言语记忆
冲程(发动机)
内嗅皮质
心脏病学
颞叶
医学
载脂蛋白E
视觉记忆
认知
心理学
内科学
海马体
听力学
神经科学
疾病
癫痫
工程类
机械工程
作者
Emilio Werden,Mohamed Salah Khlif,Laura Bird,Toby Cumming,Jennifer Bradshaw,Wasim Khan,Matthew P. Pase,Carolina Restrepo,Michele Veldsman,Natalia Egorova,Sheila K. Patel,Elie Gottlieb,Amy Brodtmann
摘要
Background:The apolipoprotein E (APOE) gene ɛ4 allele is a risk factor for Alzheimer’s disease and cardiovascular disease. However, its relationship with cognition and brain volume after stroke is not clear. Objective:We compared cognition and medial temporal lobe volumes in APOE ɛ4 carriers and no n-carriers in the first year after ischemic stroke. Methods:We sampled 20 APOE ɛ4 carriers and 20 non-carriers from a larger cohort of 135 ischemic stroke participants in the longitudinal CANVAS study. Participants were matched on a range of demographic and stroke characteristics. We used linear mixed-effect models to compare cognitive domain z-scores (attention, processing speed, executive function, verbal and visual memory, language, visuospatial function) and regional medial temporal lobe volumes (hippocampal, entorhinal cortex) between groups at each time-point (3, 12-months post-stroke), and within groups across time-points. APOE gene single nucleotide polymorphisms (SNPs; rs7412, rs429358) were genotyped on venous blood. Results:APOE ɛ4 carriers and non-carriers did not differ on any demographic, clinical, or stroke variable. Carriers performed worse than non-carriers in verbal memory at 3 months post-stroke (p = 0.046), but were better in executive function at 12 months (p = 0.035). Carriers demonstrated a significant improvement in verbal memory (p = 0.012) and executive function (p = 0.015) between time-points. Non-carriers demonstrated a significant improvement in visual memory (p = 0.0005). Carriers had smaller bilateral entorhinal cortex volumes (p < 0.05), and larger right sided and contralesional hippocampal volumes, at both time-points (p < 0.05). Conclusion:APOE ɛ4 is associated with delayed recovery of verbal memory function and reduced entorhinal cortex volumes in the first year after ischemic stroke.
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