Atherosclerosis is associated with plasma Aß levels in non-hypertension patients.

BACKGROUND: Growing evidence indicated that to develop of atherosclerosis observed more often by people with Alzheimer's disease (AD), but the underlying mechanism is not fully clarified. Considering that amyloid-ß (Aß) deposition in the brain is the key pathophysiology of AD and plasma Aß is closely relate to Aß deposition in the brain, in the present study, we investigated the relationships between atherosclerosis and plasma Aß levels. METHODS: This was a population based cross-sectional study. Patients with high risk of atherosclerosis from Qubao Village, Xi'an were underwent carotid ultrasound for assessment of atherosclerosis. Venous blood was collected on empty stomach in the morning and plasma Aß1-40 and Aß1-42 levels were measured using ELISA. Multivariate logistic regression analysis was performed to investigate the relationships between carotid atherosclerosis (CAS) and plasma Aß levels. RESULTS: Among 344 patients with high risk of atherosclerosis, 251(73.0%) had CAS. In the univariate analysis, the plasma Aß levels had no significant differences between CAS group and non-CAS group (Aß1-40: 53.07 ± 9.24 pg/ml vs. 51.67 ± 9.11pg/ml, p = 0.211; Aß1-42: 40.10 ± 5.57 pg/ml vs. 40.70 pg/ml ± 6.37pg/ml, p = 0.285). Multivariate logistic analysis showed that plasma Aß levels were not associated with CAS (Aß1-40: OR = 1.019, 95%CI: 0.985-1.054, p = 0.270;Aß1-42: OR = 1.028, 95%CI: 0.980-1.079, p = 0.256) in the total study population. After stratified by hypertension, CAS was associated with plasma Aß1-40 positively (OR = 1.063, 95%CI: 1.007-1.122, p = 0.028) in the non-hypertension group, but not in hypertensive group. When the plasma Aß concentrations were classified into four groups according to its quartile, the highest level of plasma Aß1-40 group was associated with CAS significantly (OR = 4.465, 95%CI: 1.024-19.474, p = 0.046). CONCLUSION: Among patients with high risk of atherosclerosis, CAS was associated with higher plasma Aß1-40 level in non-hypertension group, but not in hypertension group. These indicated that atherosclerosis is associated with plasma Aß level, but the relationship may be confounded by hypertension.

Fixed-dose combination treatment after stroke for secondary prevention in China: a national community-based study.

BACKGROUND AND PURPOSE: There is evidence and international consensus on the advantages and potential of a polypill for established cardiovascular disease patients to improve adherence in the secondary prevention of cardiovascular disease. This study aimed to estimate the numbers of stroke patients who would be eligible for the polypill strategy in China, and the suitable composition of a polypill, based on data of the China National Stroke Prevention Project. METHODS: A total of 717 620 residents aged ≥40 years from 6 Chinese representative provinces were screened for prevalent stroke from 2011 to 2012 with an 84.4% response rate. Participants with a history of stroke received further investigation of risk factors and treatments. The potential need for treatment was classified according to the guidelines. Rates were standardized using the population composition of the Sixth National Population Census of China. RESULTS: The standardized prevalence rate of stroke was 1.9%. Up to 93.1% of stroke patients were eligible for a polypill containing at least 2 types of medications, with 75.3% eligible for a statin and antiplatelet agent and 70.6% for antihypertensive and antiplatelet medications. Considering 3 therapies, 54% were eligible for antihypertensive, statin, and antiplatelet medications. The current treatment rate with all required combinations of separate pills was only 6.9%. CONCLUSIONS: A huge number of stroke patients in China require preventive therapy and would be eligible for a polypill. This study indicates that it would be reasonable to consider and assess the value of a polypill strategy to improve secondary prevention of stroke in China.

Oxidative stress is associated with Aß accumulation in chronic sleep deprivation model.

Amyloid-ß (Aß) accumulation is the main pathological change in Alzheimer's disease (AD), which results from the imbalance of production and clearance of Aß in the brain. Our previous study found that chronic sleep deprivation (CSD) led to the deposition of Aß in the brain by disrupting the balance of Aß production and clearance, but the specific mechanism was not clear. In the present study, we investigated the effects of oxidative stress on Aß accumulation in CSD rats. We found that the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) significantly increased after CSD, while superoxide dismutase (SOD) decreased in the brain. Furthermore, the serum ROS was elevated and SOD declined after CSD. The levels of oxidative stress in the brain were significantly correlated with ß-site APP-cleaving enzyme 1 (BACE1), low-density lipoprotein receptor-related protein-1 (LRP1), and receptor of advanced glycation end products (RAGE) levels in hippocampus and prefrontal lobe, and the concentration of serum oxidative mediators were strongly correlated with plasma levels of soluble LRP1 (sLRP1) and soluble RAGE (sRAGE). These results suggested that the oxidative stress in the brain and serum may involved in the CSD-induced Aß accumulation. The underlying mechanism may be associated with disrupting the balance of Aß production and clearance.