Accurate detection of the regions of Alzheimer's disease (AD) lesions is critical for early intervention to effectively slow down the progression of the disease. Although gray matter volumetric abnormalities are commonly detected in patients with mild cognition impairment (MCI) and patients with AD, the gray matter surface-based deterioration pattern associated with the progression of the disease from MCI to AD stages is largely unknown. To identify group differences in gray matter surface morphometry, including cortical thickness, the gyrification index (GI), and the sulcus depth, 80 subjects from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database were split into healthy controls (HCs; = 20), early MCIs (EMCI; = 20), late MCIs (LMCI; = 20), and ADs ( = 20). Regions-of-interest (ROI)-based surface morphometry was subsequently studied and compared across the four stage groups to characterize the gray matter deterioration during AD progression. Co-alteration patterns (Spearman's correlation coefficient) across the whole brain were also examined. Results showed that patients with MCI and AD exhibited a significant reduction in cortical thickness ( < 0.001) mainly in the cingulate region (four subregions) and in the temporal (thirteen subregions), parietal (five subregions), and frontal (six subregions) lobes compared to HCs. The sulcus depth of the eight temporal, four frontal, four occipital, and eight parietal subregions were also significantly affected ( < 0.001) by the progression of AD. The GI was shown to be insensitive to AD progression (only three subregions were detected with a significant difference, < 0.001). Moreover, Spearman's correlation analysis confirmed that the co-alteration pattern of the cortical thickness and sulcus depth indices is predominant during AD progression. The findings highlight the relevance between gray matter surface morphometry and the stages of AD, laying the foundation for tracking of AD progression. The co-alteration pattern of surface-based morphometry would improve the researchers' knowledge of the underlying pathologic mechanisms in AD.