ASSOCIATION OF HYPERTENSION WITH IN VIVO ALZHEIMER’S DISEASE PATHOLOGIES IN COGNITIVELY NORMAL, MCI AND DEMENTIA INDIVIDUALS

Abstract

Hypertension increases the risk of Alzheimer's disease (AD) dementia. However, the relationship between hypertension and AD pathologies is still poorly understood. This study aimed to investigate the association of hypertension with in vivo AD pathologies including cerebral Aβ burden and neuronal injury in cognitively normal (CN), mild cognitive impairment (MCI) and AD dementia (ADD) individuals. Twenty-hundred sixty CN, 71 MCI, and 59 ADD elderly subjects from the Korean Brain Aging Study for Early Diagnosis & Prediction of Alzheimer's Disease (KBASE) were included. All participants underwent comprehensive clinical assessment, 11C-labelled Pittsburgh Compound B (PiB) positron emission tomography and magnetic resonance imaging. Comorbid hypertension was identified through systematic interview with subjects and their informants by trained nurses, when subjects were diagnosed with hypertension or treated for hypertension. As an Aβ biomarker of AD, global cerebral Aβ deposition was calculated as mean cortical PiB retention value (standardized uptake value ratio, SUVR) of the region-of-interests (ROIs) including the frontal, lateral temporal, lateral parietal and precuneus/posterior cingulate cortices. Subjects were defined to be Aβ positive if they have one or more ROIs with SUVR > 1.4. As a neuronal injury biomarker of AD, AD-signature region (ADsig) cortical thickness was defined as a mean cortical thickness of the regions including the bilateral inferior and middle temporal, entorhinal cortices and fusiform gyrus. In CN and MCI, hypertension was not associated with global cerebral Aβ deposition and Aβ positivity rate. However, the presence of hypertension was significantly associated with lower global Aβ retention value and Aβ positivity rate in ADD. In terms of neuronal injury biomarkers, hypertension was significantly associated with reduced ADsig cortical thickness only in CN, but not in MCI or ADD. Hypertension appears to contribute to the occurrence of clinical ADD by increasing neural injury or lowering brain reserve rather than by increasing cerebral Aβ burden.