痴呆
神经退行性变
载脂蛋白E
医学
淀粉样蛋白(真菌学)
疾病
匹兹堡化合物B
内科学
磁共振成像
阿尔茨海默病
病理
放射科
作者
So Yeon Jeon,Min Soo Byun,Dahyun Yi,Jun Ho Lee,Young Min Choe,Kang Ko,Bo Kyung Sohn,Hyo Jung Choi,Jun‐Young Lee,Dong Young Lee
标识
DOI:10.1016/j.neurobiolaging.2018.11.001
摘要
This study aimed to investigate the relationship of hypertension with beta-amyloid (Aβ) and neurodegeneration biomarkers of Alzheimer's disease (AD) and the modulating effect of apolipoprotein E-ε4 (APOE4). In total, 259 cognitively normal (CN) and 79 AD dementia older adults received clinical assessments including the evaluation for the presence of hypertension, [11C]-Pittsburgh-compound-B–positron emission tomography, magnetic resonance imaging, and APOE genotyping. We used a clinical stage-specific approach, separately focusing on CN and AD dementia stages. For the CN group, individuals with hypertension showed reduced AD signature cortical thickness compared with those without hypertension. Subsequent subgroup analyses showed that hypertension was associated with reduced AD signature cortical thickness only in APOE4 noncarriers, whereas hypertension was associated with elevated Aβ deposition in APOE4 carriers. Meanwhile, regardless of APOE4 status, AD dementia patients with hypertension had significantly lower Aβ deposition than those without hypertension. In conclusion, the findings suggest that hypertension contributes to AD primarily through the reduction of brain reserve. In case of APOE4 carriers, however, hypertension seems to additionally facilitate AD process through amyloid-dependent pathway.
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