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.
| Identifer | oai:union.ndltd.org:TCU/oai:etd.tcu.edu:etd-05132014-112012 |
| Date | 13 May 2014 |
| Creators | Pearson, Scott James |
| Contributors | Michael J Chumley, Gary W Boehm, Giridhar R Akkaraju |
| Publisher | Texas Christian University |
| Source Sets | Texas Christian University |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.tcu.edu/etdfiles/available/etd-05132014-112012/ |
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