Study Of Relationship Between Serum Aβ 1-40,Aβ 1-42 And Cerebral Small Vessel Disease

Background and Objective:Cerebral small-vessel disease (SVD) can be visualized on MRI as white matter lesions (WML), lacunar infarcts and micro-bleedings. SVD accounts for approximately one quarter of the etiology of ischemic cerebral vascular disease, and with the development of technology more and more SVD are diagnosed. Though morbidity and mortality are lower and the neurologic deficits recover well, in the long run, patients with SVD are faced with more deaths and more stroke recurrence. SVD is also responsible for cognitive decline.Beta-amyloid peptide, as the main component of the senile plaque, is the hallmarker of Alzheimer disease. It is a peptide composed of 39-43 amino acids with a characteristic conformation of beta-sheet. It has long been suggested that soluble Aβmay exert neuronal toxicity by induction of oxidative stress, apoptosis, inflammation, calcium overload and so on. Apart from that, its vascular effect on the cerebrovasculature has also been highlighted, which could impaire the endothelium and decrease the cerebral blood flow. And that in turn will synergize with the neuronal toxicity.The importance of cerebrovascular pathology in the pathogenesis of AD has been highlighted. Several well-known vascular risk factors has been proven to be related to AD by epidemiological studies; It is suggested that vascular lesions and AD pathology often coexist and that almost 35% of AD subjects bear evidence of cerebral infarction at autopsy, and microvascular degeneration,cerebral amyloid angiopathy and periventricular white matter lesions are evident in most cases of AD. Under hypoxic condition more Aβis generated through a variety of mechanisms. Thus it is hypothized that circulating Aβmay be elevated in patients with cerebral small vessel disease. Here in this study we focus on the the relationship between plasma Aβand the existence and severity of SVD in Chinese population.Methods:Study group:63 patients (39 male,24 female, average year 67.65±8.17) were enrolled in our study. All the patients underwent an magnetic resonance imaging (MRI) examination which showed the existing of leukoaraiosis or lacunar infarction. Patients with embolism, large vascular disease, brain trauma, intracranial tumor or severe organ failure are excluded. Patients are subcategorized into two groups according to DWI:SVD patients with acute lacunar infarction and patients without acute lacunar infarctionControl group:18 age-matched patients (5 male,13 female, average year is 64.78±8.56) were also enrolled in our study. They all have risk factors for cerebral vascular disease and stroke-mimic symptoms (15 with dizziness,3 with headache,1 with epilepsy,4 with glossolalia,2 with transient limb weakness), but revealed a normal MR imaging.Medical history collection, and physical examination were done by experienced neurological doctors, and vascular risk factors were collected. White mater leision on MR image were evaluated by qualified radiologists blinded to clinical information(Fazekas scale). Blood samples were collected and Elisa was used to quantitatively detect serum Aβ.Results:1. Comparision between serum Aβ1-40 in SVD group and control groupSerum Aβ1-40 level in SVD group is 40 52.71±12.99 pg/ml, and 45.15±10.66 pg/ml in the control group. Difference is statistically significant. (p<0.05).2. Comparision between serum Aβ1-40 in SVD with acute lacunar infarction and SVD without acute lacunar infarctionSerum Aβ1-40 level in SVD subgroup with acute lacunar infarction is 48.09± 8.47pg/ml,and 56.18±14.73 pg/ml in SVD subgroup without acute lacunar infarction. Difference is statistically significant. (p<0.05).3. Comparision between serum Aβ1-40 in control group and the two SVD subgroupsSerum Aβ1-40 level in SVD subgroup with acute lacunar infarction is 48.09±8.47pg/ml, and 45.15±10.66 pg/ml in the control group, there is no significant difference. (p>0.05).Serum Aβ1-40 level in SVD subgroup without acute lacunar infarction is 56.18±14.73 pg/ml, and 45.15±10.66 pg/ml in the control group. Difference is statistically significant. (p<0.05).4. Serum Aβ1-40 and the severity of white matter leision.Serum Aβ1-40 level in SVD subgroup with mild white matter leision: 50.18±12.40 pg/ml;Serum Aβ1-40 level in SVD subgroup with moderate white matter leision: 51.67±11.52 pg/ml;Serum Aβ1-40 level in SVD subgroup with severe white matter leision: 56.37±12.99 pg/ml;There is no significant difference. (p>0.05).Conclusions:1. Serum Aβ1-40 is higher in SVD patients than in control group.2. Serum Aβ1-40 in SVD patient with acute lacunar infarction is significantly lower than in SVD patients without acute lacunar infarction.3. There is no correlation between serum Aβ1-40 level and the severity of white matter lesion.