In the Colombian kindred with autosomal dominant Alzheimer's disease (AD), Presenilin-1 (PSEN1) E280A carriers develop AD dementia by age 49 with near 100% certainty. In this ongoing study, we aim to assess longitudinal PET measures in their ability to track changes in tau and beta-amyloid (Aβ) pathology along the disease trajectory from preclinical to clinical stages. We analyzed data from 15 participants from the Colombian Kindred: 8 mutation carriers (age: 37.3±6.2 [28-45]), and 7 age-matched non-carriers (age: 38.4±6.1 [28-45]). All participants underwent two sessions of MRI, Aβ (PiB)- and Tau (Flortaucipir, FTP)-PET imaging at baseline and 2.0±0.3 [1.6-2.4] years of follow-up. To assess the anatomical distribution of Aβ and tau accumulation, rates of annual percent change (APC) for PiB (DVR, cerebellar gray reference) and FTP (SUVr, cerebellar gray reference) were calculated in 20 FreeSurfer-defined regions of interest. We then assessed the relationships between baseline and change measures of global Ab and inferior temporal (neocortical) tau, as well as carrier status and age using Spearman rho. Compared to noncarriers, PSEN1 carriers had the highest rates of APC for Aβ in caudal anterior cingulate cortex (mean=6.9, 95%CI 1.3-12.6) and for tau in superior parietal cortex (mean=9.4, 95%CI 1.3-17.5) and precuneus (mean=8.2, 95%CI 0.3-16.2). In the full sample, baseline Aβ was significantly correlated with subsequent Aβ increase (rho=0.71, p=0.004), and baseline tau was significantly correlated with subsequent tau increase (rho=0.614, p=0.017). Carriers had greater rates of change for Aβ compared to non-carriers (4.3%/year, p=0.002) across the entire age range. By contrast, only older carriers (36-45 years) showed higher rates of neocortical tau APC, compared to age-matched non-carriers (12.49%/year, p=0.024). Age and tau APC were marginally correlated in the full sample (rho=0.47, p=0.079) and significantly correlated among only carriers (r=0.73, p=0.040). These preliminary longitudinal results suggest that in autosomal dominant AD, Aβ accumulates steadily, beginning as early as 20 years prior to dementia onset; whereas rapid, widespread neocortical tau increase occurs closer to the time of symptom onset. Future analyses will focus on regional differences and relationships between Aβ and tau accumulation rates over the course of disease progression.