| Abstract | Alzheimer's disease (AD) is characterized by neurodegeneration associated with the formation of amyloid-beta (A-beta) plaques and neurofibrillary tangles in the brain. Our lab has previously shown that inflammation can lead to an increase in central A-beta;, following 7 consecutive injections of lipopolysaccharide (LPS). Using this LPS-induced inflammation model, we demonstrated an increase in Tau expression and a decrease in the phosphorylated Tau (pTau)/Tau ratio at Ser235 and Thr205. Furthermore, we demonstrated that older mice have higher basal levels of A-beta and LPS does not induce a further increase of A-beta in this population. Interestingly, in this population, we found that increases in A-beta correspond to a higher proportion of pTau and a decrease in total Tau. Together these data demonstrate that inflammation is capable of altering Tau phosphorylation and expression, and the detrimental effects of aging exacerbate pathological markers of AD |
