Review: Experimental manipulations of microglia in mouse models of A lzheimer's pathology: activation reduces amyloid but hastens tau pathology

Lee, D. C.; Rizer, J.; Hunt, J. B.; Selenica, M.‐L. B.; Gordon, M. N.; Morgan, D.

doi:10.1111/nan.12002

Cited by 57Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and Treatments

Review: Experimental manipulations of microglia in mouse models of A lzheimer's pathology: activation reduces amyloid but hastens tau pathology

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Lee, D. C., Rizer, J., Hunt, J. B., Selenica, M.‐L. B., Gordon, M. N., Morgan, D.·2013·Neuropathology and Applied Neurobiology

DOI 10.1111/nan.12002PMC PMC4300851

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Abstract

The inflammation hypothesis of A lzheimer's pathogenesis has directed much scientific effort towards ameliorating this disease. The development of mouse models of amyloid deposition permitted direct tests of the proposal that amyloid‐activated microglia could cause neurodegeneration in vivo. Many approaches to manipulating microglial activation have been applied to these mouse models, and are the subject of this review. In general, these results do not support a direct neuricidal action of microglia in mouse amyloid models under any activation state. Some of the manipulations cause both a reduction in pathology and a reduction in microglial activation. However, at least for agents like ibuprofen, this outcome may result from a direct action on amyloid production, and a reduction in the microglial‐provoking amyloid deposits, rather than from reduced microglial activation leading to a decline in amyloid deposition. Instead, a surprising number of the experimental manipulations which increase microglial activation lead to enhanced clearance of the amyloid deposits. Both the literature and new data presented here suggest that either classical or alternative activation of microglia can lead to enhanced amyloid clearance. However, a limited number of studies comparing the same treatments in amyloid‐depositing vs. tau‐depositing mice find the opposite effects. Treatments that benefit amyloid pathology accelerate tau pathology. This observation argues strongly that potential treatments be tested for impact on both amyloid and tau pathology before consideration of testing in humans.

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Studies on the role of TLRs in microglial activation have produced conflicting results.
“studies elucidating the role of TLRs in microglial activation have yielded conflicting results (109).”
From Microglia in Alzheimer's disease (2017) · cites this paper as [109]
TLR4 stimulation increases tau-related pathology in 3xTgAD and rTg4510 mice.
“A drawback of TLR4 stimulation was the observed increase in taurelated pathology in 3xTgAD and rTg4510 mice (109).”
From Microglia in Alzheimer's disease (2017) · cites this paper as [109]
IL-1β enhances amyloid-beta pathology and increases tau pathology.
“IL-1β, a key cytokine of the innate immune response, was shown to enhance Aβ pathology (126), as well as increase tau pathology (109).”
From Microglia in Alzheimer's disease (2017) · cites this paper as [109]

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Authors: Lee, D. C., Rizer, J., Hunt, J. B., Selenica, M. ‐. B., Gordon, M. N., & Morgan, D.
Affiliations: University of South Florida (US)
Corresponding author: Morgan, D.
ORCID: Lee, D. C.
Rizer, J.
Selenica, M.‐L. B.
Gordon, M. N.
Morgan, D.
Venue: Neuropathology and Applied Neurobiology
Publisher: Wiley
Published: 2013-01-22
Volume: 39
Issue: 1
Pages: 69-85
ISSN: 0305-1846 (ISSN-L)
1365-2990
DOI: 10.1111/nan.12002
PMC: PMC4300851
OpenAlex: W1960212508
Cited by: 57
References: 116
Citations by year: 2025: 2 · 2024: 4 · 2023: 5 · 2022: 2 · 2021: 3 · 2020: 6 · 2019: 1 · 2018: 1 · 2017: 4 · 2016: 4 · 2015: 11 · 2014: 8 · 2013: 6
FWCI: 0.87
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Neuropathology and Applied Neurobiology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Aging (AG 15490, AG04418, P01AG004418, R01AG015490)
National Institute of Neurological Disorders and Stroke (NS76308, R01NS076308)
Topics: Health Sciences › Medicine › Physiology › 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, microglial activation, amyloid-beta, tau pathology, neuroinflammation, ibuprofen, amyloid clearance, mouse models of Alzheimer's disease, neurodegeneration
MeSH terms: Alzheimer Disease, Animals, Disease Models, Animal, Amyloid beta-Peptides, tau Proteins, Microglia, Mice, Plaque, Amyloid

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Review: Experimental manipulations of microglia in mouse models of A lzheimer's pathology: activation reduces amyloid but hastens tau pathology

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