The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Functional Impairment of Microglia Coincides with Beta-Amyloid Deposition in Mice with Alzheimer-Like Pathology
Open accessAbstract
Microglial cells closely interact with senile plaques in Alzheimer's disease and acquire the morphological appearance of an activated phenotype. The significance of this microglial phenotype and the impact of microglia for disease progression have remained controversial. To uncover and characterize putative changes in the functionality of microglia during Alzheimer's disease, we directly assessed microglial behavior in two mouse models of Alzheimer's disease. Using in vivo two-photon microscopy and acute brain slice preparations, we found that important microglial functions - directed process motility and phagocytic activity - were strongly impaired in mice with Alzheimer's disease-like pathology compared to age-matched non-transgenic animals. Notably, impairment of microglial function temporally and spatially correlated with Aβ plaque deposition, and phagocytic capacity of microglia could be restored by interventionally decreasing amyloid burden by Aβ vaccination. These data suggest that major microglial functions progressively decline in Alzheimer's disease with the appearance of Aβ plaques, and that this functional impairment is reversible by lowering Aβ burden, e.g. by means of Aβ vaccination.
Overview
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
Cites
Statistics
Verification
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?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Notably, previous studies have shown that microglial function may be adversely affected by Aβ, particularly as a result of chronic exposure to pro-inflammatory cytokines, resulting in increased Aβ accumulation and potentially underpinning the contradiction between our in vitro and in vivo results.39,40”
From Microglial INPP5D limits plaque formation and glial reactivity in the PSAPP mouse model of Alzheimer's disease (2023) · cites this paper as [39]
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
“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 [17]
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
“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 [17]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“their phagocytic capacity declines with aging, chronic exposure to Αβ, and during sustained inflammation in the AD brain76,16,17.”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [17]
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, perturbations in microglial activity, often associated with aging, can affect the effective clearance of these neuron-derived Aβ fibrils, leading to increased plaque formation and the progression of cognitive and behavioral impairments (17–20).”
From Reducing microglial lipid load enhances β amyloid phagocytosis in an Alzheimer’s disease mouse model (2025) · cites this paper as [19]
Experimental — accuracy not yet measured
The cited source says what the claim attributes to it.
In the citing paper
“Microglial phagocytosis is believed to be dysfunctional in AD [17–19].”
From IL-1β-driven amyloid plaque clearance is associated with an expansion of transcriptionally reprogrammed microglia (2019) · cites this paper as [18]
The cited source says what the claim attributes to it.
In the citing paper
“However, several studies have shown that defects in the phagocytic function of microglia can be restored with Aβ immunization [18, 23] and anti-inflammatory drug treatment [24, 25].”
From IL-1β-driven amyloid plaque clearance is associated with an expansion of transcriptionally reprogrammed microglia (2019) · cites this paper as [18]
The cited source says what the claim attributes to it.
In the citing paper
“Notably, microglial process motility directed toward site of damage was significantly impaired in mice with A β plaques 48 .”
From Transcriptomic analysis of purified human cortical microglia reveals age-associated changes (2017) · cites this paper as [48]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo
Nimmerjahn, A., Kirchhoff, F., & Helmchen, F. (2005) · Science · doi:10.1126/science.1110647 · Cited by 5,827 · cited 1×
“To investigate a second biologically relevant microglial function we studied process motility by assessing process extensions towards an acute injury induced by a laser lesion [1,2].”
BackgroundATP mediates rapid microglial response to local brain injury in vivo
Davalos, D., Grutzendler, J., Yang, G., Kim, J. V., Zuo, Y., Jung, S., Littman, D. R., Dustin, M. L., & Gan, W.-B. (2005) · Nature Neuroscience · doi:10.1038/nn1472 · Cited by 3,913 · cited 3×
“Microglia respond to defined tissue injuries by extending their processes towards the lesion in an ATP-dependent fashion [2].”
BackgroundMethodMicroglia: Active sensor and versatile effector cells in the normal and pathologic brain
Hanisch, U.-K., & Kettenmann, H. (2007) · Nature Neuroscience · doi:10.1038/nn1997 · Cited by 3,676 · cited 1×
“process and the morphology of microglial cells does not necessarily match their functional state [14,15].”
BackgroundSelf-citationJung, S., Aliberti, J., Graemmel, P., Sunshine, M. J., Kreutzberg, G. W., Sher, A., & Littman, D. R. (2000) · Molecular and Cellular Biology · doi:10.1128/mcb.20.11.4106-4114.2000 · Cited by 2,632 · cited 2×
“1A and B and Videos S1 and S2), which were obtained by crossbreeding APPPS1 mice, a mouse model of cerebral amyloidosis [21] with Cx3cr1 mice [23], a mouse model that allows visualization of microglia.”
MethodMicroglia Shape Adult Hippocampal Neurogenesis through Apoptosis-Coupled Phagocytosis
Sierra, A., Encinas, J. M., Deudero, J. J. P., Chancey, J. H., Enikolopov, G., Overstreet-Wadiche, L. S., Tsirka, S. E., & Maletic-Savatic, M. (2010) · Cell Stem Cell · doi:10.1016/j.stem.2010.08.014 · Cited by 1,622 · cited 1×
“newborn neuroblasts [5].”
Wake, H., Moorhouse, A. J., Jinno, S., Kohsaka, S., & Nabekura, J. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.4363-08.2009 · Cited by 1,619 · cited 1×
“neuronal structure [3,4].”
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 · cited 2×
“APP23 mice, which express APP with the Swedish mutation [22] were provided by Novartis, Basel, Switzerland.”
BackgroundMethodMicroglial 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 · cited 4×
“Interestingly, expression of receptors and enzymes involved in microglial Ab-uptake and degradation is progressively downregulated in a transgenic mouse model of Alzheimer’s disease [20].”
BackgroundResultInfluentialMCGEER, P., & MCGEER, E. (1995) · Brain Research Reviews · doi:10.1016/0165-0173(95)00011-9 · Cited by 1,287 · cited 1×
“A number of in vitro studies have not only shown that administration of Ab stimulates the production of inflammatory cytokines and activation markers in microglial cells [8] but also triggers its uptake by receptor-mediated phagocytosis [16].”
BackgroundLee, J.-H., Yu, W. H., Kumar, A., Lee, S., Mohan, P. S., Peterhoff, C. M., Wolfe, D. M., Martinez-Vicente, M., Massey, A. C., Sovak, G., et al. (2010) · Cell · doi:10.1016/j.cell.2010.05.008 · Cited by 1,212
Flagged first, then by citations
Cited by
Sorted by citations
Items 101–200 of 483
Unger, M. S., Schernthaner, P., Marschallinger, J., Mrowetz, H., & Aigner, L. (2018) · Journal of Neuroinflammation · doi:10.1186/s12974-018-1304-4 · Cited by 115
“Microglia, the brains resident immune cells, are a key element in inflammatory processes of the central nervous system (CNS) and are mediating chronic neuroinflammation and aggravation of AD pathology (reviewed in [8, 10, 11]).”
Hu, G., Liao, K., Niu, F., Yang, L., Dallon, B. W., Callen, S. E., Tian, C., Shu, J., Cui, J., Sun, Z., et al. (2018) · Molecular Therapy — Nucleic Acids · doi:10.1016/j.omtn.2018.09.019 · Cited by 117
“The phagocytic activity of adult microglia of live brain slices was analyzed as described previously.(57,58) Brains from 8-week-old mice were washed in carbogen-saturated (95% O2 and 5% CO2) artificial cerebrospinal fluid (ACSF) containing (in mM): NaCl 126; KCl 2.”
MethodKey Aging-Associated Alterations in Primary Microglia Response to Beta-Amyloid Stimulation
Caldeira, C., Cunha, C., Vaz, A. R., Falcão, A. S., Barateiro, A., Seixas, E., Fernandes, A., & Brites, D. (2017) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2017.00277 · Cited by 117
“Functional impairment of microglia leading to phagocytic capacity decline was shown to coincide with Aβ deposition in a mice model of AD (Krabbe et al., 2013).”
BackgroundExcess α-synuclein compromises phagocytosis in iPSC-derived macrophages
Haenseler, W., Zambon, F., Lee, H., Vowles, J., Rinaldi, F., Duggal, G., Houlden, H., Gwinn, K. A., Wray, S., Luk, K. C., et al. (2017) · Scientific Reports · doi:10.1038/s41598-017-09362-3 · Cited by 123
Yanguas‐Casás, N., Crespo‐Castrillo, A., CEBALLOS, M. L. D., Chowen, J. A., Azcoitia, Í., Arévalo, M., & García‐Segura, L. M. (2017) · Glia · doi:10.1002/glia.23263 · Cited by 126
“…conditions after palmitic acid treatment of young microglial cells in vitro are also suggestive of a non-responsive microglial type similar to that found in the aged brain and in several mouse models of neurodegenerative disorders (Daria et al., 2017; Krabbe et al., 2013; Wendt et al., 2017).”
BackgroundResultInfluentialImpact of peripheral myeloid cells on amyloid-β pathology in Alzheimer’s disease–like mice
Prokop, S., Miller, K. R., Drost, N., Handrick, S., Mathur, V., Luo, J., Wegner, A., Wyss-Coray, T., & Heppner, F. L. (2015) · Journal of Experimental Medicine · doi:10.1084/jem.20150479 · Cited by 116
Self-citationSpermidine reduces neuroinflammation and soluble amyloid beta in an Alzheimer’s disease mouse model
Freitag, K., Sterczyk, N., Wendlinger, S., Obermayer, B., Schulz, J., Farztdinov, V. M., Mülleder, M., Ralser, M., Houtman, J., Fleck, L., et al. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02534-7 · Cited by 125
“In accordance, microglial motility in the presence of Aβ plaques was found to be decreased in APPPS1 mice compared to control mice when a focal laser lesion was induced [59].”
BackgroundSelf-citationBile acids as key modulators of the brain-Gut-Microbiota axis in alzheimer’s disease
Mulak, A. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210608 · Cited by 114
“In addition, microglia activation further impairs phagocytosis leading to the accumulation of A 42 [78, 79].”
BackgroundWoodling, N. S., Wang, Q., Priyam, P. G., Larkin, P. B., Shi, J., Johansson, J. U., Zagol-Ikapitte, I. A., Boutaud, O. G., & Andreasson, K. I. (2014) · Journal of Neuroscience · doi:10.1523/jneurosci.0410-14.2014 · Cited by 117
“…inflammatory response; alternatively, it may suggest that microglia, which can change significantly in their inflammatory and phagocytic phenotype with progressive A deposition in mutant APP models (Krabbe et al., 2013), may not successfully engage the anti-inflammatory EP4 signaling pathway.”
BackgroundVerkhratsky, A., Marutle, A., Rodríguez-Arellano, J. J., & Nordberg, A. (2015) · The Neuroscientist · doi:10.1177/1073858414547132 · Cited by 95
Xu, H., Gelyana, E., Rajsombath, M., Yang, T., Li, S., & Selkoe, D. (2016) · Journal of Neuroscience · doi:10.1523/jneurosci.1023-16.2016 · Cited by 109
“In AD and models thereof, microglial function can be impaired by A (Hickman et al., 2008; Krabbe et al., 2013) and by certain AD-linked genetic variants (Kleinberger et al.”
BackgroundThe role of neutrophil granule proteins in neuroinflammation and Alzheimer’s disease
Stock, A. J., Kasus‐Jacobi, A., & Pereira, H. A. (2018) · Journal of Neuroinflammation · doi:10.1186/s12974-018-1284-4 · Cited by 117
Systemic and CNS Inflammation Crosstalk: Implications for Alzheimer’s Disease
Paouri, E., & Georgopoulos, S. (2019) · Current Alzheimer Research · doi:10.2174/1567205016666190321154618 · Cited by 109
Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia
Colombo, A. V., Dinkel, L., Müller, S. A., Monasor, L. S., Schifferer, M., Cantuti‐Castelvetri, L., König, J., Vidatic, L., Brémovà-Ertl, T., Lieberman, A. P., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-21428-5 · Cited by 115
Inflammation and Alzheimer’s Disease: Mechanisms and Therapeutic Implications by Natural Products
Rather, M. A., Khan, A., Alshahrani, S., Rashid, H., Qadri, M. M., Rashid, S., Alsaffar, R. M., Kamal, M. A., & Rehman, M. U. (2021) · Mediators of Inflammation · doi:10.1155/2021/9982954 · Cited by 114
“The formation of A β continues during AD which leads neuroin fl ammation, which may instigate a vicious cycle that further leads to A β generation and alter the functioning of microglial cells [42, 43].”
Impairment of in vivo calcium signaling in amyloid plaque-associated microglia
Brawek, B., Schwendele, B., Riester, K., Kohsaka, S., Lerdkrai, C., Liang, Y., & Garaschuk, O. (2014) · Acta Neuropathologica · doi:10.1007/s00401-013-1242-2 · Cited by 108
“In agreement with recent data [35], we show that directed process motility is impaired in amyloid-depositing mice.”
BackgroundZádori, D., Veres, G., Szalárdy, L., Klivènyi, P., & Vécsei, L. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170929 · Cited by 108
“Beclin 1, with crucial roles in microglial phagocytosis, have been shown to be decreased in microglia isolated from brains of sporadic AD patients [144-154].”
Li, T., Lu, L., Pember, E., Li, X., Zhang, B., & Zhu, Z. (2022) · Cells · doi:10.3390/cells11121925 · Cited by 109
“Recent studies show that severe AD is associated with increased microglial dysfunction compared to healthy control brains [73].”
BackgroundHernandez, M. X., Jiang, S., Cole, T. A., Chu, S., Fonseca, M. I., Fang, M. J., Hohsfield, L. A., Torres, M. D., Green, K. N., Wetsel, R. A., et al. (2017) · Molecular Neurodegeneration · doi:10.1186/s13024-017-0210-z · Cited by 104
“Early “activation” of microglia cells has been found to be beneficial in AD models, however, as Aß plaques form, the phagocytosis and clearance of Aß is reduced [70].”
BackgroundNGF steers microglia toward a neuroprotective phenotype
Rizzi, C., Tiberi, A., Giustizieri, M., Marrone, M. C., Gobbo, F., Carucci, N. M., Meli, G., Arisi, I., D’Onofrio, M., Marinelli, S., et al. (2018) · Glia · doi:10.1002/glia.23312 · Cited by 110
“, 2007; Mandrekar-Colucci & Landreth, 2010), due to evidence suggesting that microglia near plaques are functionally impaired (Krabbe et al., 2013).”
BackgroundPrakash, P., Manchanda, P., Paouri, E., Bisht, K., Sharma, K., Rajpoot, J., Wendt, V., Hossain, A., Wijewardhane, P. R., Randolph, C. E., et al. (2025) · Immunity · doi:10.1016/j.immuni.2025.04.029 · Cited by 104
Neuroinflammation in Alzheimer’s Disease: from Pathogenesis to a Therapeutic Target
Pimplikar, S. W. (2014) · Journal of Clinical Immunology · doi:10.1007/s10875-014-0032-5 · Cited by 106
“Consistent with these observations, a recent study showed that microglia isolated from normal mouse brains showed increased phagocytic [44] activity whereas those from AD mouse models showed impaired phagocytic activity, suggesting that plaqueassociated microglia were unlikely to be in an activated state.”
ResultInteractions between inflammation, sex steroids, and Alzheimer’s disease risk factors
Uchoa, M. F., Moser, V. A., & Pike, C. J. (2016) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2016.09.001 · Cited by 105
“However, in mice with AD-like pathology, microglial motility and A phagocytosis are impaired even though cytokine production is increased (Krabbe et al., 2013).”
Liang, C., Zou, T., Zhang, M., Fan, W., Zhang, T., Jiang, Y., Cai, Y., Chen, F., Chen, X., Sun, Y., et al. (2021) · Theranostics · doi:10.7150/thno.53418 · Cited by 106
“Excessive activation of M1 microglia exacerbates AD pathological damage, as shown by a suite of phenotypic markers specific to pro-inflammatory conditions [30-32].”
BackgroundAlzheimer's disease pathophysiology in the Retina
Gaire, B. P., Koronyo, Y., Fuchs, D.-T. S., Shi, H., Rentsendorj, A., Danziger, R., Vit, J., Mirzaei, N., Doustar, J., Sheyn, J., et al. (2024) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2024.101273 · Cited by 107
Varvel, N. H., Grathwohl, S. A., Degenhardt, K., Resch, C., Bosch, A., Jucker, M., & Neher, J. J. (2015) · Journal of Experimental Medicine · doi:10.1084/jem.20150478 · Cited by 99
“Furthermore, dystrophic neuritic structures that microglial dysfunction, as part of the normal aging process or as the result of pathological changes, may be a driver of AD pathology (Streit et al., 2009; Krabbe et al., 2013; Hefendehl et al., 2014).”
BackgroundCytokine-producing microglia have an altered beta-amyloid load in aged APP/PS1 Tg mice
Babcock, A. A., Ilkjær, L., Clausen, B. H., Villadsen, B., Dissing-Olesen, L., Bendixen, A. T. M., Lyck, L., Lambertsen, K. L., & Finsen, B. (2015) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2015.03.006 · Cited by 107
Walker, D. G., Tang, T. M., & Lue, L. (2017) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2017.00244 · Cited by 95
“The potential for manipulation of microglia to enhance amyloid beta (Aβ) phagocytosis through antibody or immunization as a therapeutic strategy has highlighted the other functions of microglia that need to be maintained (Zotova et al., 2011; Krabbe et al., 2013).”
BackgroundXie, Y., Ba, L., Wang, M., Deng, S., Chen, S., Huang, L., Zhang, M., Wang, W., & Ding, F. (2019) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.13218 · Cited by 102
From the Cajal alumni Achúcarro and Río-Hortega to the rediscovery of never-resting microglia
Tremblay, M., Lecours, C., Samson, L., Sánchez-Zafra, V., & Sierra, A. (2015) · Frontiers in Neuroanatomy · doi:10.3389/fnana.2015.00045 · Cited by 96
“In these conditions, their surveillance of the environment (motility) is concomitantly reduced (Damani et al., 2011; Dibaj et al., 2011; Krabbe et al., 2013; Hefendehl et al., 2014), possibly because they become involved with many other tasks that are required for the inflammatory response.”
BackgroundMolecular imaging of neuroinflammation in Alzheimer's disease and mild cognitive impairment
Knezevic, D., & Mizrahi, R. (2018) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2017.05.007 · Cited by 97
“Furthermore, activated microglia begin to produce pro-inflammatory cytokines, chemokines, complement proteins, and upon strong activation may release toxic free radicals (McGeer and McGeer, 2010; Krabbe et al., 2013).”
Altered microglial phagocytosis in GPR34‐deficient mice
Preissler, J., Grosche, A., Lede, V., Duc, D. L., Krügel, K., Matyash, V., Szulzewsky, F., Kallendrusch, S., Immig, K., Kettenmann, H., et al. (2014) · Glia · doi:10.1002/glia.22744 · Cited by 99
“Morphological changes in microglia together with reduced phagocytosis abilities were also seen in Alzheimer models (Krabbe et al., 2013) implicating functional stages additionally to “resting” or “activated” microglia.”
BackgroundSelf-citationGullotta, G. S., Costantino, G., Sortino, M. A., & Spampinato, S. F. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24119144 · Cited by 97
Amyloid-beta uptake by blood monocytes is reduced with ageing and Alzheimer’s disease
Chen, S.-H., Tian, D.-Y., Shen, Y.-Y., Cheng, Y., Fan, D.-Y., Sun, H.-L., He, C.-Y., Sun, P.-Y., Bu, X.-L., Zeng, F., et al. (2020) · Translational Psychiatry · doi:10.1038/s41398-020-01113-9 · Cited by 89
Phagocytic astrocytes: Emerging from the shadows of microglia
Konishi, H., Koizumi, S., & Kiyama, H. (2022) · Glia · doi:10.1002/glia.24145 · Cited by 88
“In a mouse model of AD (APP/PS1 mouse), microglial phagocytic capacity declined according to the disease progression (Krabbe et al., 2013).”
BackgroundMicroglia communication: parallels between aging and Alzheimer's disease
Udeochu, J. C., Shea, J. M., & Villeda, S. A. (2016) · Clinical and Experimental Neuroimmunology · doi:10.1111/cen3.12307 · Cited by 87
“laser microlesion was significantly delayed compared with age-matched wild-type controls.(72) Ab pathology likely causes this disease-associated impairment in”
MethodFaivre, É., Coelho, J. E., Zornbach, K., Malik, E. M., Baqi, Y., Schneider, M., Cellai, L., Carvalho, K., Sebda, S., Figeac, M., et al. (2018) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2018.00235 · Cited by 93
Self-citationAltered morphological dynamics of activated microglia after induction of status epilepticus
Avignone, E., Lepleux, M., Angibaud, J., & Nägerl, U. V. (2015) · Journal of Neuroinflammation · doi:10.1186/s12974-015-0421-6 · Cited by 95
“In contrast, in an Alzheimer’s model, microglial processes moved faster towards an ATP-containing pipette [35], while responses to a laser lesion and phagocytosis were impaired [36], and basal motility remained unaffected [37].”
ResultTargeting microglia for the treatment of Alzheimer’s disease
McGeer, P. L., & McGeer, E. G. (2014) · Expert Opinion on Therapeutic Targets · doi:10.1517/14728222.2014.988707 · Cited by 92
“[62] found that the phagocytic activity of microglia in Tg mice coincided with Ab plaque deposition and could be restored by Ab vaccination.”
BackgroundHuman CNS immune senescence and neurodegeneration
Streit, W. J., & Xue, Q.-S. (2014) · Current Opinion in Immunology · doi:10.1016/j.coi.2014.05.005 · Cited by 86
Hellwig, S., Masuch, A., Nestel, S., Katzmarski, N., Meyer-Luehmann, M., & Biber, K. (2015) · Scientific Reports · doi:10.1038/srep14624 · Cited by 91
Mulder, S. D., Nielsen, H. M., Blankenstein, M. A., Eikelenboom, P., & Veerhuis, R. (2014) · Glia · doi:10.1002/glia.22619 · Cited by 86
“A plausible explanation for this comes from a very recent study (Krabbe et al., 2013) in which microglia in APP-PS1 mouse brain were elegantly shown to become dysfunctional in phagocytosing Ab when amyloid deposition becomes apparent in the brain.”
ResultSayed, A., Bahbah, E. I., Kamel, S., Barreto, G. E., Ashraf, G. M., & Elfil, M. (2020) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2020.577398 · Cited by 88
Pannell, M., Szulzewsky, F., Matyash, V., Wolf, S. A., & Kettenmann, H. (2014) · Glia · doi:10.1002/glia.22633 · Cited by 86
“Recently, we have demonstrated that (morphologically activated) microglial cells in a mouse model of Alzheimer’s disease decrease their phagocytic activity coincident with the appearance of plaques (Krabbe et al., 2013).”
BackgroundSelf-citationSynaptic dysfunction in early phases of Alzheimer's Disease
Pelucchi, S., Gardoni, F., Luca, M. D., & Marcello, E. E. (2022) · Handbook of clinical neurology · doi:10.1016/b978-0-12-819410-2.00022-9 · Cited by 95
Senescent Microglia: The Key to the Ageing Brain?
Greenwood, E. K., & Brown, D. R. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22094402 · Cited by 84
“An intriguing suggestion for future study is that that the accumulation of iron in microglia could function initially as a protective mechanism, to defend the brain from the neurotoxic effects of excess iron, with the eventual consequence that microglia themselves begin to experience those effects, leading to dystroph…”
BackgroundMatyash, M., Zabiegalov, O., Wendt, S., Matyash, V., & Kettenmann, H. (2017) · PLoS ONE · doi:10.1371/journal.pone.0175012 · Cited by 86
Self-citationHashemiaghdam, A., & Mroczek, M. (2020) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2020.577185 · Cited by 79
An update on the interactions between Alzheimer's disease, autophagy and inflammation
Bostancıklıoğlu, M. (2019) · Gene · doi:10.1016/j.gene.2019.04.040 · Cited by 78
Pomilio, C. J., Pavía, P., Gorojod, R. M., Vinuesa, Á., Alaimo, A., Galván, V., Kotler, M. L., Beauquis, J., & Saravia, F. (2015) · Hippocampus · doi:10.1002/hipo.22503 · Cited by 82
“Strong evidence indicates that the amyloid apparition is related to functional microglia impairment as it was elegantly demonstrated by Krabbe and co-workers (Krabbe et al., 2013).”
BackgroundZuo, Z., Qi, F., Yang, J., Wang, X., Wu, Y., Wen, Y., Yuan, Q., Zou, J., Guo, K., & Yao, Z. B. (2017) · Neurobiology of Disease · doi:10.1016/j.nbd.2017.02.001 · Cited by 78
Hopperton, K. E., Trépanier, M., Giuliano, V., & Bazinet, R. P. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0721-5 · Cited by 85
“While an amoeboid phenotype is classically associated with microglial activation, it is now known that amyloid-β contributes to microglial dysfunction, including decreased phagocytic capacity, so that microglia in AD may be phenotypically, but not functionally, activated [60, 72].”
BackgroundMicroglial activation occurs late during preclinical Alzheimer's disease
Streit, W. J., Braak, H., Del Tredici, K., Leyh, J., Lier, J., Khoshbouei, H., Eisenlöffel, C., Müller, W., & Bechmann, I. (2018) · Glia · doi:10.1002/glia.23510 · Cited by 98
Role of Microglia Adenosine A2AReceptors in Retinal and Brain Neurodegenerative Diseases
Santiago, A. R., Baptista, F. I., Santos, P. F., Cristóvão, G., Ambrósio, A. F., Cunha, R. A., & Gomes, C. A. (2014) · Mediators of Inflammation · doi:10.1155/2014/465694 · Cited by 81
“In animalmodels ofAD it has been shown in late stages of cerebral amyloidosis that the phagocytic capacity of microglia is impaired [102], and this impairment was described to accelerate pathology progression [103].”
BackgroundMicroRNA deregulation and chemotaxis and phagocytosis impairment in Alzheimer's disease
Guedes, J. R., Santana, I. J., Cunha, C., Duro, D., Almeida, M. R., Cardoso, A. M., de Lima, M. C. P., & Cardoso, A. L. (2015) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2015.11.004 · Cited by 77
“Deficiencies in microglia-mediated Ab phagocytosis have also been reported in AD [43], suggesting that microglia lose their ability to clear Ab deposits with age and disease.”
BackgroundRivera-Escalera, F., Pinney, J. J., Owlett, L., Ahmed, H., Thakar, J., Olschowka, J. A., Elliott, M. R., & O’Banion, M. K. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1645-7 · Cited by 75
Role of purinergic receptors in the Alzheimer’s disease
Cieślak, M., & Wojtczak, A. (2018) · Purinergic Signalling · doi:10.1007/s11302-018-9629-0 · Cited by 77
“The role of microglia in CNS is similar to that of monocytes/macrophages in the peripheral blood [118, 119].”
Castranio, E. L., Hasel, P., Haure‐Mirande, J., Ramirez Jimenez, A. V., Hamilton, B. W., Kim, R. D., Glabe, C. G., Wang, M., Zhang, B., Gandy, S., et al. (2023) · Alzheimer's & Dementia · doi:10.1002/alz.12821 · Cited by 74
“12 We hypothesize that under chronic stimulation from A β in the mouse model, microglia that lack Inpp5d undergo functional impairment in association with A β plaque deposition as was described previously, 39 resulting in more plaques.”
Kluge, M. G., Abdolhoseini, M., Zalewska, K., Ong, L. K., Johnson, S. J., Nilsson, M., & Walker, F. R. (2018) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x18797346 · Cited by 74
Joshi, Y. B., & Praticò, D. (2015) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00436 · Cited by 75
“…effectively phagocytate high concentrations (or insoluble conformations) of it resulting in aberrantly activated microglia that associate with both Aβ plaques and neurofibrillary tangles (Hickman et al., 2008; Johnston et al., 2011; D’Andrea et al., 2004; Krabbe et al., 2013; Morales et al., 2013).”
BackgroundMicroglia as Dynamic and Essential Components of the Amyloid Hypothesis
Gandy, S., & Heppner, F. L. (2013) · Neuron · doi:10.1016/j.neuron.2013.05.007 · Cited by 74
“This result may provide a molecular explanation for the Ab-mediated dysfunction of microglia evidenced by the failure of microglia to reduce Ab burden in a transgenic mouse model of AD (Krabbe et al., 2013), ultimately resulting in microglial senescence (Miller and Streit, 2007).”
BackgroundSelf-citationChowdhury, A. A., Gawali, N. B., Munshi, R., & Juvekar, A. R. (2017) · Metabolic Brain Disease · doi:10.1007/s11011-017-0147-5 · Cited by 76
“AD has been attributed to inept Aβ clearance by microglia (Hickman et al. 2008; Krabbe et al. 2013) and increased cytokine concentrations (Patel et al. 2005).”
BackgroundGlial Calcium Signalling in Alzheimer’s Disease
Lim, D., Ronco, V., Grolla, A. A., Verkhratsky, A., & Genazzani, A. A. (2014) · Reviews of physiology, biochemistry and pharmacology · doi:10.1007/112_2014_19 · Cited by 72
Association of Peripheral Blood Cell Profile With Alzheimer's Disease: A Meta-Analysis
Huang, L., Zhang, C., Wang, Y., & Wang, J. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.888946 · Cited by 76
“Subsequently, an increasing number of inflammatory cytokines are released, and the number of macrophages increase in an attempt to combat plaque deposition (Stalder et al., 2005; Krabbe et al., 2013).”
BackgroundEarly morphofunctional plasticity of microglia in response to acute lipopolysaccharide
Madore, C., Joffre, C., Delpech, J.-C., Smedt, V. D., Aubert, A., Coste, L., Layé, S., & Nadjar, A. (2013) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2013.08.008 · Cited by 70
“know from previous reports that microglia in slices are still able to respond to stimuli (Krabbe et al., 2013).”
ResultChiozzi, P., Sarti, A. C., Sanz, J. M., Giuliani, A. L., Adinolfi, E., Vultaggio-Poma, V., Falzoni, S., & Virgilio, F. D. (2019) · Scientific Reports · doi:10.1038/s41598-019-42931-2 · Cited by 71
Lana, D., Ugolini, F., Nosi, D., Wenk, G. L., & Giovannini, M. G. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.651973 · Cited by 73
Phenotypic and functional differences between senescent and aged murine microglia
Stojiljkovic, M. R., Ain, Q., Bondeva, T., Heller, R., Schmeer, C., & Witte, O. W. (2019) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2018.10.007 · Cited by 71
Wendt, S., Maricos, M., Vana, N., Meyer, N., Guneykaya, D., Semtner, M., & Kettenmann, H. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.05.027 · Cited by 69
“Microglial phagocytic activity was previously shown to be impaired in the APP/PS1 model of Alzheimer’s disease, and this decrease was correlated to the presence of Abeta plaques (Krabbe et al., 2013).”
InfluentialSelf-citationTREM2 alters the phagocytic, apoptotic and inflammatory response to Aβ42 in HMC3 cells
Akhter, R., Shao, Y., Formica, S., Khrestian, M., & Bekris, L. M. (2021) · Molecular Immunology · doi:10.1016/j.molimm.2020.12.035 · Cited by 68
Reducing microglial lipid load enhances β amyloid phagocytosis in an Alzheimer’s disease mouse model
Wu, X., Miller, J. A., Lee, B. T. K., Wang, Y., & Ruedl, C. (2025) · Science Advances · doi:10.1126/sciadv.adq6038 · Cited by 67
Nagu, P., Parashar, A., Behl, T., & Mehta, V. (2021) · Journal of Molecular Neuroscience · doi:10.1007/s12031-021-01829-3 · Cited by 68
“Recently it was revealed that in AD, the microglial cells lose their phagocytic potential and thereby are not capable of phagocyting Aβ, which further intensifies the neuroinflammation and AD pathogenesis (Krabbe et al. 2013).”
BackgroundHelin, J. S., Lopez‐Picon, F. R., Majidi, R. A., Eskola, O., Krzyczmonik, A., Keller, T., Löyttyniemi, E., Solin, O. H., Rinne, J. O., & Haaparanta‐Solin, M. (2016) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x16677990 · Cited by 66
“Our in vivo and ex vivo data were in line with data from previous preclinical studies of AD.”
BackgroundInfluentialThe leukotriene signaling pathway: a druggable target in Alzheimer’s disease
Michael, J., Marschallinger, J., & Aigner, L. (2018) · Drug Discovery Today · doi:10.1016/j.drudis.2018.09.008 · Cited by 70
“In addition, during the course of AD pathology, microglia become increasingly dysfunctional in phagocytosis [39], and this functional decline of microglia correlates with A b deposition [40].”
BackgroundModulation of β-Amyloid Fibril Formation in Alzheimer’s Disease by Microglia and Infection
Brown, M. R., Radford, S. E., & Hewitt, E. W. (2020) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2020.609073 · Cited by 67
Fox, B. M., Beck, H. P., Roveto, P. M., Kayser, F., Cheng, Q., Dou, H., Williamson, T. L., Treanor, J. J. S., Liu, H., Jin, L., et al. (2015) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.5b00567 · Cited by 64
Microglial motility in Alzheimer’s disease and after Aβ42 immunotherapy: a human post-mortem study
Franco-Bocanegra, D. K., George, B., Lau, L. C., Holmes, C., Nicoll, J. A. R., & Boche, D. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0828-x · Cited by 64
“Alterations of microglial motility have been documented in AD, with (i) microglial clusters identified around Aβ plaques indicating movement of microglia as part of their response to Aβ aggregation [16, 57], (ii) in AD mouse models, impairment of directed motility and phagocytic activity [23], and (iii) morphological…”
Prevention and Treatment of Alzheimer’s Disease: Biological Mechanisms of Exercise
McGurran, H., Glenn, J. M., Madero, E. N., & Bott, N. T. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-180958 · Cited by 63
“This also coincides with microglial function impairment correlating to A (cid:2) levels [134].”
Teng, E., Taylor, K. M., Bilousova, T. V., Weiland, D. A., Pham, T., Zuo, X., Yang, F., Chen, P., Glabe, C. G., Takacs, A., et al. (2015) · Neurobiology of Disease · doi:10.1016/j.nbd.2015.09.002 · Cited by 65
Cornejo, F., Vruwink, M., Metz, C., Muñoz, P., Salgado, N., Poblete, J., Andrés, M. E., Eugenín, J., & von Bernhardi, R. (2018) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2017.12.007 · Cited by 59
“, 2010), being microglia the main cell involved in Ab removal (Daria et al., 2017; Efthymiou and Goate, 2017; Frautschy et al., 1998; Hickman et al., 2008; Krabbe et al., 2013; Paresce et al., 1996).”
BackgroundMishra, P., Silva, A., Sharma, J., Nguyen, J., Pizzo, D. P., Hinz, D., Sahoo, D., & Cherqui, S. (2023) · Cell Reports · doi:10.1016/j.celrep.2023.112956 · Cited by 64
“60,66–68 In contrast, microglia derived from the transplanted WT HSPCs displayed a more rami-fied ‘‘resting’’ phenotype, but co-localized with 6E10 + plaques that appear smaller, suggesting engulfment of the A b plaques by the WT microglia in 5xFAD/WT HSPC mice.”
Novel targets in Alzheimer’s disease: A special focus on microglia
Balducci, C., & Forloni, G. (2018) · Pharmacological Research · doi:10.1016/j.phrs.2018.01.017 · Cited by 62
Stress Granules Modulate SYK to Cause Microglial Cell Dysfunction in Alzheimer's Disease
Ghosh, S., & Geahlen, R. L. (2015) · EBioMedicine · doi:10.1016/j.ebiom.2015.09.053 · Cited by 62
“MG in aged and AD brain fail to clear Aβ plaques, but display an activated, pro-inflammatory phenotype (Krabbe et al., 2013; Hickman et al., 2008; Mosher and Wyss-Coray, 2014).”
BackgroundInfluentialWang, Y.-B., Li, X., Bing, Y., Zhang, Q., Fei-Tong, J., Minghong, W., Xiangxiang, Z., Le, K., Li, Y., Ping, S., et al. (2022) · Cell Death and Disease · doi:10.1038/s41419-022-04765-1 · Cited by 60
“Sustained activation of microglia weakens their capacity to bind and phagocytise Aβ and decreases Aβ degradation [48].”
BackgroundMicroglial Responses to Brain Injury and Disease: Functional Diversity and New Opportunities
Lyu, J., Jiang, X., Leak, R. K., Shi, Y., Hu, X., & Chen, J. (2020) · Translational Stroke Research · doi:10.1007/s12975-020-00857-2 · Cited by 63
Actin dynamics shape microglia effector functions.
Uhlemann, R., Gertz, K., Boehmerle, W., Schwarz, T., Nolte, C., Freyer, D., Kettenmann, H., Endres, M., & Kronenberg, G. (2016) · Brain Structure and Function · doi:10.1007/s00429-015-1067-y · Cited by 61
Self-citationMyeloid Cells in Alzheimer's Disease: Culprits, Victims or Innocent Bystanders?
Meyer‐Luehmann, M., & Prinz, M. (2015) · Trends in Neurosciences · doi:10.1016/j.tins.2015.08.011 · Cited by 58
Fernando, K., & Wijayasinghe, Y. S. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.746631 · Cited by 57
Inflammaging and Brain: Curcumin and Its Beneficial Potential as Regulator of Microglia Activation
Cianciulli, A., Calvello, R., Ruggiero, M., & Panaro, M. A. (2022) · Molecules · doi:10.3390/molecules27020341 · Cited by 60
“Furthermore, while it was seen that microglial cells of young animals, after administration of ATP rapidly stretch their ramifications and increase their motility, it seems that microglial cells are much less mobile during aging [76].”
BackgroundMicroglial Priming in Infections and Its Risk to Neurodegenerative Diseases
Lima, M. N., Barbosa‐Silva, M. C., & Maron‐Gutierrez, T. (2022) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2022.878987 · Cited by 66
Aβ promotes CD38 expression in senescent microglia in Alzheimer’s disease
Hu, Y., Huang, Y., Xing, S., Chen, C., Shen, D., & Chen, J. (2022) · Biological Research · doi:10.1186/s40659-022-00379-1 · Cited by 58
Park, M. H., Lee, M., Nam, G., Kim, M., Kang, J., Choi, B. J., Jeong, M. S., Park, K. H., Han, W. H., Tak, E., et al. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1916318116 · Cited by 54
“Overall, our immunohistological studies demonstrate that DAPPD can restore the phagocytic activity of microglia, defective in APP/PS1 mice (16, 48), as evidenced by the increased colocalization of Aβ plaques and lysosomes within microglia, the shifts in microglial morphology, and the changes in the size distribution o…”
BackgroundImpaired microglia process dynamics post‐stroke are specific to sites of secondary neurodegeneration
Kluge, M. G., Kracht, L., Abdolhoseini, M., Ong, L. K., Johnson, S. J., Nilsson, M., & Walker, F. R. (2017) · Glia · doi:10.1002/glia.23201 · Cited by 52
“also observed a reduction of phagocytic capacity (Figure 9; Krabbe et al., 2013).”
BackgroundResultInfluentialAstillero‐Lopez, V., Villar‐Conde, S., González-Rodríguez, M., Flores‐Cuadrado, A., Úbeda‐Bañón, I., Saiz‐Sánchez, D., & Martínez-Marcos, A. (2024) · Brain Pathology · doi:10.1111/bpa.13235 · Cited by 54
“However, whether both glial cell populations facilitate the clearance [6, 7] and/or the spread [8 – 10] of A β and tau pathological proteins remains unclear.”
BackgroundImaging of Leukocyte Trafficking in Alzheimer’s Disease
Pietronigro, E. C., Zenaro, E., & Constantin, G. (2016) · Frontiers in Immunology · doi:10.3389/fimmu.2016.00033 · Cited by 52
“Two-photon laser scanning microscopy has also facilitated the characterization of impaired microglial functionality near amyloid deposits in AD mice, suggesting a correlation between plaque deposition and microglial behavior (64).”
BackgroundIn Vivo Imaging of Microglial Calcium Signaling in Brain Inflammation and Injury
Tvrdík, P., & Kalani, M. Y. S. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18112366 · Cited by 52
“This dysfunction is manifested by a marked decrease in directed process motility and phagocytic activity in mice with AD-like pathology [98].”
BackgroundAlzheimer’s Disease: A Molecular View of β-Amyloid Induced Morbific Events
Asik, R. M., Suganthy, N., Aarifa, M. A., Kumar, A., Szigeti, K., Máthé, D., Gulyás, B. Z., Archunan, G., & Padmanabhan, P. (2021) · Biomedicines · doi:10.3390/biomedicines9091126 · Cited by 54
Altered motility of plaque-associated microglia in a model of Alzheimer’s disease
Gyoneva, S., Swanger, S. A., Zhang, J., Weinshenker, D., & Traynelis, S. F. (2016) · Neuroscience · doi:10.1016/j.neuroscience.2016.05.061 · Cited by 51
“These results extend the findings in the APP/PS1 model (Krabbe et al., 2013) to the 5xFAD model and from laser-induced damage to modest mechanical damage.”
BackgroundMethodResultInfluentialSynergistic Actions of Microglia and Astrocytes in the Progression of Alzheimer's Disease
Bouvier, D. S., & Murai, K. K. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-143156 · Cited by 52
“Interestingly the intrinsic ability of microglia to clear amyloid peptide is progressively impaired in AD mouse models [71, 74, 75].”
BackgroundSchmöle, A., Lundt, R., Toporowski, G., Hansen, J. N., Beins, E. C., Halle, A., & Zimmer, A. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180230 · Cited by 51
“…studies that demonstrated that microglial phagocytic capacity was decreased in activated microglial cells in the vicinity of A (cid:2) plaques [46, 47] and a decreased internalized A (cid:2) load was found in activated TNF-(cid:4) – or IL-(cid:2) -positive microglial from AD mouse models as…”
Self-citation
Metadata
- Authors
- Krabbe, G., Halle, A., Matyash, V., Rinnenthal, J. L., Eom, G. D., Bernhardt, U., Miller, K. R., Prokop, S., Kettenmann, H., & Heppner, F. L.
- Affiliations
- Max Delbrück Center (DE)
- Center of Advanced European Studies and Research (DE)
- Charité – Universitätsmedizin Berlin (DE)
- Corresponding author
- Kettenmann, Helmut
- Heppner, Frank L.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-04-08
- Volume
- 8
- Issue
- 4
- Pages
- e60921
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3620049
- OpenAlex
- W2044090829
- Cited by
- 478
- References
- 41
- Citations by year
- 2026: 15 · 2025: 29 · 2024: 31 · 2023: 25 · 2022: 44 · 2021: 56 · 2020: 40 · 2019: 41 · 2018: 38 · 2017: 38 · 2016: 33 · 2015: 39 · 2014: 34 · 2013: 13
- FWCI
- 22.45
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- MDC Repository (Max-Delbrueck-Center for Molecular Medicine) (acceptedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Max Planck Digital Library (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Funders
- European Commission (FP7 HEALTH)
- Deutsche Forschungsgemeinschaft (SFB TRR 43, NeuroCure EXC257, GRK1258, EXC257)
- Jung-Stiftung für Wissenschaft und Forschung
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (R01NS046006, NS046006)
- FP7 Health
- 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
- microglia, Alzheimer's disease, amyloid plaques, microglial activation, microglial phagocytosis, mouse models of Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Animals, Cell Movement, Disease Models, Animal, Female, Humans, Male, Mice, Transgenic, Mutation, Phagocytosis, Amyloid beta-Peptides, Protein Structure, Secondary, Microglia, Mice, Protein Multimerization, Plaque, Amyloid, Spatio-Temporal Analysis
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
