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- W4385667068 abstract "Glial activation and inflammation coincide with neurofibrillary tangles (NFT) formation in neurons. However, the mechanism behind tau fibril and glia interaction is poorly understood. Here, we found that tau preformed fibrils (PFF) caused induction of inflammation in microglia by specifically activating the TLR2-MyD88, but not TLR4-MyD88, pathway. Accordingly, TLR2 interacting domain of MyD88 (wtTIDM) peptide inhibited tau PFF-induced activation of TLR2-MyD88-NF-κB pathway resulting in reduced inflammation. Nasal administration of wtTIDM in P301S tau-expressing PS19 mice was found to inhibit gliosis and inflammatory markers, along with reduction of pathogenic tau in the hippocampus, resulting in improved cognitive behavior in PS19 mice. The inhibitory effect of wtTIDM on tau pathology was absent in PS19 mice lacking TLR2, reinforcing the essential involvement of TLR2 in wtTIDM- mediated effects in vivo. While understanding the mechanism further, we found that tau promoter harboured a potential NF-κB binding site and that proinflammatory molecules increased the transcription of tau in neurons via NF-κB. These results suggest that tau-induced neuroinflammation and neuropathology require TLR2 and that neuroinflammation directly upregulates tau in neurons via NF-κB, highlighting a direct connection between inflammation and tauopathy." @default.
- W4385667068 created "2023-08-09" @default.
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- W4385667068 date "2023-09-15" @default.
- W4385667068 modified "2023-09-25" @default.
- W4385667068 title "Tau fibrils induce glial inflammation and neuropathology via TLR2 in Alzheimer’s disease-related mouse models" @default.
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- W4385667068 doi "https://doi.org/10.1172/jci161987" @default.
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