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Vascular Risk and β ‐Amyloid Are Synergistically Associated with Cortical Tau
Author(s) -
Rabin Jennifer S.,
Yang HyunSik,
Schultz Aaron P.,
Hanseeuw Bernard J.,
Hedden Trey,
Viswanathan Anand,
Gatchel Jennifer R.,
Marshall Gad A.,
Kilpatrick Emily,
Klein Hannah,
Rao Vaishnavi,
Buckley Rachel F.,
Yau WaiYing Wendy,
Kirn Dylan R.,
Rentz Dorene M.,
Johnson Keith A.,
Sperling Reisa A.,
Chhatwal Jasmeer P.
Publication year - 2019
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.25399
Subject(s) - pittsburgh compound b , medicine , positron emission tomography , entorhinal cortex , cardiology , tau pathology , disease , alzheimer's disease , framingham heart study , pathology , framingham risk score , oncology , nuclear medicine , hippocampus
Objective Neuropathological studies have demonstrated that cerebrovascular disease and Alzheimer disease (AD) pathology frequently co‐occur in older adults. The extent to which cerebrovascular disease influences the progression of AD pathology remains unclear. Leveraging newly available positron emission tomography (PET) imaging, we examined whether a well‐validated measure of systemic vascular risk and β ‐amyloid (A β ) burden have an interactive association with regional tau burden. Methods Vascular risk was quantified at baseline in 152 clinically normal older adults (mean age = 73.5 ± 6.1 years) with the office‐based Framingham Heart Study cardiovascular disease risk algorithm (FHS‐CVD). We acquired A β ( 11 C‐Pittsburgh compound B) and tau ( 18 F‐flortaucipir) PET imaging on the same participants. A β PET was performed at baseline; tau PET was acquired on average 2.98 ± 1.1 years later. Tau was measured in the entorhinal cortex (EC), an early site of tau deposition, and in the inferior temporal cortex (ITC), an early site of neocortical tau accumulation associated with AD. Linear regression models examined FHS‐CVD and A β as interactive predictors of tau deposition, adjusting for age, sex, APOE ε4 status, and the time interval between baseline and the tau PET scan. Results We observed a significant interaction between FHS‐CVD and A β burden on subsequently measured ITC tau ( p < 0.001), whereby combined higher FHS‐CVD and elevated A β burden was associated with increased tau. The interaction was not significant for EC tau ( p = 0.16). Interpretation Elevated vascular risk may influence tau burden when coupled with high A β burden. These results suggest a potential link between vascular risk and tau pathology in preclinical AD. Ann Neurol 2019; 1–8 ANN NEUROL 2019;85:272–279.