Association between the use of antihypertensive medication and amyloid‐beta deposition in older adults with hypertension
Musung Keum, Min Soo Byun, Dahyun Yi, Hyejin Ahn, Gijung Jung, Joon Hyung Jung, Nayeong Kong, Jun‐Young Lee, Yu Kyeong Kim, Yun‐Sang Lee, Koung Mi Kang, Chul‐Ho Sohn, Dong Young Lee,- Psychiatry and Mental health
- Cellular and Molecular Neuroscience
- Geriatrics and Gerontology
- Neurology (clinical)
- Developmental Neuroscience
- Health Policy
- Epidemiology
Abstract
Background
Recent evidences suggest that the use of antihypertensive medications (HTNmed) may decrease the incidence of Alzheimer’s disease (AD) dementia. We investigated whether the use of HTNmed is associated with in vivo AD pathologies, particularly cerebral beta‐amyloid (Aβ) deposition, and whether the relationship between HTNmed and cerebral Aβ deposition differs according to the characteristics of HTNmed in older adults.
Method
Participants were recruited from the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease (KBASE) cohort. Both cognitively normal and cognitively impaired older adults (age range: 55‐90 years) who met the following criteria of hypertension (HTN) were included for this study: i) clinical diagnosis of hypertension or ii) systolic blood pressure higher than 130mmHg or diastolic blood pressure higher than 80mmHg measured at baseline. All participants underwent comprehensive clinical assessment and [11C] Pittsburgh Compound B positron emission tomography PET for measuring Aβ deposition.
Result
Among total 413 older adults with hypertension, 227(54.8%) were taking HTNmed. Overall, individuals taking HTNmed showed significantly lower Aβ deposition compared to those without HTNmed (B = ‐0.104, p = 0.007), even after controlling age, sex, apolipoprotein E e4 positivity, and mean arterial blood pressure(MAP). Drug‐class specific analyses showed that the use of renin angiotensin system (RAS) inhibitor (i.e., angiotensin converting enzyme inhibitor and angiotensin receptor blocker) was associated with less cerebral Aβ deposition among older adults with HTNmed (B = ‐0.142, p = 0.006), but the use of other HTNmeds was not. In addition, the blood‐brain barrier permeability of HTNmed also did not have any relationship with Aβ deposition.
Conclusion
The present finding suggests that the use of HTNmed, particularly RAS inhibitor, is associated with less Aβ deposition in older adults with hypertension. Further studies to explore the mechanism underlying the effect of RAS inhibitor on Aβ accumulation may provide clues for new therapeutic targets of AD.