E., & Schachner, M. (2007) · Molecular Psychiatry · doi:10.1038/sj.mp.4002077 · Cited by 139
β Amyloid peptide (Aβ 42 ) is internalized via the G‐protein‐coupled receptor FPRL1 and forms fibrillar aggregates in macrophages 1
YAZAWA, H., YU, Z.-X., TAKEDA, K., LE, Y., GONG, W., FERRANS, V. J., OPPENHEIM, J. J., LI, C. C. H., & WANG, J. M. (2001) · The FASEB Journal · doi:10.1096/fj.01-0251com · Cited by 105
Extracellular amyloid formation and associated pathology in neural grafts
Meyer‐Luehmann, M., Stalder, M., Herzig, M. C., Kaeser, S. A., Kohler, E., Pfeifer, M., Boncristiano, S., Mathews, P. M., Mercken, M. H., Abramowski, D., et al. (2003) · Nature Neuroscience · doi:10.1038/nn1022 · Cited by 137
Self-citation
Inflammatory changes are tightly associated with neurodegeneration in the brain and spinal cord of the APP/PS1KI mouse model of Alzheimer's disease
Wirths, O., Breyhan, H., Marcello, A., Côtel, M.-C., Brück, W., & Bayer, T. A. (2008) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2008.06.011 · Cited by 140
Secretase Targets for Alzheimer's Disease: Identification and Therapeutic Potential
Wolfe, M. S. (2001) · Journal of Medicinal Chemistry · doi:10.1021/jm0004897 · Cited by 135
Induction of Brain-Derived Neurotrophic Factor in Plaque-Associated Glial Cells of Aged APP23 Transgenic Mice
Burbach, G. J., Hellweg, R., Haas, C. A., Del Turco, D., Deicke, U., Abramowski, D., Jucker, M., Staufenbiel, M., & Deller, T. (2004) · The Journal of Neuroscience · doi:10.1523/jneurosci.5599-03.2004 · Cited by 132
Self-citation
Spatial learning, exploration, anxiety, and motor coordination in female APP23 transgenic mice with the Swedish mutation
Lalonde, R., Dumont, M., Staufenbiel, M., Sturchler, C., & Strazielle, C. (2002) · Brain Research · doi:10.1016/s0006-8993(02)03476-5 · Cited by 135
Self-citation
Does my mouse have Alzheimer's disease?
Dodart, J., Mathis, C., Bales, K. R., & Paul, S. M. (2002) · Genes Brain & Behavior · doi:10.1034/j.1601-183x.2002.10302.x · Cited by 126
Microglia in Aging and Alzheimer’s Disease: A Comparative Species Review
Edler, M. K., Mhatre-Winters, I., & Richardson, J. R. (2021) · Cells · doi:10.3390/cells10051138 · Cited by 126
Nuclear receptors as therapeutic targets for Alzheimer's disease
Mandrekar-Colucci, S., & Landreth, G. E. (2011) · Expert Opinion on Therapeutic Targets · doi:10.1517/14728222.2011.594043 · Cited by 126
Microglial cells are the driving force in fibrillar plaque formation, whereas astrocytes are a leading factor in plaque degradation
Wegiel, J., Wang, K. C., Tarnawski, M., & Lach, B. (2000) · Acta Neuropathologica · doi:10.1007/s004010000199 · Cited by 124
Tracking neuroinflammation in Alzheimer’s disease: the role of positron emission tomography imaging
Zimmer, E. R., Leuzy, A., Benedet, A. L., Breitner, J., Gauthier, S., & Rosa-Neto, P. (2014) · Journal of Neuroinflammation · doi:10.1186/1742-2094-11-120 · Cited by 121
Changes in extracellular space size and geometry in APP23 transgenic mice: A model of Alzheimer's disease
Syková, E., Voříšek, I., Antonova, T., Mazel, T., Meyer-Luehmann, M., Jucker, M., Hájek, M., Or, M., & Bureš, J. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0408235102 · Cited by 121
Self-citation

Authors: Stalder, M., Phinney, A., Probst, A., Sommer, B., Staufenbiel, M., & Jucker, M.
Affiliations: University of Basel (CH)
Novartis (Switzerland) (CH)
Corresponding author: Jucker, Mathias
ORCID: Sommer, Bernd
Jucker, Mathias
Venue: The American Journal of Pathology
Publisher: Elsevier BV
Published: 1999-06
Volume: 154
Issue: 6
Pages: 1673-1684
ISSN: 0002-9440 (ISSN-L)
DOI: 10.1016/s0002-9440(10)65423-5
PMC: PMC1866618
OpenAlex: W2090811490
Cited by: 345
References: 48
Citations by year: 2026: 3 · 2025: 11 · 2024: 11 · 2023: 9 · 2022: 14 · 2021: 19 · 2020: 9 · 2019: 6 · 2018: 11 · 2017: 12 · 2016: 12 · 2015: 12 · 2014: 9 · 2013: 10 · 2012: 16
FWCI: 9.44
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: American Journal Of Pathology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Universität Basel
Novartis Pharma
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords: microglial activation, amyloid plaques, APP23 transgenic mice, cerebral amyloidosis, Alzheimer's disease, amyloid-beta deposition, amyloid fibrils, phagocytosis, Mac-1, phosphotyrosine, hippocampus, neocortex, dystrophic neurites, neuroinflammation
MeSH terms: Animals, Brain, Congo Red, Immunohistochemistry, Male, Mice, Transgenic, Microscopy, Immunoelectron, Microglia, Mice, Plaque, Amyloid

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

Association of Microglia with Amyloid Plaques in Brains of APP23 Transgenic Mice

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Self-check

Citations

Cites

Cited by

Related

Metadata

Record

About these checks