The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Astrocytes Regulate Microglial Phagocytosis of Senile Plaque Cores of Alzheimer's Disease
Abstract
We have developed an in vitro model in which isolated senile plaque (SP) cores are presented to rat microglial cells in culture. Microglia rapidly phagocytosed, broke apart, and cleared SP cores. However, when cocultured with astrocytes, microglial phagocytosis was markedly suppressed, allowing the SPs to persist. Suppression of phagocytosis by astrocytes appears to be a general phenomena since microglia in the presence of astrocytes showed reduced capacity to phagocytose latex beads as well. The astrocyte effect on microglia is related in part to a diffusible factor(s) since astrocyte- but not fibroblast-conditioned media also reduced phagocytosis. These results suggest that while microglia have the capacity to phagocytose and remove SPs, astrocytes which lie in close association to microglia may help prevent the efficient clearance of SP material allowing them to persist in Alzheimer's disease.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
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?
In the citing paper
“Moreover, astrocytes can also modulate microglial responses to Aβ [55, 58, 59].”
From IL-1β-driven amyloid plaque clearance is associated with an expansion of transcriptionally reprogrammed microglia (2019) · cites this paper as [59]
Citations
Cites
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
Relationship of microglia and astrocytes to amyloid deposits of Alzheimer disease
Itagaki, S., McGeer, P. L., Akiyama, H., Zhu, S., & Selkoe, D. (1989) · Journal of Neuroimmunology · doi:10.1016/0165-5728(89)90115-x · Cited by 940
Release of Excess Amyloid β Protein from a Mutant Amyloid β Protein Precursor
Cai, X.-D., Golde, T. E., & Younkin, S. G. (1993) · Science · doi:10.1126/science.8424174 · Cited by 913
McGeer, P. L., Itagaki, S., Tago, H., & McGeer, E. G. (1987) · Neuroscience Letters · doi:10.1016/0304-3940(87)90696-3 · Cited by 836
Flagged first, then by citations
Research works printed but not linked: 65
- Abd-El-Basset, 1995, Effect of bacterial wall lipopolysaccharide (LPS) on morphology, motility and cytoskeletal organization of microglia in cultures, J. Neurosci. Res., 41, 222, 10.1002/jnr.490410210 · DOI
- Araujo, 1992, β-Amyloid stimulates glial cells in vitro to produce growth factors that accumulate in senile plaques in Alzheimer's disease, Brain Res., 569, 141, 10.1016/0006-8993(92)90380-R · DOI
- Ard, 1996, Scavenging of Alzheimer's amyloid β-protein by microglia in culture, J. Neurosci. Res., 43, 190, 10.1002/(SICI)1097-4547(19960115)43:2<190::AID-JNR7>3.0.CO;2-B · DOI
- Ashwell, 1989, Development of microglia in the albino rabbit retina, J. Comp. Neurol., 287, 286, 10.1002/cne.902870303 · DOI
- Bell, 1994, Upregulation of the macrophage scavenger receptor in response to different forms of injury in the CNS, J. Neurocytol., 23, 605, 10.1007/BF01191555 · DOI
- Berbel, 1988, The development of the corpus callosum in cats: A light and electron-microscopic study, J. Comp. Neurol., 276, 132, 10.1002/cne.902760109 · DOI
- Bignami, 1991, Brain extracellular matrix and nerve regeneration, Adv. Exp. Med. Biol., 296, 197, 10.1007/978-1-4684-8047-4_19 · DOI
- Canning, 1993, β-amyloid of Alzheimer's disease induces reactive gliosis that inhibits axon outgrowth, Exp. Neurol., 124, 289, 10.1006/exnr.1993.1199 · DOI
- Chamak, 1991, Fibronectin and laminin regulate the in vitro differentiation of microglial cells, Neuroscience, 45, 513, 10.1016/0306-4522(91)90267-R · DOI
- Christie, 1996, Expression of the macrophage scavenger receptor, a multifunctional lipoprotein receptor, in microglia associated with senile plaques in Alzheimer's disease, Am. J. Pathol., 148, 399
- Cras, 1990, Neuronal and microglial involvement in β-amyloid protein deposition in Alzheimer's disease, Am. J. Pathol., 137, 241
- Davis, 1994, Cellular Forms and Functions of Brain Microglia, Brain Res. Bull., 34, 73, 10.1016/0361-9230(94)90189-9 · DOI
- Elkabes, 1996, Brain microglia/macrophages express neurotrophins that selectively regulate microglia proliferation and function, J. Neurosci., 16, 2508, 10.1523/JNEUROSCI.16-08-02508.1996 · DOI
- Ferrer, 1990, Naturally occurring cell death in the cerebral cortex of the rat and removal of dead cells by transitory phagocytes, Neuroscience, 39, 451, 10.1016/0306-4522(90)90281-8 · DOI
- Frackowiak, 1992, Ultrastructure of the microglia that phagocytose amyloid and the microglia that produce β-amyloid fibrils, Acta Neuropathol., 84, 225, 10.1007/BF00227813 · DOI · Paper page
- Frank, 1996, Cellular reaction at the lesion site after crushing of the rat optic nerve, Glia, 16, 227, 10.1002/(SICI)1098-1136(199603)16:3<227::AID-GLIA5>3.0.CO;2-Z · DOI
- Frautschy, 1992, Phagocytosis and deposition of vascular beta-amyloid in rat brains injected with Alzheimer beta amyloid, Am. J. Pathol., 140, 1389
- Gehrmann, 1995, Microglia: Intrinsic immunoeffector cell of the brain, Brain Res. Rev., 20, 269, 10.1016/0165-0173(94)00015-H · DOI
- Giordana, 1994, Reactive Cell Proliferation and microglia following injury to the rat brain, Neuropathol. Applied Neurobiol., 20, 163, 10.1111/j.1365-2990.1994.tb01175.x · DOI
- Giulian, 1986, Characterization of ameboid microglia isolated from developing mammalian brain, J. Neurosci., 6, 2163, 10.1523/JNEUROSCI.06-08-02163.1986 · DOI
- Giulian, 1989, The role of mononuclear phagocytes in wound healing after traumatic injury to adult mammalian brain, J. Neurosci., 9, 4416, 10.1523/JNEUROSCI.09-12-04416.1989 · DOI
- Giulian, 1995, Senile plaques stimulate microglia to release a neurotoxin found in Alzheimer's brain, Neurochem. Int., 27, 119, 10.1016/0197-0186(95)00067-I · DOI · Paper page
- Giulian, 1995, Cell surface morphology identifies microglia as a distinct class of mononuclear phagocyte, J. Neurosci., 15, 7712, 10.1523/JNEUROSCI.15-11-07712.1995 · DOI
- Hachimi, 1994, Do microglial cells phagocyte the β/A4-amyloid senile plaque core of Alzheimer disease, C. R. Acad. Sci. III, 317, 445
- Haga, 1989, Demonstration of microglia cells in and around senile (neuritic) plaques in the Alzheimer brain: An immunohistochemical study using a novel monoclonal antibody, Acta Neuropathol., 77, 569, 10.1007/BF00687883 · DOI
- Haga, 1993, Synthetic Alzheimer amyloid beta/A4 peptides enhance production of complement C3 component by cultured microglial cells, Brain Res, 601, 88, 10.1016/0006-8993(93)91698-R · DOI
- Hume, 1983, Immunohistochemical localization of a macrophage-specific antigen in developing mouse retina: phagocytosis of dying neurons and differentiation of microglial cells to form a regular array in the plexiform layers, J. Cell Biol., 97, 253, 10.1083/jcb.97.1.253 · DOI
- Hyman, 1993, The lack of accumulation of senile plaques or amyloid burden in Alzheimer's disease suggests a dynamic balance between amyloid deposition and resolution, J. Neuropathol. Exp. Neurol., 52, 594, 10.1097/00005072-199311000-00006 · DOI
- Innocenti, 1983, Transitory macrophages in the white matter of the developing visual cortex I. Light and electron microscopic characteristics and distribution, Brain Res., 313, 39, 10.1016/0165-3806(83)90200-6 · DOI
- Innocenti, 1983, Transitory macrophages in the white matter of the developing visual cortex. II. Development and relations with axonal pathways, Brain Res., 313, 55, 10.1016/0165-3806(83)90201-8 · DOI
- Killackey, 1984, Glia and the elimination of transient cortical projections, Trends Neurosci., 7, 225, 10.1016/S0166-2236(84)80209-X · DOI
- Kim, 1988, Production and characterization of monoclonal antibodies reactive to synthetic cerebrovascular amyloid peptide, Neurosci. Res. Commun., 2, 121
- Lawson, 1994, Quantification of the mononuclear phagocyte response to Wallerian degeneration of the optic nerve, J. Neurocytol., 23, 729, 10.1007/BF01268086 · DOI
- Linden, 1986, Mononuclear phagocytes in the retina of developing rats, Histochemistry, 85, 335, 10.1007/BF00493486 · DOI
- Liu, 1994, Macrophage colony-stimulating factor mediates astrocyte-induced microglial ramification in human fetal central nervous system culture, Am. J. Pathol., 145, 48
- Liu, 1997, Neuronal and glial apoptosis after traumatic spinal cord injury, J. Neurosci., 17, 5395, 10.1523/JNEUROSCI.17-14-05395.1997 · DOI · Paper page
- Mackenzie, 1995, Role of microglia in senile plaque formation, Neurobiol. Aging, 16, 797, 10.1016/0197-4580(95)00092-S · DOI · Paper page
- Mandybur, 1990, Astrocytes and the plaques of Alzheimer's disease, Neurology, 40, 635, 10.1212/WNL.40.4.635 · DOI
- McMillian, 1994, Brain injury in a dish: A model for reactive gliosis, Trends Neurosci., 17, 138, 10.1016/0166-2236(94)90086-8 · DOI
- Milligan, 1991, Differential immunocytochemical markers reveal the normal distribution of brain macrophages and microglia in the developing rat brain, J. Comp. Neurol., 314, 125, 10.1002/cne.903140112 · DOI
- Naruse, 1991, Mis-sense mutation Val-Ile in exon 17 of the amyloid precursor protein gene in Japanese familial Alzheimer's disease, Lancet, 337, 978, 10.1016/0140-6736(91)91612-X · DOI
- Nieto-Sampedro, 1994, Active microglia, sick astroglia and Alzheimer type dementias, Neuroreport, 5, 375, 10.1097/00001756-199401120-00001 · DOI
- Paresce, 1996, Microglial cells internalize aggregates of the Alzheimer's disease Amyloid β-Protein via a scavenger receptor, Neuron, 17, 553, 10.1016/S0896-6273(00)80187-7 · DOI · Paper page
- Perlmutter, 1992, MHC class II-positive microglia in human brain: association with Alzheimer lesions, J. Neurosci. Res., 33, 549, 10.1002/jnr.490330407 · DOI
- Perry, 1987, The macrophage response to central and peripheral nerve injury. A possible role for macrophages in regeneration, J. Exp. Med., 165, 1218, 10.1084/jem.165.4.1218 · DOI
- Perry, 1987, Macrophages and microglia in the nervous system, Trends Neuroci., 11, 273, 10.1016/0166-2236(88)90110-5 · DOI
- Pike, 1995, Early association of reactive astrocytes with senile plaques in Alzheimer's disease, Exp. Neurol., 132, 172, 10.1016/0014-4886(95)90022-5 · DOI · Paper page
- Rogers, 1992, Complement activation by β-amyloid in Alzheimer disease, Proc. Natl. Acad. Sci. USA, 89, 10016, 10.1073/pnas.89.21.10016 · DOI · Paper page
- Rosana, 1996, Microtubules can modulate pseudopod activity from a distance inside macrophages, Cell Motil. Cytoskeleton, 34, 230, 10.1002/(SICI)1097-0169(1996)34:3<230::AID-CM6>3.0.CO;2-D · DOI
- Selkoe, 1991, The molecular pathology of Alzheimer's disease, Neuron, 6, 487, 10.1016/0896-6273(91)90052-2 · DOI · Paper page
- Selkoe, 1986, Isolation of low-molecular-weight proteins from the amyloid plaque fibers in Alzheimer's disease, J. Neurochem., 46, 1820, 10.1111/j.1471-4159.1986.tb08501.x · DOI
- Shaffer, 1995, Amyloid β protein (Aβ) removal by neuroglial cells in culture, Neurobiol. Aging, 16, 737, 10.1016/0197-4580(95)00055-J · DOI
- Sievers, 1994, Blood monocytes and spleen macrophages differentiate into microglia-like cells on monolayers of Astrocytes: Morphology, Glia, 12, 245, 10.1002/glia.440120402 · DOI
- Stoll, 1989, Macrophage function during Wallerian degeneration of rat brain optic nerve: Clearance of degenerating myelin and Ia expression, J. Neurosci., 9, 2327, 10.1523/JNEUROSCI.09-07-02327.1989 · DOI
- Streit, 1990, An Improved Staining Method for Rat Microglial Cells Using the Lectin from Griffonia simplicifolia (GSA I-B4, J. Histochem. Cytochem., 38, 1683, 10.1177/38.11.2212623 · DOI
- Streit, 1988, Response of endogenous glial cells to motor neuron degeneration induced by toxin ricin, J. Comp. Neurol., 268, 248, 10.1002/cne.902680209 · DOI
- Suzuki, 1994, An increased percentage of long amyloid beta protein secreted by familial amyloid beta protein precursor (beta APP717) mutants, Science, 264, 1336, 10.1126/science.8191290 · DOI · Paper page
- Suzumura, 1991, Morphological transformation of microgliain vitro, Brain Res., 545, 301, 10.1016/0006-8993(91)91302-H · DOI
- Suzumura, 1993, Transforming Growth Factor-β Suppresses Activation and Proliferation of microgliain vitro, J. Immunol., 151, 2150, 10.4049/jimmunol.151.4.2150 · DOI
- Tanaka, 1996, Microglial ramification requires nondiffusible factors derived from astrocytes, Exp. Neurol., 137, 367, 10.1006/exnr.1996.0038 · DOI
- Thomas, 1992, Brain macrophages: evaluation of microglia and their functions, Brain Res. Rev., 17, 61, 10.1016/0165-0173(92)90007-9 · DOI
- Ward, 1991, Characterization of ramified microglia in tissue culture: Pinocytosis and motility, J. Neurosci. Res., 29, 13, 10.1002/jnr.490290103 · DOI
- Wisniewski, 1991, Phagocytosis of β/A4, Acta Neuropathol., 81, 588, 10.1007/BF00310142 · DOI
- Wisniewski, 1993, Migration of perivascular cells into the neuropil and their involvement in β-amyloid plaque formation, Acta Neuropathol., 85, 586, 10.1007/BF00334667 · DOI
- Wood, 1979, The failure of microglia in normal brain to exhibit mononuclear phagocyte markers, J. Neuropathol. Exp. Neurol., 38, 369, 10.1097/00005072-197907000-00002 · DOI
Cited by
Sorted by citations
Items 201–233 of 233
Neuroinflammation and Alteration of the Blood-Brain Barrier in Alzheimer´s Disease
Soto-Rojas, L. O., de la Cruz‐López, F., Ontiveros‐Torres, M. Á., Viramontes‐Pintos, A., Cárdenas‐Aguayo, M. D. C., Meraz‐Ríos, M. A., Salinas‐Lara, C., Florán, B., & Luna‐Muñoz, J. (2015) · InTech eBooks · doi:10.5772/60024 · Cited by 21
“Attenuate the production of FRs and tumor necrosis factor α (TNF-α) [61], reduces microglial activation by Aβ [62] and alter their phagocytic activity [63].”
BackgroundThe Alzheimer Pandemic: Is Paracetamol to Blame?
Jones, G. R. N. (2014) · Inflammation & Allergy - Drug Targets · doi:10.2174/1871528112666131219163405 · Cited by 11
Iribarren, P., Chen, K., Gong, W., Cho, E. H., Lockett, S., Uranchimeg, B., & Wang, J. M. (2007) · Neurobiology of Disease · doi:10.1016/j.nbd.2007.04.010 · Cited by 11
Behl, T., Kaur, I., Sehgal, A., Singh, S., Makeen, H. A., Albratty, M., Alhazmi, H. A., Bhatia, S., & BUNGAU, S. G. (2022) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2022.113179 · Cited by 12
High spatial-resolution imaging of label-free in vivo protein aggregates by VISTA
Lin, L., Miao, K., Qian, C., & Wei, L. (2021) · The Analyst · doi:10.1039/d1an00060h · Cited by 18
Benhamron, S., Rozenstein‐Tsalkovich, L., Nitzan, K., Abramsky, O., & Rosenmann, H. (2018) · Experimental Neurology · doi:10.1016/j.expneurol.2018.02.004 · Cited by 11
“A decrease in astrocyte burden may facilitate the phagocytotic activity of the microglia, since suppression of phagocytosis by astrocytes has been reported (DeWitt et al., 1998).”
Immune Responses in Neurodegenerative Diseases
Shrestha, R., Shrestha, S., Millington, O. R., Brewer, J. M., & Bushell, T. J. (2015) · Kathmandu University Medical Journal · doi:10.3126/kumj.v12i1.13646 · Cited by 7
Decline of Immune Responsiveness: A Pathogenetic Factor in Alzheimer’s Disease?
Richartz-Salzburger, E., & Koehler, N. K. U. (2009) · Springer eBooks · doi:10.1007/978-1-4020-9063-9_61 · Cited by 2
Canet, G., Zussy, C., Vitalis, M., Morin, F., Chevallier, N., Hunt, H., Claeysen, S., Blaquière, M., Marchi, N., Planel, E., et al. (2025) · British Journal of Pharmacology · doi:10.1111/bph.17457 · Cited by 7
“Moreover, there is a crosstalk between reactive astrocytes and microglia, where each cell type can inhibit the phagocytic capacity of the other (DeWitt et al., 1998; Liddelow et al., 2017).”
Modulation of the Complement System by Neoplastic Disease of the Central Nervous System
Yarmoska, S. K., Alawieh, A., Tomlinson, S., & Hoang, K. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.689435 · Cited by 7
“In the CNS, C1q is recognized by microglia during the process of synaptic pruning (39, 40), a mechanism that can also be carried out by astrocytes (88, 89).”
BackgroundKanuri, S. H., & Sirrkay, P. J. (2025) · Neurology International · doi:10.3390/neurolint17090134 · Cited by 7
“In a previous study by DeWitt D.A. et al., macrophages grown in astrocyte-conditioned medium demonstrated a decreased ability to engulf and degrade senile plaques in AD due to inhibitory factors present in the vicinity of neurons [15].”
Rodriguez, J. J., Gardenal, E., Zallo, F., Arrúe, A., Cabot, J., & Busquets, X. (2023) · Acta Histochemica · doi:10.1016/j.acthis.2023.152131 · Cited by 8
Josepha, J. A. (2001) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00206-2 · Cited by 6
Self-citationThe Pathophysiology of Alzheimer’s Disease
Selkoe, D. J. (2000) · Humana Press eBooks · doi:10.1007/978-1-59259-005-6_4 · Cited by 9
A Question of Origins: Non-neuronal Sources of Amyloid-β
Sasmita, A. O., & Depp, C. (2026) · Neuroscience Bulletin · doi:10.1007/s12264-025-01572-4 · Cited by 4
“In AD mouse models, they have been described to acquire a disease-associated microglial (DAM) transcriptional state [89] and are associated with Aβ plaques [144, 145].”
Tada, A. M., Hamezah, H. S., Arrozi, A. P., Bakar, Z. H. A., Yanagisawa, D., & Tooyama, I. (2022) · Journal of Alzheimer's Disease · doi:10.3233/jad-220192 · Cited by 4
Neuroinflammatory Environments Promote Amyloid-ß Deposition and Posttranslational Modification
Atwood, C., Smith, M. A., Martins, R. N., Tanzi, R. E., Roher, A. E., Bush, A. I., & Perry, G. L. (2003) · Humana Press eBooks · doi:10.1007/978-1-59259-297-5_12 · Cited by 3
Self-citationBeta Amyloid Protein Clearance and Microglial Activation
Frautschy, S. A., Cole, G. M., & Ard, M. D. (2002) · Springer eBooks · doi:10.1007/978-1-4757-4139-1_12 · Cited by 3
Cellular and molecular mechanisms of Alzheimer’s disease inflammation
Peery, H. E., Strohmeyer, R., & Rogers, J. (2001) · Birkhäuser Basel eBooks · doi:10.1007/978-3-0348-8350-4_1 · Cited by 2
Liu, M., Beckett, T. L., Thomason, L. A. M., Dorr, A. E., Stefanovic, B., & McLaurin, J. (2021) · Brain Research · doi:10.1016/j.brainres.2020.147233 · Cited by 5
Aging and Cognitive Decline: Neuroprotective Strategies
do Couto, F. S., & de Mendonça, A. (2007) · Springer eBooks · doi:10.1007/978-0-387-70830-0_11 · Cited by 1
“On the other hand, some studies claim a protective role for astrocytes by Aβ uptake (Shaffer et al., 1995), or by modulation of microglial activity (DeWitt et al., 1998).”
BackgroundMicroglial and Astrocytic Reactions in Alzheimer’s Disease
Walker, D. G., & Beach, T. G. (2002) · Humana Press eBooks · doi:10.1007/978-1-59259-105-3_19 · Cited by 2
Alzheimer-related pathogenesis is dependent on neuronal receptor PTPσPreprint
Gu, Y., Shu, Y., Corona, A. W., Xu, K., Yi, A. F., Chen, S., Luo, M., Tremblay, M. L., Nelson, R. J., Landreth, G. E., et al. (2016) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/079806 · Cited by 1
Self-citationNeuroglia in Alzheimer’s Disease
Arellano, J. R., Matute, C., & Verkhratsky, A. (2011) · CRC Press eBooks · doi:10.1201/b11450-16 · Cited by 1
Specific reaction of Met 35 in amyloid beta peptide with hypochlorous acid
Nakamura, M., Shishido, N., Nunomura, A., Smith, M. A., Perry, G. L., Akutsu, H., & Hayashi, T. (2010) · Free Radical Research · doi:10.3109/10715761003745954 · Cited by 1
Self-citationThe Role of Connexin 43 in Vascular Cognitive Diseases
Li, X., Wu, Y.-J., Wang, Y., Luo, M., Yang, L., & Zhang, X. (2018) · doi:10.4172/neuropsychiatry.1000518 · Cited by 1
“Astrocytes might be activated by human amyloid- β (Aβ) [28].”
BackgroundNeurodegeneration and Neuroglia: Emphasis on Astroglia in Alzheimer’s Disease
Verkhratsky, A., Parpura, V., & Rodriguez, J. J. (2014) · Springer eBooks · doi:10.1007/978-1-4939-0974-2_12
“β-amyloid is reported to trigger reactive changes in astrocytes in vitro (DeWitt et al. 1998).”
BackgroundExternal Validation of a Mathematical Model of Brain HealthPreprint
Sadia, H., Doyon, N., Duchesne, S., & Initiative, A. D. N. (2026) · medRxiv · doi:10.64898/2026.09.01.26361929
Pittà, M. D. (2017) · doi:10.48550/arxiv.1708.00731
“Astrocytes have indeed been shown to promote reactive microglia proliferation [38] as well as suppress phagocytic migroglia activity [39].”
BackgroundAmyloid- _ and _ in Alzheimer’s Disease
Nunomura, A., Lee, H., Zhu, X., Perry, G. L., Castellani, R. J., & Smith, M. A. (2005) · Oxidative stress and disease · doi:10.1201/9781420026559.ch6
Self-citationUnravelling the role of nutraceutical supplements in treatment of Parkinson’s Disease
Kakoty, V., Kumar, S., Parasar, S., Pamthied, S., Wardhan, Y., Vishwas, S., Gulati, M., Gupta, G., Sulakhiya, K., Dua, K., et al. (2024) · BIO Web of Conferences · doi:10.1051/bioconf/20248601045
“In the brain, microglial cells are one of the crucial phagocytes, Microglia’s phagocytosis of misfolded proteins can accelerate the degeneration of the neurons, via releasing of chemokines and cytokines[38] – [40].”
BackgroundAmyloid-beta signaling in physiology and pathology: from astrocytes to SUMO
Lee, L. (2013) · doi:10.7916/d80z79hs
“On the other hand, astrocytes can also regulate microglia functions, including microglial phagocytosis of plaques and cytokine production (DeWitt et al., 1998; Farina et al., 2007; Minagar et al., 2002).”
BackgroundGlial Cells and Aβ Peptides in Alzheimer’s Disease Pathogenesis
Siu, G., Clifford, P., Kosciuk, M. C., Venkataraman, V., & Nagele, R. G. (2006) · Springer eBooks · doi:10.1007/978-1-84628-440-3_13
Metadata
- Authors
- DeWitt, D. A., Perry, G., Cohen, M., Doller, C., & Silver, J.
- Affiliations
- Case Western Reserve University (US)
- Venue
- Experimental Neurology
- Publisher
- Elsevier BV
- Published
- 1998-02
- Volume
- 149
- Issue
- 2
- Pages
- 329-340
- ISSN
- 0014-4886 (ISSN-L)
- OpenAlex
- W2164956116
- Cited by
- 261
- References
- 69
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 6 · 2023: 11 · 2022: 6 · 2021: 12 · 2020: 3 · 2019: 7 · 2018: 8 · 2017: 6 · 2016: 12 · 2015: 13 · 2014: 11 · 2013: 8 · 2012: 13
- FWCI
- 6.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Scholars Crossing (Liberty University) (submittedVersion)
- Funders
- National Institutes of Health (5r01ag009287-08)
- National Institute on Aging (AG-00105-11A1, T32AG000105, AG 09287)
- National Institute of Neurological Disorders and Stroke (NS 25713)
- 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
- astrocytes, microglia, phagocytosis, amyloid plaques, Alzheimer's disease, plaque clearance, astrocyte-microglia interaction, conditioned medium, diffusible factors, latex bead phagocytosis, fibroblasts
- MeSH terms
- Alzheimer Disease, Animals, Animals, Newborn, Astrocytes, Brain, Cells, Cultured, Cerebral Cortex, Frontal Lobe, Humans, Phagocytosis, Temporal Lobe, Rats, Sprague-Dawley, Microglia, Coculture Techniques, Rats, 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