Triglyceride and VLDL cholesterol are lower in cognitively healthy individuals with Amyloid pathologies than those without

Abstract

AbstractBackgroundFramingham, or cardiovascular (CVD) risk score, as a composite score can accurately predict long‐term CVD risk in the general population. General lipid profiles contribute to CVD risk and Alzheimer’s disease (AD) with inconsistent reports: both high and low triglyceride or body mass index (BMI) have been linked with AD risk. However, the knowledge of their contribution to early AD is limited. To study the changes of CVD risk score and lipid in early AD, we explored the CVD risk score and lipid profile risk factors in our aging cohort.MethodWe compared estimated CVD risk score (Erisk) between cognitively healthy (CH, n=137) individuals, in participants with mild cognitive impairment (MCI, n=54), AD (n=42), and other dementia (OD) (n=23). We also compared lipid profile risk factors (BMI, triglyceride, cholesterol, high‐density lipoprotein (HDL) cholesterol, low‐density lipoprotein (LDL) cholesterol, and very low‐density lipoprotein (VLDL) cholesterol). Furthermore, we compared those risk factors in CH participants subgroups with different status of CSF amyloid (A), phospho‐tau (T), and total‐tau (N): between those with AD risk (A+T±N±: ChA+) and those without (ChA‐T‐N‐). Bonferroni correction was used for multiple comparisons.ResultErisk and lipid profiles were not different between CH, MCI, AD, or OD. We observed lower triglyceride and VLDL cholesterol, and marginally lower BMI, in ChA+ group than in ChA‐T‐N‐ group (p<0.008, Fig 1).ConclusionThese pilot results suggest that CH participants with amyloid pathology presented with lower triglyceride and VLDL cholesterol values, and marginally lower BMI. Although these data need to be confirmed in a larger population, our study supports the concept that lower levels of triglycerides, VLDL cholesterol, or BMI may be linked to amyloid pathology in the CH stage. Further studies examining related factors and pathways that contribute to amyloid pathology such as APOE genotype and VLDL‐receptor expression are needed to fully understand the implications of our findings.