Abstract
Angiotensin-converting enzyme-1 (ACE1) and apolipoproteins (APOs) may play important roles in the development of Alzheimer’s disease (AD) and cardiovascular diseases (CVDs). This study aimed to examine the associations of AD, CVD, and endocrine-metabolic diseases (EMDs) with the levels of ACE1 and 9 APO proteins (ApoAI, ApoAII, ApoAIV, ApoB, ApoCI, ApoCIII, ApoD, ApoE, and ApoH). Non-Hispanic white individuals including 109 patients with AD, 356 mild cognitive impairment (MCI), 373 CVD, 198 EMD and controls were selected from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) dataset. Multivariable general linear model (GLM) was used to examine the associations. ApoE ε4 allele was associated with AD, as well as ApoAIV, ApoB and ApoE proteins, but not associated with CVD and EMD. Both AD and CVD were associated with levels of ACE1, ApoB, and ApoH proteins. AD, MCI and EMD were associated with levels of ACE1, ApoAII, and ApoE proteins. This is the first study to report associations of ACE1 and several APO proteins with AD, MCI, CVD and EMD, respectively, including upregulated and downregulated protein levels. In conclusion, as specific or shared biomarkers, the levels of ACE1 and APO proteins are implicated for AD, CVD, EMD and ApoE ε4 allele. Further studies are required for validation to establish reliable biomarkers for these health conditions.
Highlights
Alzheimer’s disease (AD) is a progressive disease that affects memory through the degeneration of brain cell connections and the cells themselves [1]
Gender, and education level were not associated with AD diagnosis (p = 0.9176, 0.1449 and 0.2134, respectively), a significant association was observed of apolipoprotein E (ApoE) ε4 allele with AD diagnosis (p < 0.0001) (Table 1)
There were no significant associations between Cardiovascular disease (CVD) diagnostic status and age, education level, and ApoE ε4 allele, but a significant difference was observed between gender and CVD diagnosis (p = 0.0306)
Summary
Alzheimer’s disease (AD) is a progressive disease that affects memory through the degeneration of brain cell connections and the cells themselves [1]. The pathogenesis of AD is associated with abnormal lipid metabolism [2]. Abnormal aplipoprotein metabolism may lead to an increased clearance by macrophages and result in atherosclerosis. The human ApoE gene is functionally polymorphic and consists of three allele variants—ε2, ε3, and ε4 [3]. Due to its distinct role in lipid metabolism, ApoE variants naturally influence cholesterol transport and homeostasis. ApoE absence results in a spike in the plasma cholesterol levels, and the start of atherosclerosis [5]. Functions of ApoE involve cholesterol efflux, involved in cholesterol-loaded macrophage foam cells, and other atherosclerosis-relevant cells [9]. There is limited study of ApoE genetic variants in association with the level of other apolipoproteins (APOs)
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