| Background and Purpose: Cerebral infarction is the leading cause of death and the most common cause of adul neurologic disability. Despite of advances in acute and prophylactic therapies, rates of cerebral infarction and cerebral infarction-related deaths continue to increase. Not only may inflammatory and immune process play a role in atherosclerosis and cerebral infarction occurrence, but it also play a critical role in postischemic injury. C-reactive protein ( CRP ) has been suggested as a marker for inflammatory process and seems to correlate with poor prognosis after cerebral infarction. Changes of T lymphocyte subsets in the peripheral blood have been found in patients with cerebral infarction, the clinical implication of the changes has not been known clearly. In the brains of Alzheimer's disease ( AD ) patients amyloid beta-peptide ( Aβ) is the major component of senile plaque. Aβ( Aβ40 and Aβ42 ) is a proteolytic product of the larger beta amyloid precursor protein ( βAPP ). In the brains of AD, a cardinal role for Aβhas been postulated as a major trigger of neuronal injury, Aβcompromises neurons via an excitotoxic pathway including extracellular glutamate accumulation, N-methyl-D-aspartate ( NMDA ) receptor activation and an intracellular Ca2+ overload leading to cell death. Aβalso appears to be associated with an inflammatory response in AD brains. In ischemic stress, βAPP and Aβwere reported to be changed. The change of Aβlevels and the biological significance of Aβin patient with ischemic stroke have not been known clearly, the interplay among various pathogenic role in the progression of cerebral infarction remains unclear. Neuroprotective agents that change the pathophysiological processes could be beneficial to patients with cerebral infarction and alter the course of the disease. Many neuroprotective drugs reduce ischemic damage in animal models of stroke, but the side effects are severe. Many are searching for a safe agent that can limit ischemic damage in human stroke. In the last few years, several studies appear to show that statins have effects that extend beyond cholesterol reduction, statins seem to be able to decrease inflammatory response, have pleiotropic immunomodulatory effects, reduce deleterious effects of excitatory neurotransmitter on cells, and have anti-oxidant effects. Some studies show that the use of statins is associated with a lower risk of developing AD. Cell and animal experiments have revealed a connection between cholesterol metabolism and the processing of βAPP, it has been suggested that βAPP processing is altered by statins and that leads to changes in Aβconcentration. Pleiotropic effects of statins might be implicated in any potential benefit in ischemic stroke. This implys statins might have protective effect on cerebral infarction. Studies about the role of statins in patients with cerebral infarction are few. Thus, we measured serum Aβ40, plasma Aβ42 levels, serum CRP levels, T lymphocyte subsets in the peripheral blood, serum levels of total cholesterol ( TC ), triglyceride ( TG ), high density lipoprotein cholesterol ( HDL-C ) and low density lipoprotein cholesterol ( LDL-C ), serum aspartate aminotransferase ( AST ) levels and serum creatine kinase ( CK ) levels in acute cerebral infarction subjects before and after statins treatment. All patients were examined with National Institutes of Health Stroke Scale ( NIHSS ) and Barthel Index ( BI ) score at admission and 3 months after admission. To investigate the changes and clinical implication of serum Aβ40 and plasma Aβ42 concentration and the effect of statins intervention on former parameters and the outcome of cerebral infarction. Methods: Participant were healthy control and cerebral infarction patients. Cerebral infarction patients were consistent with the diagnosis and exclusion criteria of the study, the course of disease were no more than 2 weeks. Patients entered a randomized, double-blind, placebo-controlled intervention trial. They were randomized to one of the two treatment...
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