아밀로이드 양성인 인지기능저하군에서 APOE ε4 유전형이 내측두엽 위축에 미치는 영향: 자기공명영상 장기연구
The Effect of Apolipoprotein E ε4 Genotype on the Medial Temporal Lobe Atrophy in Cognitively Impaired Patients With Amyloid Deposition: 2 Years Longitudinal Magnetic Resonance Imaging Study
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Objective: Apolipoprotein E (APOE) genotype is associated with risk of Alzheimer’s disease (AD), but the association of APOE ε4 allele with longitudinal medial temporal lobe atrophy (MTA) has been controversial. This study aims to evaluate the effect of APOE genotype on longitudinal MTA over a 2-year period in cognitively impaired patients with amyloid deposition. Methods: This retrospective longitudinal study included 65 cognitively impaired subjects with amyloid deposition (subjective memory impairment, mild cognitive impairment, and mild AD). Participants were divided into carriers (n=27) and non-carriers (n=38) of the ε4 allele. The main outcome is longitudinal reduction of medial temporal lobe (hippocampus, entorhinal cortex, and parahippocampal gyrus) over 2 years. Analysis of covariance was conducted to compare the differences in longitudinal MTA between groups, controlling for covariates. Results: At baseline, hippocampal volume was 4.6% smaller (6.38±1.13 vs. 6.69±0.83, p=0.026) and entorhinal thickness was 6.4% thinner (3.51±0.57 vs. 3.75±0.52, p=0.033) in APOE ε4 carriers than non-carriers. Furthermore, APOE ε4 carriers had significantly 72% greater longitudinal hippocampal atrophy compared to non-carriers (-0.43±0.30 vs. -0.25±0.31, p=0.041). Conclusion: Our findings of baseline or longitudinal MTA in APOE ε4 carriers suggest that APOE ε4 genotype may contribute to underlying pathophysiology of medial temporal lobe in AD.
Abstract
Objective: Apolipoprotein E (APOE) genotype is associated with risk of Alzheimer’s disease (AD), but the association of APOE ε4 allele with longitudinal medial temporal lobe atrophy (MTA) has been controversial. This study aims to evaluate the effect of APOE genotype on longitudinal MTA over a 2-year period in cognitively impaired patients with amyloid deposition. Methods: This retrospective longitudinal study included 65 cognitively impaired subjects with amyloid deposition (subjective memory impairment, mild cognitive impairment, and mild AD). Participants were divided into carriers (n=27) and non-carriers (n=38) of the ε4 allele. The main outcome is longitudinal reduction of medial temporal lobe (hippocampus, entorhinal cortex, and parahippocampal gyrus) over 2 years. Analysis of covariance was conducted to compare the differences in longitudinal MTA between groups, controlling for covariates. Results: At baseline, hippocampal volume was 4.6% smaller (6.38±1.13 vs. 6.69±0.83, p=0.026) and entorhinal thickness was 6.4% thinner (3.51±0.57 vs. 3.75±0.52, p=0.033) in APOE ε4 carriers than non-carriers. Furthermore, APOE ε4 carriers had significantly 72% greater longitudinal hippocampal atrophy compared to non-carriers (-0.43±0.30 vs. -0.25±0.31, p=0.041). Conclusion: Our findings of baseline or longitudinal MTA in APOE ε4 carriers suggest that APOE ε4 genotype may contribute to underlying pathophysiology of medial temporal lobe in AD.
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