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- W4311143821 abstract "Increasing evidence supports the pathogenic role of neuroinflammation in psychiatric diseases, including major depressive disorder (MDD) and neuropsychiatric symptoms of Coronavirus disease 2019 (COVID-19); however, the precise mechanism and therapeutic strategy are poorly understood. Here, we report that myeloid differentiation factor 88 (MyD88), a pivotal adaptor that bridges toll-like receptors to their downstream signaling by recruiting the signaling complex called 'myddosome', was up-regulated in the medial prefrontal cortex (mPFC) after exposure to chronic social defeat stress (CSDS) or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein. The inducible expression of MyD88 in the mPFC primed neuroinflammation and conferred stress susceptibility via amplifying immune danger signals, such as high-mobility group box 1 and SARS-CoV-2 spike protein. Overexpression of MyD88 aggravated, whereas knockout or pharmacological inhibition of MyD88 ameliorated CSDS-induced depressive-like behavior. Notably, TJ-M2010-5, a novel synthesized targeting inhibitor of MyD88 dimerization, alleviated both CSDS- and SARS-CoV-2 spike protein-induced depressive-like behavior. Taken together, our findings indicate that inhibiting MyD88 signaling represents a promising therapeutic strategy for stress-related mental disorders, such as MDD and COVID-19-related neuropsychiatric symptoms." @default.
- W4311143821 created "2022-12-23" @default.
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- W4311143821 date "2023-02-01" @default.
- W4311143821 modified "2023-10-18" @default.
- W4311143821 title "Adaptor protein MyD88 confers the susceptibility to stress via amplifying immune danger signals" @default.
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- W4311143821 doi "https://doi.org/10.1016/j.bbi.2022.12.007" @default.
- W4311143821 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36496170" @default.
- W4311143821 hasPublicationYear "2023" @default.
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