In men only, ApoE E4 associated with CVD (adjusted OR (aOR)=1.46, 95%CI 0.76, 2.80) and with 18-year mortality (adjusted HR (aHR) =1.47, 95%CI 0.95, 2.26), adjusting for age, ethnicity, physical activity, hypertension, diabetes, LDL-cholesterol, HDL-cholesterol, triglycerides and lipid-lowering medications.
The combination of MASP, apolipoprotein E (apoE) and adiponectin improved diabetes prediction on top of both reference models, while prediabetes prediction was improved by MASP plus CRP on top of the HbA1c model.
Age (B = -0.07, SE = 0.01), APOE*4 carriage (B = -0.41, SE = 0.18), and diabetes (B = -0.18, SE = 0.10) were independently associated with faster cognitive decline (p < 0.05 for all).
Our study indicates that APOE ε4 carriers have a greater propensity to glycation than non-carriers which may further increase their risk for diabetes and dementia.
The role of apolipoprotein E gene (APOE) in lipid metabolism has been well established, and APOE is associated with the risk of cardiovascular disease (CVD) and diabetes mellitus (DM).
Multiple linear regression models were fit to explore associations between baseline EDS and ΔPiB while adjusting for baseline age, sex, presence of the apolipoprotein E ε4 allele, educational level, baseline PiB uptake, global PiB positivity (standardized uptake value ratio ≥1.4), physical activity, cardiovascular comorbidities (obesity, hypertension, hyperlipidemia, and diabetes), reduced sleep duration, respiratory symptoms during sleep, depression, and interval between scans.
In apolipoprotein E-deficient mice, chronic treatment of streptozotocin-induced diabetes mellitus with NRG-1 corrected titin phosphorylation via increased PKG (protein kinase G) and ERK1/2 activity and reduced PKCα activity, which reversed the diabetes mellitus-associated changes in titin-based passive tension.
Apolipoprotein E knockout mice exhibiting insulin resistance after 6 weeks of high-fat diet were administered with a low dose of streptozotocin (STZ) to induce diabetes.
We also find that both level and slope of cognitive age are inversely related to education, as well as increased for persons with APOE ε4 and/or diabetes.
Apolipoprotein E (ApoE) gene polymorphism has been implicated in predisposition to diabetes and dementia in old population, but the results from the different studies were inconclusive.
We presume that risk factors of AD, including genetic factors (e.g., the apolipoprotein E ε4 allele and genetic mutations) and non-genetic factors (such as fat, diabetes, and cardiac failure) accelerate biomembrane aging and lead to the onset and development of the disease.
This study performed fasting blood sugar (FBS) and blood pressure measurements and investigated the presence of the ε4 allele of apolipoprotein E (APOE4) to determine the prevalence of diabetes, hypertension and the genetic risk of NCDs.
In the experimental model of streptozotocin-induced diabetes in apolipoprotein E-deficient mice, treatment with tBHQ increased Nrf2 activity in macrophages and vascular smooth muscle cells within atherosclerotic lesions.
Diabetes was an effect modifier of the relationship between APOE-ε4 and IMT, such that ε4 carriers with diabetes had greater IMT in the CCA and ICA than those without diabetes.
Plasma Aβ40 and Aβ42 were measured in 194 participants with diabetes recruited from the community-based Fremantle Diabetes Study Phase II cohort (mean age 71 years, 59% males) and 194 age-, sex-, and APOEɛ4 allele-matched, control subjects without diabetes from the Australian Imaging, Biomarkers and Lifestyle Study using a multiplex microsphere-based immunoassay.
APOE e4 carriers with either a self-reported diagnosis of diabetes (β = 0.160, p = 0.002) or higher glycated hemoglobin levels (β = 0.114, p = 0.014) exhibited greater WMH progression, and the former survived correction for multiple testing.
The association between diabetes and AD-associated amyloid pathology is stronger among carriers of the apolipoprotein E (APOE) ε4 gene allele, the strongest genetic risk factor for late-onset AD.