IC‐P‐170: In Vitro Characterization of Fibrillar Amyloid, TAU Deposition, and Activated Astrocytes in Arctic AD Brain in Comparison With Sporadic AD Brain Using 3H‐PIB, 3H‐THK5117 and 3H‐Deprenyl

(MCI) during the follow-up, we found close matches between PK11195 images and DBSI neuroinflammation images (Fig. 1 Left). More strikingly, DBSI neuroinflammation increased over the course of the follow-up visits (Fig.1 Right), consistent with the participant’s clinical outcome. For an amyloid-positive participant who remained CN, the distribution and severity of DBSI-detected inflammation did not change from 2008 to 2015, suggesting slow neuroinflammation progression.We also examined two amyloid-positive CN participants who later converted to very mild AD. Increased levels of DBSI neuroinflammation in the follow-up examination were found. Five grey and white matter ROIs in these four participants were selected to quantitatively assess the temporal evolution of neuroinflammation change detected by DBSI. Whereas the level of DBSI neuroinflammation remained stable in the participant who remained CN, DBSI neuroinflammation levels dramatically increased in participants who developed symptoms at follow-up visits (Fig. 2). Additionally, we found the longitudinal neuroinflammation rate of change, not the baseline DBSI neuroinflammation strength, related strongly to disease progression. Conclusions: DBSI provides a noninvasive, non-radiative means to quantify neuroinflammation and predict clinical AD progression. Additionally, we demonstrate that a 3T clinical MRl scanner running FDA-approved diffusion sequences could reliably generate DBSI neuroinflammation images.