The Study In Hypercholesteremia And Change Of Aβ_1-40 And Aβ_1-42 Levels

Objective:Cholesterol is necessary ingredient of biomenbrane. It participate to exchange of cell molecular substance and signal transduction,regulate liquidity of celluar membrane. It also play significant role to keep biomembrane structure and function . The metabolism of cholesterol in brain play significant role in growing brain cells and remodeling nervous. Hyperlipoidemia is a major risk factor of stroke. The synthetic rate-limiting enzyme of cholesterol is 3-hydroxy-3-methylglutarul CoA reductase . Statins drugs inhibit synthesize of cholesterol. It utend treatment of hyper- cholestermia widespread. In the brains of Alzheimer's disease patients amyloid beta-peptide(Aβ) is the major component of senile plaque. Aβis formed by sequential breakdown ofβ-amyloid precursor protein (βAPP). Cleavage ofβAPP byγ-secretase results in the production of the Aβ_1-40 and Aβ_1-42.The abnormality metabolism of APP is relate to abnormality pathway of cholesterol.. Cholesterol play important role in process of generating Aβand aggregating Aβ. Cholesterol direct influence metabolism of APP to promote generating Aβ. Cholesterol also cause the change ofβcleavage site of APP and promote amyloid metabolic pathway of APP to generate more Aβ. Recent research mostly approach to stroke and change of blood-fat horizontal ,but the correlations between Aβlevels and blood-fat have not been known clearly. Thus, we investigate the changes of blood Aβ_1-40, Aβ_1-42 and total cholesterol, trigly ceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol in patients with acute ischemic stroke. Method:We prospectively enrolled 47 patients with acute ischemic stroke and 10 controls to detect the serum total cholesterol, triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, Aβ_1-40 and plasma Aβ_1-42. (at admission and one week after admission ). The blood Aβlevels were determined using the double sandwich enzyme linked immunosorbent assay(ELISA).Results:1. We found that baseline and week 1 serum Aβ_1-40 levels of AIS group were higher than those of control group(P<0.01).Plasma Aβ_1-42 levels of AIS group were lower than those of control group(P<0.01).1 week levels of blood Aβ_1-40 and Aβ_1-42 were not different significantly compared with baseline levels in AIS group. Baseline plasma Aβ_1-42 levels were positively correlated with age(P<0.05).2.Baseline serum Aβ_1-40 levels were positively correlated with hyperlipoidemia . (P<0.05).Conclusions:1.In patients with acute ischemic stroke serum Aβ_1-40 levels are negatively correlated with plasma Aβ_1-42 levels.Plasma Aβ_1-42 levels are increased in older patients.2. In patients with acute ischemic stroke plasma Aβ_1-42 levels were positively correlated with hyperlipoidemia.. Hyperlipoidemia is a possibly important factor influence plasma Aβ_1-42 levels.