Associations between an abbreviated CAIDE score and amyloid chronicity

Abstract

AbstractBackgroundEfforts to quantify dementia risk have led to the development of indices that include health factors, like the Cardiovascular Risk Factors, Aging, and Incidence of Dementia (CAIDE) index. Prior studies demonstrate that higher CAIDE is associated with cognitive decline and neurodegeneration. Few studies have analyzed the association between CAIDE and Alzheimer’s disease (AD)‐related pathophysiology, like beta‐amyloid. Recent studies suggest that duration of beta‐amyloid positivity (amyloid chronicity) is associated with cognitive decline. It is unclear whether health factors contribute to the onset of beta‐amyloid accumulation. This study examines the relationship between the three cardiovascular components of the CAIDE score and amyloid chronicity as assessed by [C‐11]PiB PET imaging.MethodParticipants (n=272; Table 1) from the Wisconsin Registry for Alzheimer’s Prevention were included in this study based on the availability of PiB‐PET imaging data, APOE information, and cardiovascular CAIDE components (total cholesterol, BMI, and systolic blood pressure; CAIDE range 0‐3). Based on observed stability of CAIDE scores (Figure 1), a within‐person average was used in linear regression models assessing whether average CAIDE was associated with amyloid chronicity (calculated as last CAIDE assessment age – estimated age PiB(+)) or estimated age of PiB(+) onset (sensitivity analysis).ResultThe median average CAIDE was 0.4 (1st and 3rd quartiles = 0 and 1 CAIDE, respectively). The mean(SD) age of last PiB scan and last CAIDE ages were 66.55(6.74) and 66.53(6.45), respectively. After adjusting for covariates (education, sex, APOE status, last scan age), CAIDE score was not associated with amyloid chronicity (beta=‐0.47; p=0.74). Sensitivity analyses examining amyloid onset and amyloid positivity since last scan were consistent with our primary analysis. In secondary analyses, we found that CAIDE did not modify associations between APOE status and amyloid chronicity at time of last CAIDE (beta=‐0.28; p=0.87; see Table 2 for full model output).ConclusionOur results suggest that peripheral measures of vascular health do not relate to beta‐amyloid duration in a relatively healthy sample. These results add to recent findings suggesting the independent pathways leading to cognitive decline for vascular factors and amyloid. In the future, we will probe the relationship between health factors, AD‐related pathology, and cognition.