Apolipoprotein is genetically associated with the risk of Alzheimer's disease (AD). The APOA1, APOC3, and APOA4 genes are closely linked and located on human chromosome 11. There was a decreased trend for levels of APOA1, APOC3, and APOA4 in AD patients. CONCLUSION: Low levels of APOA1, APOC3, and APOA4 are associated with risk of AD. APOA1, APOC3, and APOA4 should be developed as combined drμgs for the therapy of AD. SNP(single nucleotide polymorphisms)in APOA1and APOA4 genes influences atherogenic characteristics of LDL particles in response to diet.
Apolipoprotein B is a major protein constituent of chylomicrons (apo B-48), LDL (apo B-100) and VLDL (apo B-100). Apo B-100 functions as a recognition signal for the cellular binding and internalization of LDL particles by the apoB/E receptor.
Apolipoprotein-D (ApoD) is an atypical apolipoprotein and, based on its primary structure, it also a member of the lipocalin family. ApoD is mainly associated with high density lipoproteins in human plasma. ApoD is expressed in numerous tissues having high levels of expression in spleen, testes and brain. ApoD plays a role in maintenance and repair within the central and peripheral nervous systems. ApoD occurs in the macromolecular complex with lecithin-cholesterol acyltransferase. It is a multi-ligand, multi-functional transporter and transports a ligand from 1 cell to another. ApoD is probably involved in the transport and binding of bilin, it appears to be able to transport a variety of ligands in a number of different contexts.
Apolipoprotein H (APOH), also known as Beta-2-glycoprotein 1, Activated protein C-binding protein, B2GPI, and B2G1, is a glycoprotein synthesized by liver cells and it is present in the blood associated with plasma lipoproteins. It is an essential cofactor for the binding of certain antiphospholipid antibodies (APA) to anionic phospholipid. APOH binds to various kinds of negatively charged substances such as heparin, phospholipids, and dextran sulfate. APOH may prevent activation of the intrinsic blood coagulation cascade by binding to phospholipids on the surface of damaged cells. The activity of APOH appears to involve the binding of agglutenating, negatively charged compounds, and inhibits agglutenation by the contact activation of the intrinsic blood coagulation pathway. APOH causes a reduction of the prothrombinase binding sites on platelets and reduces the activation caused by collagen when thrombin is present at physiological serum concentrations of APOH suggesting a regulatory role of APOH in coagulation. APOH plasma concentrations are strongly associated to metabolic syndrome alterations and vascular disease in type 2 diabetic and could be considered as a clinical marker of cardiovascular risk. APOH is found on several classes of lipoproteins, and is involved in the activation of lipoprotein lipase in lipid metabolism. This single-chain glycoprotein also has been implicated in several physiologic pathways including coagulation and the production of hypertension, which are related to the pathogenesis of primary cerebral hemorrhage (PICH).
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