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Tauopathies are neurodegenerative diseases, including Alzheimer’s disease, that are associated with pathological accumulation of the microtubule associated protein tau (MAPT, or tau) (Lee et al., 2001). Abnormal hyperphosphorylated tau (pTau) strongly correlate with cognitive impairment (Nelson et al., 2012). Neuroinflammation is also associated with tauopathies (Gerhard et al., 2006b; Edison et al., 2008) and is implicated in driving tau pathology (Yoshiyama et al., 2007, Maphis et al., 2015b). Therefore, it is compelling to understand the role of anti-inflammatory cytokines in limiting neuroinflammation and tau pathology. Interleukin-10 (IL-10) is a well-established anti-inflammatory cytokine with roles in limiting inflammation in the central nervous system (CNS) (Strle et al., 2001; Lobo- Silva et al., 2016; Burmeister and Marriott, 2018). Here, we determine if IL-10 regulates inflammation-induced tau pathology by examining the role of IL-10 on tau phosphorylation during an acute inflammatory challenge. We also examined IL-10 in the context of slow progression of neuroinflammation and pTau progression in a human tau expressing (hTau) mouse model. Our findings suggest a distinct importance of IL-10 in limiting tau hyperphosphorylation after an acute inflammatory challenge, however, its role in limiting early expression and/or chronic progression of cytokines and tau phosphorylation remains unclear.


Poster presented at the Brain & Behavioral Health Research Day 2021



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