In preclinical Alzheimer's disease (AD), AD neuropathology is present in cognitively normal (CN) individuals. It is not yet clear how long this phase of the disease may be present prior to symptoms. The “AD signature” MRI biomarker, a measure of cortical thinning in specific limbic and association regions, is detectable in CN individuals nearly a decade prior to dementia. Here we characterize the age-associated trajectory of the AD-signature thickness in a large Colombian kindred with the E280A presenilin 1 (PSEN1) mutation, one goal of which is to assess the potential duration of neurodegeneration prior to symptoms. 56 pre-symptomatic carriers (age = 22.9 ± 9.3 years), 11 symptomatic carriers (MCI or dementia; MMSE 23.1 ± 3.5; 47.5 ± 5 years), and 57 CN non-carriers (23.8 ± 9.4 years) from the Colombian kindred were evaluated. T1-weighted volumetric MRI images were acquired using a Siemens 1.5T scanner. Cortical thickness was measured in a fully automated fashion using FreeSurfer. A priori regions of interest (ROIs) were used to obtain thickness from “AD-signature regions”. ANOVA was used to compare the groups using the entire summary measure as well as individual regions. Regression curves for the trajectory of the AD-cortical signature associated with age were estimated and compared. As a whole, the presymptomatic PSEN1 carrier group did not show cortical thinning compared to non-carriers. However, symptomatic carriers demonstrated cortical thinning in the AD-signature summary measure and in all individual nine ROIs (P <0.001). Compared to non-carriers, preliminary regression curve analysis suggested that PSEN1 mutation carriers had a greater slope in which advancing age was associated with thinner cortex in the AD-signature measure (P <0.05). It is critical to begin using opportunities afforded by this and other large early-onset familial AD cohorts to investigate the potential duration of preclinical AD. Further analyses of this quantitative MRI biomarker are ongoing.