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These results strengthen the proposed pathogenic effect of T H 17 cells on cognition during AD, suggesting that their accumulation is possibly dependent on commensal-derived signals

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This allows lower weekly doses while achieving higher peak and trough drug concentrations, which may translate to more consistent GLP-1 receptor activation throughout the week

[19] pointed out that this might result from the S-glutathionylation of several cysteine residues within the RyR1 molecule

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