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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.
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“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]
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“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]
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“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]
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“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]
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“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]
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“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]
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“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]
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“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]
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Citations
Cites
Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo
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“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
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“process and the morphology of microglial cells does not necessarily match their functional state [14,15].”
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MethodMicroglia Shape Adult Hippocampal Neurogenesis through Apoptosis-Coupled Phagocytosis
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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×
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“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
Microglia: new roles for the synaptic stripper
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“neuronal structure [3,4].”
Self-citationApoE-Directed Therapeutics Rapidly Clear β-Amyloid and Reverse Deficits in AD Mouse Models
Cramer, P. E., Cirrito, J. R., Wesson, D. W., Lee, C. Y. D., Karlo, J. C., Zinn, A. E., Casali, B. T., Restivo, J. L., Goebel, W. D., James, M. J., et al. (2012) · Science · doi:10.1126/science.1217697 · Cited by 1,050
The Role of Microglia in the Healthy Brain: Figure 1.
Tremblay, M.-È., Stevens, B., Sierra, A., Wake, H., Bessis, A., & Nimmerjahn, A. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.4158-11.2011 · Cited by 992 · cited 1×
“by their intrinsic phagocytic activity [6].”
Aβ42‐driven cerebral amyloidosis in transgenic mice reveals early and robust pathology
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“Mouse Models APPPS1 mice, a transgenic mouse model of cerebral amyloidosis expressing human APP with the Swedish mutation (KM670/ 671NL) and human mutated PS1 (PS1-L166P) [21] were kindly provided by Mathias Jucker, University of Tübingen, Germany.”
BackgroundMethodInfluentialInflammation in Alzheimer Disease--A Brief Review of the Basic Science and Clinical Literature
Wyss-Coray, T., & Rogers, J. (2012) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006346 · Cited by 975 · cited 1×
“changes of microglia are commonly interpreted as an ‘‘activated’’ state [12,13].”
A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines
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“morphology [7–11].”
The role of microglia in amyloid clearance from the AD brain
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“However, the question of whether resident microglia restrict Ab plaque growth in AD has remained controversial, as the recruitment of microglia to Ab plaques does not seem to result in their degradation [13,18].”
BackgroundInfluentialMicroglial response to amyloid plaques in APPsw transgenic mice.
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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 · cited 2×
“Further studies found that microglial cells internalize soluble, protofibrillar and fibrillar forms of Ab [9,17,18] in vitro and in vivo by several mechanisms such as macropinocytosis or endocytosis, highlighting the general aptitude of microglia to remove Ab.”
BackgroundAre senescence and exhaustion intertwined or unrelated processes that compromise immunity?
Akbar, A. N., & Henson, S. M. (2011) · Nature Reviews Immunology · doi:10.1038/nri2959 · Cited by 474 · cited 1×
“In contrast to the microglial phenotype reported here, cellular senescence is irreversible, at least in lymphocytes and at late stages of cellular senescence [40].”
ResultThe microglial "activation" continuum: from innate to adaptive responses
Town, T., Nikolic, V., & Tan, J. (2005) · Journal of Neuroinflammation · doi:10.1186/1742-2094-2-24 · Cited by 466
Microglial Phagocytosis of Fibrillar β-Amyloid through a β1Integrin-Dependent Mechanism
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“deposits and increase in microglial response was observed by in vivo imaging after stimulation with Ab-specific antibodies when administered directly to an open skull preparation in a mouse model of AD [31].”
BackgroundInhibition of IL-12/IL-23 signaling reduces Alzheimer's disease–like pathology and cognitive decline
vom Berg, J., Prokop, S., Miller, K. R., Obst, J., Kälin, R. E., Lopategui-Cabezas, I., Wegner, A., Mair, F., Schipke, C. G., Peters, O., et al. (2012) · Nature Medicine · doi:10.1038/nm.2965 · Cited by 416 · cited 1×
“morphology [7–11].”
Self-citationMicroglia Mediate the Clearance of Soluble Aβ through Fluid Phase Macropinocytosis
Mandrekar, S., Jiang, Q., Lee, C. Y. D., Koenigsknecht-Talboo, J., Holtzman, D. M., & Landreth, G. E. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.5572-08.2009 · Cited by 415 · cited 1×
“Further studies found that microglial cells internalize soluble, protofibrillar and fibrillar forms of Ab [9,17,18] in vitro and in vivo by several mechanisms such as macropinocytosis or endocytosis, highlighting the general aptitude of microglia to remove Ab.”
BackgroundFormation 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 · cited 2×
“The Ab plaque-associated functional decline of microglia we have shown here may explain why temporary ablation of microglia for up to 30 days in APPPS1 mice does not change the formation and maintenance of Ab burden [19].”
BackgroundSelf-citationMicroglial Activation Resulting from CD40-CD40L Interaction After β-Amyloid Stimulation
Tan, J., Town, T., Paris, D., Mori, T., Suo, Z., Crawford, F., Mattson, M. P., Flavell, R. A., & MULLAN, M. J. (1999) · Science · doi:10.1126/science.286.5448.2352 · Cited by 353 · cited 1×
“Such chronic production of inflammatory molecules by microglia and/or constant exposure to a proinflammatory microenvironment within plaque-bearing AD brains may present another explanation of why microglial function may be influenced negatively [13,37,38].”
BackgroundCombs, C. K., Johnson, D. E., Cannady, S. B., Lehman, T. M., & Landreth, G. E. (1999) · Journal of Neuroscience · doi:10.1523/jneurosci.19-03-00928.1999 · Cited by 349 · cited 1×
“A large number of in vitro studies have shown that microglial cells release a battery of proinflammatory mediators, including nitric oxide and tumor necrosis factor alpha (TNFa), when stimulated with Ab peptides [34–36].”
BackgroundLiu, Z., Condello, C., Schain, A., Harb, R., & Grutzendler, J. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.4403-10.2010 · Cited by 275
Evidence That Aging And Amyloid Promote Microglial Cell Senescence
Flanary, B. E., Sammons, N. W., Nguyen, C., Walker, D., & Streit, W. J. (2007) · Rejuvenation Research · doi:10.1089/rej.2006.9096 · Cited by 272 · cited 1×
“Microglial senescence has been described in the human brain during aging and in Alzheimer’s disease and is associated with telomere shortening and reduced telomerase activity [39].”
BackgroundSpecific Domains of β-Amyloid from Alzheimer Plaque Elicit Neuron Killing in Human Microglia
Giulian, D., Haverkamp, L. J., Yu, J., Karshin, W. L., Tom, D., Li, J., Kirkpatrick, J. B., Kuo, Y., & Roher, A. E. (1996) · Journal of Neuroscience · doi:10.1523/jneurosci.16-19-06021.1996 · Cited by 268 · cited 1×
“A large number of in vitro studies have shown that microglial cells release a battery of proinflammatory mediators, including nitric oxide and tumor necrosis factor alpha (TNFa), when stimulated with Ab peptides [34–36].”
BackgroundAβ Species Removal After Aβ 42 Immunization
Nicoll, J. A. R., Barton, E., Boche, D., Neal, J. W., Ferrer, I., Thompson, P., Vlachouli, C., Wilkinson, D., Bayer, A., Games, D., et al. (2006) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/01.jnen.0000240466.10758.ce · Cited by 265
Role of CD40 ligand in amyloidosis in transgenic Alzheimer's mice
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“Such chronic production of inflammatory molecules by microglia and/or constant exposure to a proinflammatory microenvironment within plaque-bearing AD brains may present another explanation of why microglial function may be influenced negatively [13,37,38].”
BackgroundLevites, Y. (2005) · Journal of Clinical Investigation · doi:10.1172/jci25410 · Cited by 209
McLellan, M. E., Kajdasz, S. T., Hyman, B. T., & Bacskai, B. J. (2003) · The Journal of Neuroscience · doi:10.1523/jneurosci.23-06-02212.2003 · Cited by 174 · cited 1×
“1 M PB, thereby labeling the b-sheet structure of dense core plaques [26].”
BackgroundKrabbe, G., Matyash, V., Pannasch, U., Mamer, L., Boddeke, H. W. G. M., & Kettenmann, H. (2011) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2011.12.002 · Cited by 170 · cited 2×
“As microglia in different brain regions, including cerebellum and hippocampus, can be readily evaluated with this in situ method, we used cerebral slice preparations to investigate microglial phagocytic capacity and quantified uptake of fluorescent polystyrene microparticles by microglia of APPPS1 mice as described pr…”
MethodSelf-citationKoenigsknecht-Talboo, J., Meyer-Luehmann, M., Parsadanian, M., Garcia-Alloza, M., Finn, M. B., Hyman, B. T., Bacskai, B. J., & Holtzman, D. M. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.4147-08.2008 · Cited by 149 · cited 3×
“In vivo Imaging For intravital imaging, b-amyloid plaques were labeled with methoxy-XO4 (10 mg/kg) as described [27].”
MethodInfluentialThe effects of aging, injury and disease on microglial function: a case for cellular senescence
Miller, K. R., & Streit, W. J. (2007) · Neuron Glia Biology · doi:10.1017/s1740925x08000136 · Cited by 134 · cited 1×
“Our findings may also give an explanation as to why microglia fail to sufficiently remove Ab plaques in AD in vivo [18,20], and would support the notion of a dystrophic rather than an activated phenotype of microglia at late stages of AD [33].”
ResultSelf-citationPrinz, M., Kann, O., Draheim, H. J., Schumann, R. R., Kettenmann, H., Weber, J. R., & Hanisch, U. (1999) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/00005072-199910000-00006 · Cited by 111 · cited 1×
“Primary Microglial Cell Culture Microglial cultures were prepared from cerebral cortex of 1–3 day old APPPS1 and wildtype mice as previously described [24] and cultured in DMEM supplemented with 10% fetal calf serum, 2 mM L-glutamine, 100 units/ml penicillin and 100 mg/ml streptomycin.”
MethodSelf-citationγ‐Secretase component presenilin is important for microglia β‐amyloid clearance
Farfara, D., Trudler, D., Segev‐Amzaleg, N., Galron, R., Stein, R., & Frenkel, D. (2010) · Annals of Neurology · doi:10.1002/ana.22191 · Cited by 57
β-Amyloid(25–35) induces the production of interleukin-8 from human monocytes
Meda, L., Bonaiuto, C., Szendrei, G. I., Ceska, M., Rossi, F., & Cassatella, M. A. (1995) · Journal of Neuroimmunology · doi:10.1016/0165-5728(95)00021-s · Cited by 44
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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
“The sustained exposure to A β itself, chemokines, cytokines, and other inflammatory mediators seems responsible for the persistent functional impairment of microglial cells observed at plaque sites 40,41 .”
Self-citationInflammation 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
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 in physiology and disease
Wolf, S. A., Boddeke, H. W. G. M., & Kettenmann, H. (2017) · Annual Review of Physiology · doi:10.1146/annurev-physiol-022516-034406 · Cited by 1,426
Self-citationMicroglia and brain macrophages in the molecular age: from origin to neuropsychiatric disease
Prinz, M., & Priller, J. (2014) · Nature Reviews Neuroscience · doi:10.1038/nrn3722 · Cited by 1,329
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
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