O2‐13‐06: Development of NLRP3 Inflammasome Inhibitors for Alzheimer's Disease

sults for IP-10), although ceiling effects may limit MSD for some markers (Figure 1D). We analyzed the association of these and other markers with the ratio of CSF total-tau (t-tau) to Ab42, a widely used index of disease progression. Even in this limited sample, we observed significant correlation (p <0.05) between IL-1b, IL-8, IP-10, MCP-1, or TNF-a (all measurable using both platforms) and log t-tau/Ab42 (e.g., Figure 1A, 1B). MCP-4 and TARC were also correlated with log t-tau/Ab42, but were measurable by MSD only. Conclusions: Changes in markers of AD progression may be used in high-risk populations to assess potential of candidate preventive interventions. The importance of inflammatory processes in AD pathogenesis is suggested by a strong association between several inflammatory markers and an established index of AD progression. Our results suggest a rationale for testing anti-inflammatory treatments as potential preventives that may delay onset of AD symptoms – now under investigation in INTREPAD. The longitudinal pattern of individual inflammatory markers and their response to NSAID treatment may reveal much about the etio-pathogenesis of AD.