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Neurobiol Aging. 2018 Nov 16;75:62-70. doi: 10.1016/j.neurobiolaging.2018.11.001. [Epub ahead of print]

Influence of hypertension on brain amyloid deposition and Alzheimer's disease signature neurodegeneration.

Author information

1
Department of Neuropsychiatry, Seoul National University Hospital, Seoul, Republic of Korea.
2
Institute of Human Behavioral Medicine, Medical Research Center, Seoul National University, Seoul, Republic of Korea.
3
Department of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine, Seoul, Republic of Korea.
4
Department of Neuropsychiatry, Hallym University Dongtan Sacred Hospital, Dongtan, Republic of Korea.
5
Department of Psychiatry, Sanggye Paik Hospital, Inje University College of Medicine, Seoul, Republic of Korea.
6
Department of Neuropsychiatry, SMG-SNU Boramae Medical Center, Seoul, Republic of Korea.
7
Department of Neuropsychiatry, SMG-SNU Boramae Medical Center, Seoul, Republic of Korea; Department of Psychiatry, Seoul National University College of Medicine, Seoul, Republic of Korea.
8
Department of Neuropsychiatry, Seoul National University Hospital, Seoul, Republic of Korea; Institute of Human Behavioral Medicine, Medical Research Center, Seoul National University, Seoul, Republic of Korea; Department of Psychiatry, Seoul National University College of Medicine, Seoul, Republic of Korea. Electronic address: selfpsy@snu.ac.kr.

Abstract

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.

KEYWORDS:

Alzheimer's disease; Apolipoprotein E ε4; Beta-amyloid; Hypertension; Neurodegeneration

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