The DOI matches its Crossref record; 22 of the 22 references it cites were found in a registry or an index.
Formation and maintenance of Alzheimer's disease β-amyloid plaques in the absence of microglia
Open accessAbstract
In Alzheimer's disease, microglia cluster around beta-amyloid deposits, suggesting that these cells are important for amyloid plaque formation, maintenance and/or clearance. We crossed two distinct APP transgenic mouse strains with CD11b-HSVTK mice, in which nearly complete ablation of microglia was achieved for up to 4 weeks after ganciclovir application. Neither amyloid plaque formation and maintenance nor amyloid-associated neuritic dystrophy depended on the presence of microglia.
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
“it remains unclear to what extent microglia are capable of removing amyloid from pre-existing fibrillar congophilic plaques (Stalder et al., 2001) or of preventing the deposition of smaller protofibrillar Aβ aggregates (Grathwohl et al., 2009).”
From CX3CR1 in Microglia Regulates Brain Amyloid Deposition through Selective Protofibrillar Amyloid-β Phagocytosis (2010) · cites this paper as Grathwohl et al., 2009
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
“Finally, a recent study provided evidence that gancyclovir-mediated depletion of microglia expressing thymidine kinase had no demonstrable effect on A pathology in two mouse models of AD. 57”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [57]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Previous in vivo results range from showing that microglia are effective at phagocytosis of fibrillar amyloid (Frautschy et al., 1991; Bacskai et al., 2002; Bolmont et al., 2008) to suggesting that microglia play no role in the control of amyloid deposition (Grathwohl et al., 2009).”
From CX3CR1 in Microglia Regulates Brain Amyloid Deposition through Selective Protofibrillar Amyloid-β Phagocytosis (2010) · cites this paper as Grathwohl et al., 2009
In the citing paper
“Unlike with synapse loss, the formation and maintenance of β-amyloid plaques in amyloidosis models does not seem to be affected by CSF1R inhibition or other methods of microglia depletion (Grathwohl et al., 2009; Olmos-Alonso et al., 2016; Spangenberg et al., 2016).”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Grathwohl et al., 2009
In the citing paper
“Despite this response, however, Aβ clearance and plaque modulation/dynamics is unaffected10–12”
From Sustained microglial depletion with CSF1R inhibitor impairs parenchymal plaque development in an Alzheimer’s disease model (2019) · cites this paper as [11]
In the citing paper
“depleting microglia after amyloid-β pathology onset via pharmacological inhibition of colony-stimulating factor 1 receptor (CSF1R) signalling38 or by using the CD11b-HSVTK (TK) system39 for 4 weeks, does not affect total plaque burden.”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [39]
In the citing paper
“Similarly, data examining the effects of microglia and inflammatory mediators on Aβ deposition in APP transgenic mice are mixed, with some studies demonstrating reduced and others exacerbated Aβ accumulation [120–122].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [122]
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
Microglia: 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
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-citationWyss-Coray (2006) · doi:10.1038/nm1484 · Cited by 1,284
Simard, A. R., Soulet, D., Gowing, G., Julien, J.-P., & Rivest, S. (2006) · Neuron · doi:10.1016/j.neuron.2006.01.022 · Cited by 1,265
Kawarabayashi, T., Younkin, L. H., Saido, T. C., Shoji, M., Ashe, K. H., & Younkin, S. G. (2001) · The Journal of Neuroscience · doi:10.1523/jneurosci.21-02-00372.2001 · Cited by 1,053
Rapid appearance and local toxicity of amyloid-β plaques in a mouse model of Alzheimer’s disease
Meyer-Luehmann, M., Spires-Jones, T. L., Prada, C., Garcia-Alloza, M., de Calignon, A., Rozkalne, A., Koenigsknecht-Talboo, J., Holtzman, D. M., Bacskai, B. J., & Hyman, B. T. (2008) · Nature · doi:10.1038/nature06616 · Cited by 987
Aβ42‐driven cerebral amyloidosis in transgenic mice reveals early and robust pathology
Radde, R., Bolmont, T., Kaeser, S. A., Coomaraswamy, J., Lindau, D., Stoltze, L., Calhoun, M. E., Jäggi, F., Wolburg, H., Gengler, S., et al. (2006) · The EMBO Reports · doi:10.1038/sj.embor.7400784 · Cited by 986
Self-citationExperimental autoimmune encephalomyelitis repressed by microglial paralysis
Heppner, F. L., Greter, M., Marino, D., Falsig, J., Raivich, G., Hövelmeyer, N., Waisman, A., Rülicke, T., Prinz, M., Priller, J., et al. (2005) · Nature Medicine · doi:10.1038/nm1177 · Cited by 732
Self-citationDynamics 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-citationAmyloid-β immunotherapy for Alzheimer's disease: the end of the beginning
Schenk, D. (2002) · Nature Reviews Neuroscience · doi:10.1038/nrn938 · Cited by 436
Blocking TGF-β–Smad2/3 innate immune signaling mitigates Alzheimer-like pathology
Town, T., Laouar, Y., Pittenger, C., Mori, T., Szekely, C. A., Tan, J., Duman, R. S., & Flavell, R. A. (2008) · Nature Medicine · doi:10.1038/nm1781 · Cited by 422
Herzig, M. C., Winkler, D. T., Burgermeister, P., Pfeifer, M., Kohler, E., Schmidt, S. D., Danner, S., Abramowski, D., Stürchler-Pierrat, C., Bürki, K., et al. (2004) · Nature Neuroscience · doi:10.1038/nn1302 · Cited by 391
Self-citationAssociation of Microglia with Amyloid Plaques in Brains of APP23 Transgenic Mice
Stalder, M., Phinney, A., Probst, A., Sommer, B., Staufenbiel, M., & Jucker, M. (1999) · The American Journal of Pathology · doi:10.1016/s0002-9440(10)65423-5 · Cited by 345
Self-citationSpontaneous Hemorrhagic Stroke in a Mouse Model of Cerebral Amyloid Angiopathy
Winkler, D. T., Bondolfi, L., Herzig, M. C., Jann, L., Calhoun, M. E., Wiederhold, K., Tolnay, M., Staufenbiel, M., & Jucker, M. (2001) · Journal of Neuroscience · doi:10.1523/jneurosci.21-05-01619.2001 · Cited by 290
Self-citationBondolfi, 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-citationVisualization of microglia in living tissues using Iba1‐EGFP transgenic mice
Hirasawa, T., Ohsawa, K., Imai, Y., Ondo, Y., Akazawa, C., Uchino, S., & Kohsaka, S. (2005) · Journal of Neuroscience Research · doi:10.1002/jnr.20480 · Cited by 186
Mechanisms of microglia accumulation in Alzheimer’s disease: therapeutic implications
Khoury, J. E., & Luster, A. D. (2008) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2008.08.004 · Cited by 171
Spectral Unmixing of Multicolored Bioluminescence Emitted from Heterogeneous Biological Sources
Gammon, S. T., Leevy, W. M., Gross, S., Gokel, G. W., & Piwnica-Worms, D. R. (2006) · Analytical Chemistry · doi:10.1021/ac051999h · Cited by 97
Stereological estimation of total microglia number in mouse hippocampus
Long, J. M., Kalehua, A. N., Muth, N. J., Hengemihle, J. M., Jucker, M., Calhoun, M. E., Ingram, D. K., & Mouton, P. R. (1998) · Journal of Neuroscience Methods · doi:10.1016/s0165-0270(98)00100-9 · Cited by 87
Self-citationCerebral and Peripheral Amyloid Phagocytes— an Old Liaison with a New Twist
Jucker, M., & Heppner, F. L. (2008) · Neuron · doi:10.1016/j.neuron.2008.06.014 · Cited by 27
Self-citationGruys, E., Timmermans, H. J. F., & van Ederen, A. M. (1979) · Laboratory Animals · doi:10.1258/002367779781071230 · Cited by 21
Research works printed but not linked: 1
- Wyss-Coray, T. Nat. Med. 12, 1005–1015 (2006).
Cited by
Sorted by citations
Neuroinflammation in Alzheimer's disease
Heneka, M. T., Carson, M. J., Khoury, J. E., Landreth, G. E., Brosseron, F., Feinstein, D. L., Jacobs, A. H., Wyss-Coray, T., Vitorica, J., Ransohoff, R. M., et al. (2015) · The Lancet Neurology · doi:10.1016/s1474-4422(15)70016-5 · Cited by 6,226
Mechanisms underlying inflammation in neurodegeneration
Glass, C. K., Saijo, K., Winner, B., Marchetto, M. C., & Gage, F. H. (2010) · Cell · doi:10.1016/j.cell.2010.02.016 · Cited by 3,580
Kettenmann, H., Hanisch, U.-K., Noda, M., & Verkhratsky, A. (2011) · Physiological Reviews · doi:10.1152/physrev.00011.2010 · Cited by 3,547
Immune attack: the role of inflammation in Alzheimer disease
Heppner, F. L., Ransohoff, R. M., & Becher, B. (2015) · Nature Reviews Neuroscience · doi:10.1038/nrn3880 · Cited by 2,134
Self-citationMicroglia and macrophages in brain homeostasis and disease
Li, Q., & Barres, B. A. (2018) · Nature Reviews Immunology · doi:10.1038/nri.2017.125 · Cited by 1,999
Metadata
- Authors
- Grathwohl, S. A., Kälin, R. E., Bolmont, T., Prokop, S., Winkelmann, G., Kaeser, S. A., Odenthal, J., Radde, R., Eldh, T., Gandy, S., Aguzzi, A., Staufenbiel, M., Mathews, P. M., Wolburg, H., Heppner, F. L., & Jucker, M.
- Affiliations
- Hertie Institute for Clinical Brain Research (DE)
- Charité – Universitätsmedizin Berlin (DE)
- German Center for Neurodegenerative Diseases (DE)
- University of Tübingen (DE)
- Icahn School of Medicine at Mount Sinai (US)
- University Hospital Zurich (CH)
- Novartis (Switzerland) (CH)
- Nathan Kline Institute for Psychiatric Research (US)
- Corresponding author
- Heppner, Frank L
- Jucker, Mathias
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2009-10-18
- Volume
- 12
- Issue
- 11
- Pages
- 1361-1363
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC4721582
- OpenAlex
- W2066165659
- Cited by
- 401
- References
- 22
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 11 · 2023: 19 · 2022: 8 · 2021: 27 · 2020: 20 · 2019: 21 · 2018: 26 · 2017: 33 · 2016: 21 · 2015: 38 · 2014: 27 · 2013: 33 · 2012: 43
- FWCI
- 22.61
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Funders
- National Institute on Aging (P01AG010491, AG017617, P01AG017617)
- National Institute of Neurological Disorders and Stroke (NS045205, R01NS045205, R01NS046006)
- 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
- Alzheimer's disease, amyloid plaques, microglia, ganciclovir, APP transgenic mice, neuritic dystrophy, plaque clearance, mouse models of Alzheimer's disease
- MeSH terms
- CD68 Molecule, Alzheimer Disease, Animals, Antiviral Agents, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Female, Gene Expression Regulation, Humans, Injections, Intra-Articular, Male, Mice, Transgenic, Mutation, Plague, Thymidine Kinase, Antigens, Differentiation, Myelomonocytic, Antigens, CD, Ganciclovir, Amyloid beta-Peptides, Microscopy, Immunoelectron, Amyloid beta-Protein Precursor, Microglia, Neuroaxonal Dystrophies, CD11b Antigen, Green Fluorescent Proteins, Mice, Presenilin-1
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
