161 Longitudinal change in biomarkers (negative-negative), negative at baseline and positive at follow-up (negative-positive), positive at baseline and negative at follow-up (positive-negative) and positive at baseline and follow-up (positive-positive). We investigated change in amyloid status in relation to actual BPND values at baseline and follow-up, using a division into low, grey zone and high BPND with previously described thresholds by our group of 0.19 and 0.29 BPND (6). Next, we investigated which factors were associated with change from a negative to a positive amyloid status using logistic regression analyses. In model 1, baseline age, sex, education, baseline MMSE score and APOE ε4 carriership were evaluated as individual predictors, with the group remaining A- at follow-up as reference group. In model 2, all predictors were entered simultaneously. In an additional analysis, we used amyloid accumulation rate as outcome, using linear mixed models (outcome: BPND composite ROI). We again assessed baseline age, sex, education, baseline MMSE score and APOE ε4 carriership as predictors. In model 1, variables were assessed individually, and each analysis included the variable of interest, time and the interaction between the variable and time. Model 2 included all predictors simultaneously (including time and all interactions between predictors and time). Last, we used change in amyloid status as predictor of cognitive test performance over time, using linear mixed models. We used our four-level variable reflecting change in amyloid status, time and their interaction as predictors (negative-negative (reference), negative-positive, positive-negative and positive-positive). Baseline age, sex and education were used as covariates. Outcome were neuropsychological test scores. Models included a random intercept, and additionally a random slope when it improved the model (random slope included for VAT-A, TMT-A, Stroop I-III and MMSE). Separate analyses were run with different tests as outcome. RESULTS Demographics Ninety-two individuals were on average 65±8 years old, 39 (42%) were female and 27 (31%) APOE ε4 carrier (Table 1). At baseline, 24 (26%) individuals were A+. By design, A+ individuals had higher baseline amyloid burden. Additionally, they were more often APOE ε4 carrier and had higher baseline tau burden than those who were A-. MTA score, Fazekas score, number of microbleeds and baseline neuropsychological test scores did not differ between A- and A+ individuals. There were no significant differences in baseline demographics between individuals with complete ATN biomarker information at follow-up and those who did not have complete ATN biomarker information at follow-up available. 7