MRI decline pattern in early onset MCI due to Alzheimer’s disease

Abstract

AbstractBackgroundStructural neuroimaging longitudinal studies in Alzheimer’s disease (AD) have consistently defined a “cortical signature” of gray matter loss. Apparently, early‐onset AD (EOAD) has a greater density of amyloid, a more generalized atrophy and a more aggressive evolution than late‐onset AD (LOAD). We hypothesize EOAD would show pronounced longitudinal cortical atrophy, especially in associative areas like precuneus and in addition to temporal lobe loss.MethodsWe investigate longitudinal 3T‐MRI structural data from the Alzheimer’s disease Neuroimaging Initiative (ADNI) 2 cohort. We included patients aged ≤65 years with a baseline mild cognitive impairment (MCI) diagnosis. According to AD biomarkers at baseline, patients were divided into MCI due to AD with high likelihood (MCI‐AD) and MCI unlikely due to AD (MCI‐nonAD). We downloaded the summary of longitudinal measures for volume and cortical thickness. We used linear mixed effects in SPSS25 with data at baseline and month 24 to compare atrophy progression between groups. We focused on “AD's cortical signature”, including entorhinal, inferior temporal, middle temporal, inferior parietal, fusiform areas, and also precuneus and posterior cingulate. In addition, we studied volume of hippocampus (HpV) and total subcortical supratentorial (SSupratV). We tested for group by time interactions and significance level was set at p<0.05, FDR corrected.ResultsWe included 22 MCI‐AD and 26 MCI‐nonAD patients. MMSE mean score was lower in MCI‐AD [Table1]. MCI‐AD had significant lower baseline Cth in precuneus, middle temporal and entorhinal and lower HpV. At group by time interactions, MCI‐AD showed significant greater CTh atrophy in middle temporal, enthorhinal and posterior cingulate, and higher volume decrease in HpV and SSupratV than MCI‐nonAD [Figure1]. Notably, the rest of areas studied were not significantly different at baseline or at group by time effects.ConclusionCompared to MCI‐nonAD, MCI‐AD showed greater decline in only some of the areas previously defined as the cortical AD signature and in hippocampal volume and global subcortical volume. The study could be biased by the small sample size, by the age being close to LOAD and by no stratification by clinical symptoms. Further analyses are needed to understand AD atrophy progression pattern in relation to age at onset.