ABSTRACT
With the development of imaging, molecular biology, and pathology, the pathogenesis of cerebral small vessel disease (CSVD) has been deeply understood, but the exact pathogenesis is still unclear. This article reviews the pathogenesis of CSVD, including oxidative stress, inflammatory reaction, amyloid beta amyloid deposition, vascular endothelial dysfunction, and blood-brain barrier damage.
ABSTRACT
Cerebral smal vessel disease (CSVD) refers to cerebral smal perforating arteries and arterioles (diameter 40 - 200 μm), capilaries, and venules caused syndromes of clinical, cognitive and pathological manifestations. Its imaging classification includes lacunar infarcts, white matter lesions, cerebral microbleed, and perivascular space enlargement, etc. The pathogenesis of CSVD is stil being explored, and imaging findings can not completely reflect the change process of its pathophysiology, especialy the early lesions. Therefore, the difficulties have increased for the prevention and treatment of CSVD. This article summarizes the progress in research on CSVD biomarkers in recent years in order to provide ideas for its etiology, pathogenesis, and clinical prevention and treatment.
ABSTRACT
The research of the secondary damage remote from middle cerebral artery territory infarction has made significant progress in recent years.More animal experiments from the cellular,biochemical and molecular levels have been performed for in-depth and detailed research on remote site damage. The injury mechanisms such as oxidative damage and β amyloid deposition have been found.The new imaging detection technologies,such as magnetic resonance diffusion tensor imaging(DTI),have gradually been applied to the diagnosis of remote site damage.
ABSTRACT
Objective To investigate the learning and memory functions,expression changes of disintegrin and metalloprotease 10 (ADAM10) mRNA in hippocampus in the aged rats with chronic cerebral hypoperfusion as well as the effect of atorvastatin on them.Methods A total of 72 rats were randomly divided into sham operation,cerebral hypoperfusion and atorvastatin treatment groups.A permanent bilateral common carotid artery occlusion (2VO)model was induced.Atorvastatin 10 mg/(kg · d) was administered orally after procedure in the atorvastatin treatment group.Real-time fluorescence quantitative polymerase chain reaction was used to detect the expression of ADAM10 mRNA in bilateral hippoocampus at 1,2,4,and 16 weeks after modeling,Results Two weeks after modeling,the learning and memory functions were decreased significantly in the cerebral hypoperfusion group compared to the sham operation group (P < 0.05).At 4 and 16 weeks after modeling,they were further decreased (P <0.01); there were no significant differences in the learning and memory functions at 1,2,and 3 weeks after modeling between the atorvastatin treatment group and the cerebral hypoperfusion group,however,they were improved significantly at 16 weeks compared to the cerebral hypoperfusion group (P<0.01).The expression of ADAM10 mRNA in hippocampus at different time points after modeling in the cerebral hypoperfusion group was down-regulated by 22%,43%,35%,and 50%,respectively compared to the sham operation group (all P <0.05).The expression of ADAM 10 mRNA in hippocampus at 2 weeks in the atorvastatin treatment group was higher than 22% in the cerebral hypoperfusion group (P<0.05).There were not significant differences at other time points.Conelusions Chronic cerebral hypoperfusion results in the down-regulation of the expression of ADAM10 mRNA in hippocampus in the aged rats,and atorvastatin may inhibit down-regulation of the expression of ADAM10 mRNA at early stage.
ABSTRACT
Cerebral amyloid angiopathy (CAA) is characterized by leptomeningeal and β-amyloid deposition in arteriole wall in cortex, and it is one of the common cerebral vascular diseases in the elderly. It is correlated with Alzheimer's disease, intracerebral hemorrhage, cerebral infarction and leukoencephalopathy. CAA is divided into hereditary and sporadic types, and the latter is most common. This article reviews the advances in research on the pathophysiological mechanisms of sporadic CAA, particularly the production of β-amyloid protein and clearance mechanism in brain tissue.