摘要
The amyloid framework forms the central medical theory related to Alzheimer disease (AD), and the in vivo demonstration of amyloid positivity is essential for diagnosing AD. On the basis of a longitudinal cohort design, the study investigated clinical progressive patterns by obtaining cognitive and structural measurements from a group of patients with amnestic mild cognitive impairment (MCI); the measurements were classified by the positivity (A beta+) or absence (A beta-) of the amyloid biomarker. We enrolled 185 patients (64 controls, 121 patients with MCI). The patients with MCI were classified into two groups on the basis of their [F-18]flubetaben or [F-18]florbetapir amyloid positron-emission tomography scan (A beta+ vs. A beta-, 67 vs. 54 patients) results. Data from annual cognitive measurements and three-dimensional T1 magnetic resonance imaging scans were used for between-group comparisons. To obtain longitudinal cognitive test scores, generalized estimating equations were applied. A linear mixed effects model was used to compare the time effect of cortical thickness degeneration. The cognitive decline trajectory of the A beta+ group was obvious, whereas the A beta- and control groups did not exhibit a noticeable decline over time. The group effects of cortical thickness indicated decreased entorhinal cortex in the A beta+ group and supramarginal gyrus in the A beta- group. The topology of neurodegeneration in the A beta- group was emphasized in posterior cortical regions. A comparison of the changes in the A beta+ and A beta- groups over time revealed a higher rate of cortical thickness decline in the A beta+ group than in the A beta- group in the default mode network. The A beta+ and A beta- groups experienced different APOE epsilon 4 effects. For cortical-cognitive correlations, the regions associated with cognitive decline in the A beta+ group were mainly localized in the perisylvian and anterior cingulate regions. By contrast, the degenerative topography of A beta- MCI was scattered. The memory learning curves, cognitive decline patterns, and cortical degeneration topographies of the two MCI groups were revealed to be different, suggesting a difference in pathophysiology. Longitudinal analysis may help to differentiate between these two MCI groups if biomarker access is unavailable in clinical settings.