Low systolic blood pressure modifies the association of amyloid‐β with tau neuropathology: Human neuropathology/amyloid. (7th December 2020)

• Record Type: Journal Article
• Authors: Oveisgharan, Shahram; Capuano, Ana W.; Kapasi, Alifiya; Buchman, Aron S.; Schneider, Julie A.; Bennett, David A.; Arvanitakis, Zoe
• Is Part Of: Alzheimer's & dementia. Volume 16(2020)Supplement 2
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-12-07
• Subjects: Alzheimer's disease -- Periodicals; Alzheimer Disease -- Periodicals; Dementia -- Periodicals; Démence; Maladie d'Alzheimer; Périodique électronique (Descripteur de forme); Ressource Internet (Descripteur de forme); 616.83
• DOI: 10.1002/alz.038324
• Languages: English
• ISSNs: 1552-5260

Abstract

Abstract: Background: Few pathological studies have examined the association of the vascular risk factors with Alzheimer's disease (AD) pathology. In this clinical‐pathologic study, we examined the association of vascular risk factors with the amyloid‐β and tau depositions, hallmarks of AD pathology. Method: We leveraged post mortem data of 1580 participants from two longitudinal community‐based studies of older adults. Amyloid‐β and tau were quantified by postmortem examination. Vascular risk factors were summarized by calculating the Framingham risk score (FRS) proximate to death. Using linear regressions, we examined the association of the FRS with the amyloid‐β and tau levels, and examined if the FRS modified the association of the amyloid‐β with tau. Result: On average, participants were nearly 90 years old at the time of death and two thirds were women. The FRS was not associated wtih amyloid‐β (r = ‐0.01, p = 0.844), or tau levels (r = 0.02, p = 0.412). However, the FRS as a whole, and specifically the systolic blood pressure (SBP) component, modified the association of the amyloid‐β with the tau, such that the association was stronger at lower levels of FRS, and lower SBP specifically. Taking levels of SBP into account showed that the slope of tau accumulation per unit increase in the amyloid‐β was 40% steeper in participants who had a SBP < 120 mmhg, compared to those with a 130 ≤ SBP < 140 (estimate of slope difference = 0.197, S.E. = 0.087, p = 0.024). Conclusion: Lower levels of SBP in late‐life is associated with a stronger association of amyloid‐β with tau neuropathology. These data suggest that vascular risk factors may modify the relation of AD pathology markers to one another.