Cited by 347Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and Treatments

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Association of Microglia with Amyloid Plaques in Brains of APP23 Transgenic Mice

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Stalder, Martina, Phinney, Amie, Probst, Alphonse, Sommer, Bernd, Staufenbiel, Matthias, Jucker, Mathias·1999·The American Journal of Pathology

DOI 10.1016/s0002-9440(10)65423-5PMC PMC1866618

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Abstract

Microglia are a key component of the inflammatory response in the brain and are associated with senile plaques in Alzheimer's disease (AD). Although there is evidence that microglial activation is important for the pathogenesis of AD, the role of microglia in cerebral amyloidosis remains obscure. The present study was undertaken to investigate the relationship between beta-amyloid deposition and microglia activation in APP23 transgenic mice which express human mutated amyloid-beta precursor protein (betaPP) under the control of a neuron-specific promoter element. Light microscopic analysis revealed that the majority of the amyloid plaques in neocortex and hippocampus of 14- to 18- month-old APP23 mice are congophilic and associated with clusters of hypertrophic microglia with intensely stained Mac-1- and phosphotyrosine-positive processes. No association of such activated microglia was observed with diffuse plaques. In young APP23 mice, early amyloid deposits were already of dense core nature and were associated with a strong microglial response. Ultrastructurally, bundles of amyloid fibrils, sometimes surrounded by an incomplete membrane, were observed within the microglial cytoplasm. However, microglia with the typical characteristics of phagocytosis were associated more frequently with dystrophic neurites than with amyloid fibrils. Although the present observations cannot unequivocally determine whether microglia are causal, contributory, or consequential to cerebral amyloidosis, our results suggest that microglia are involved in cerebral amyloidosis either by participating in the processing of neuron-derived betaPP into amyloid fibrils and/or by ingesting amyloid fibrils via an uncommon phagocytotic mechanism. In any case, our observations demonstrate that neuron-derived betaPP is sufficient to induce not only amyloid plaque formation but also amyloid-associated microglial activation similar to that reported in AD. Moreover, our results are consistent with the idea that microglia activation may be important for the amyloid-associated neuron loss previously reported in these mice.

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Authors: Stalder, M., Phinney, A., Probst, A., Sommer, B., Staufenbiel, M., & Jucker, M.
Affiliations: University of Basel (CH)
Novartis (Switzerland) (CH)
Corresponding author: Jucker, Mathias
ORCID: Sommer, Bernd
Jucker, Mathias
Venue: The American Journal of Pathology
Publisher: Elsevier BV
Published: 1999-06
Volume: 154
Issue: 6
Pages: 1673-1684
ISSN: 0002-9440 (ISSN-L)
DOI: 10.1016/s0002-9440(10)65423-5
PMC: PMC1866618
OpenAlex: W2090811490
Cited by: 345
References: 48
Citations by year: 2026: 3 · 2025: 11 · 2024: 11 · 2023: 9 · 2022: 14 · 2021: 19 · 2020: 9 · 2019: 6 · 2018: 11 · 2017: 12 · 2016: 12 · 2015: 12 · 2014: 9 · 2013: 10 · 2012: 16
FWCI: 9.44
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: American Journal Of Pathology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Universität Basel
Novartis Pharma
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: microglial activation, amyloid plaques, APP23 transgenic mice, cerebral amyloidosis, Alzheimer's disease, amyloid-beta deposition, amyloid fibrils, phagocytosis, Mac-1, phosphotyrosine, hippocampus, neocortex, dystrophic neurites, neuroinflammation
MeSH terms: Animals, Brain, Congo Red, Immunohistochemistry, Male, Mice, Transgenic, Microscopy, Immunoelectron, Microglia, Mice, Plaque, Amyloid

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Association of Microglia with Amyloid Plaques in Brains of APP23 Transgenic Mice

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