Previous research suggests that grey and white matter contrast ratio (GWR) seen on MRI is significantly higher (healthier) in cognitively normal elders compared to individuals with Alzheimer's disease (AD) or mild cognitive impairment (MCI). We examined GWR and conversion status after a 3-year follow-up period in a small cohort of individuals with MCI. Data was analyzed on n = 138 participants from the Alzheimer's Disease Neuroimaging Initiative who met the following inclusion criteria: (1) baseline diagnosis of MCI; (2) 1.5T MRI acquisition on either a Siemens or GE scanner; (3) 36-month follow-up data. Participants, matched on Mini-Mental State Examination scores, were categorized into two groups according to their 36-month follow-up diagnoses: 1) non-converters (n = 69, 75 ± 7, 26% female), and 2) converters, who had an AD diagnosis at follow-up (n = 69, 75 ± 7, 30% female). FreeSurfer was used to generate GWR data using T1 structural MR images. For the GWR calculation, white matter was defined as 1mm below the grey-white boundary, and grey matter included 35% from the boundary through the cortex. GWR surfaces were smoothed prior to analyses. Higher GWR values represented better brain integrity (i.e., less degradation in tissue contrast). Using a general linear model with a threshold of P <0.01, converters evidenced significantly lower GWR values than non-converters (i.e., more degradation in tissue contrast), specifically within the left and right temporal lobe. Secondary analyses regressing out hippocampal volume (i.e., a proxy measure of AD pathology) increased the region of GWR significance in the left hemisphere, but attenuated the area of GWR significance in the right hemisphere. We observed differences in GWR between MCI individuals who convert to AD versus those individuals who remain diagnostically stable over a three-year period. Such differences persisted even after adjusting for a traditional neuroimaging marker of AD pathology (i.e., hippocampal volume). GWR may represent an early neuroimaging marker of abnormal brain aging that precedes AD pathology or a second pathway of brain injury independent of AD pathology. Future research is needed to better understand the pathological and clinical implications of GWR.