Cited by 156Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and Treatments

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Accumulation of tau induced in neurites by microglial proinflammatory mediators

Gorlovoy, Philipp, Larionov, Sergey, Pham, Thao Thi Hien, Neumann, Harald·2009·The FASEB Journal

DOI 10.1096/fj.08-123877

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Abstract

Aggregated fibrillary microtubule‐associated protein tau is the major component of neurofibrillary tangles in Alzheimer's disease. The exact molecular mechanism of tau aggregation is unknown. Microglial cell activation and migration toward amyloid‐β plaques precede the appearance of dysmorphic neurites and formation of neurofibrillary tangles. Here, we analyzed the accumulation of tau at a distance range of expected spontaneous aggregation by fluorescence lifetime‐based Förster resonance energy transfer in cultured primary murine neurons cotransfected with the human tau gene tagged to the green fluorescent protein variants Citrine (tau‐Citrine) and Cerulean (tau‐Cerulean). No spontaneous accumulation of cotransfected tau‐Citrine and tau‐Cerulean was detected in untreated neurons. Coculture of neurons with activated microglia induced aggregation of tau in neurites. Treatment of neurons with tumor necrosis factor‐α (TNF‐α) stimulated reactive oxygen species generation and resulted in the accumulation of tau‐Citrine and tau‐Cerulean in neurites, which was inhibited by neutralization of TNF and the free radical inhibitor 6‐hydroxy‐2,5,7,8‐tetramethylchromane‐2‐carboxylic acid (Trolox). These data demonstrate that activated microglia and the microglial‐derived proinflammatory cytokine TNF can induce accumulation of the aggregation‐prone tau molecules in neurites via reactive oxygen species.— Gorlovoy, P.,Larionov, S., Pham, T. T. H., Neumann, H. Accumulation of tau induced in neurites by microglial proinflammatory mediators. FASEB J. 23, 2502–2513 (2009)

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Background
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Authors: Gorlovoy, P., Larionov, S., Pham, T. T. H., & Neumann, H.
Affiliations: University of Bonn (DE)
ORCID: Neumann, Harald
Venue: The FASEB Journal
Publisher: Wiley
Published: 2009-03-16
Volume: 23
Issue: 8
Pages: 2502-2513
ISSN: 0892-6638 (ISSN-L)
1530-6860
DOI: 10.1096/fj.08-123877
OpenAlex: W2161849052
Cited by: 156
References: 54
Citations by year: 2026: 2 · 2025: 7 · 2024: 14 · 2023: 12 · 2022: 11 · 2021: 9 · 2020: 12 · 2019: 6 · 2018: 13 · 2017: 7 · 2016: 9 · 2015: 11 · 2014: 4 · 2013: 8 · 2012: 14
FWCI: 6.85
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: The FASEB Journal (publishedVersion)
PubMed (publishedVersion)
Funders: Deutsche Forschungsgemeinschaft
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: tau protein, tau aggregation, neurofibrillary tangles, Alzheimer's disease, microglial activation, TNF-α, reactive oxygen species, neurites, inflammatory cytokines, Trolox
MeSH terms: Animals, Cells, Cultured, Humans, Neurons, Recombinant Fusion Proteins, Transfection, Tumor Necrosis Factor-alpha, Neurites, Neurofibrillary Tangles, tau Proteins, Reactive Oxygen Species, Microglia, Inflammation Mediators, Coculture Techniques, Fluorescence Resonance Energy Transfer, Multiprotein Complexes, Green Fluorescent Proteins, Mice

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Accumulation of tau induced in neurites by microglial proinflammatory mediators

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