The incidence of poststroke dementia is high and the burden of disease is heavy. It is very important to prevent or delay its occurrence and progression. In recent years, the lifestyle adjustments, such as the intervention for vascular risk factors, adhering to the diet management, and functional exercise have been confirmed to prevent poststroke dementia to a certaln extent. Acetylcholinesterase inhibitor and glutamate receptor antagonist, etc. play an important role in delaying the progression of poststroke dementia and vascular cognitive impalrment. This article reviews the latest progress in research on the prevention and treatment of poststroke dementia.

Mesenchymal stem cells (MSCs) play a neuroproteetive effect via a variety of mechanisms.They provide a new idea for the treatment of cerebral ischemia.However,the inadequate sources have significantly limited the possible clinical applications.Carbon nanotubes (CNTs),a new nanomaterials,can not only promote the adhesion,proliferation and differentiation of MSCs in vitro,but also as the cell carriers they can provide good microenvironmental guarantee for the survival of MSCs through the regulation of secretion of cytokines and neurotrophic factors,as well as regulation of biological characteristics of neurons,glial cells,and macrophages after their cell transplantation,provide a good microenvironment guarantee for the survival of MSCs,and promote the effect of MSCs on the therapeutic effect of cerebral ischemia.

Membrane-associated guanylate kinases (MAGUKs) is a class of postsynaptic density proteins (PSDs) in the postsynaptic dense of the postsynaptic membrane,including PSD-95,SAP-102,PSD-93,and SAP-97.MAGUK family members contain several protein binding sites,and these special binding sites are responsible for mediating a variety of signal transduction.MAGUKs participate in the occurrence and development mechanisms in central nervous system diseases,and has become a topic of general interest of neuroscience.This article briefly reviews the roles of MAGUKs in ischemic brain injury.

Carotid stenosis is one of the important causes of cerebral infarction. It has been demonstrated that carotid angioplasty and stenting (CAS) can prevent the occurrence of stroke, and its clinical application is continuously increasing. Although CAS is a microinvasive technique, it has some potential complications, such as hemodynamic abnormalities, hyperperfusion syndrome, cerebral infarction, and restenosis. This article reviews the complications of CAS and their management strategies.

Different from Westerners,intracranial atherosclerosis (ICAS) is a main cause for acute ischemic stroke in Eastern population.Studies have shown that ICAS is associated with the risk factors including metabolic syndrome,dyslipidemia,diabetes mellitus,and inflammation.Adiponectin is involved in oxidative stress and glycolipid metabolism,its reduced level is the most important risk factor for metabolic syndrome and the most prominent inflammatory markers.Numerous studies have suggested that adiponectin is associated with cardiovascular diseases,and it is used as a preventive marker.In recent years,the relationship between adiponectin and ICAS has become a hot research topic.This article mainly reviews the roles of adiponectin in ICAS.

Objective To explore the expression of brain-derived neurotrophic factor(BDNF) mRNA and high-affinity receptor TrkB mRNA in the prefrontal cortex of the post stroke depression in the rats.Methods Focal cerebral ischemic rat models were made with thread embolism method.Post stroke depression(PSD) rat models were established with comprehensive separately breeding and chronic unpredicted mild stress (CUMS) on this basis.Normal control group,depression group and stroke group were used to compare with PSD group.8 rats were used in each group.RT-PCR was employed to detect gene expression of BDNF and TrkB.GADPH was used as control at 29th day after the CUMS.Results The results showed that the gene level of BNDF in the prefrontal cortex of rat subjected PSD was lowest among all groups(0.75 ± 0.21).And the expression of BNDF mRNA in the normal control rats was (0.83 ± 0.16) and was highest among all groups.While it was (0.77 ± 0.22) in the depression group and (0.80 ± 0.20) in the stroke group.The one-way analysis of variance showed the expression of BDNF mRNA in the prefrontal cortex decreased significantly in the PSD group compared with normal control rats (P ＜ 0.05).Whereas,the expression of TrkB mRNA had no statistical difference among groups (P ＞ 0.05).Conclusion The downregulation of BDNF mRNA in the prefrontal cortex may be responsible for the pathogenesis of PSD.

Objective To explore the expression of brain-derived neurotrophic factor(BDNF) and highaffinity receptors tropomyosin receptor kinase B(TrkB) protien in the prefrontal cortex of the post stroke depression in the rats.Methods Focal cerebral ischemic rat models were made with thread embolization method.Post stroke depression rat models were established with comprehensive separately breeding and chronic unpredicted mild stress (CUMS) on this basis.Normal control group,depression group and stroke group were used to compared with PSD group.6 rats were used in each group.Immunohistochemistry for detecting the expression of BDNF and TrkB in the prefrontal was used at 29th day since the CUMS.Results The number of BNDF immunopositive cells in PSD group was the least ((21.00 ± 12.41) per microscope field of vision) than other groups.Whereas there was no statistical difference among groups(P＞ 0.05).The number of TrkB immunopositive cells in the prefrontal cortex in PSD group was the least (20.78 ± 7.20) among three groups,and depreesion group was secondary (21.00 ±5.61).Stroke group has the most number of immunopositive cells(31.67 ± 7.38) in the prefrontal cortex among four groups.One way ANOVA statistical analysis showed the number of TrkB immunopositive cells decreased significantly in the PSD group and depression group compared with stroke group (P＜0.05).Conclusion The downregulation of TrkB immunopositive cells in the prefrontal cortex may be responsible for the pathogenesis of PSD.

Objective To explore the relationships between cognitive emotion regulation and behavioral inhibition system(BIS)/behavioral activation system (BAS) of adolescents.Methods Seven hundreds forty-two adolescents were tested by Behavioral Inhibition/Activation System Scale(BIS/BAS Scale) and Cognitive Emotion Regulation Questionnaire Chinese version (CERQ-C).Results (1) Maladaptive emotion regulation,such as selfblame,rumination,catastrophizing and blame others were positively corrected with BIS (r =0.13 ～ 0.38,P ＜0.01).But adaptive ER had no significantly correlations with BIS (r =-0.05,P ＞ 0.05).Maladaptive emotion regulation was positively correlated with BAS (r =0.24,P ＜ 0.01),and adaptive emotion regulation was negatively correlated with BAS(r =-0.028,P＜ 0.01).(2)Except acceptance,BIS/BAS had significant effect on the other eight cognitive emotion regulation(P ＜ 0.01).Conclusion BIS/BAS are closely related with cognitive emotion regulation,and have important influences on selection of adolescents'cognitive emotion regulation.

Objective:To investigate the feasibility,effectiveness and safety in the treatment of symptomatic middle cerebral artery stenosis with stenting.Methods:Twelve patients with middle cerebral artery stenosis were treated with stenting from August 2005 to December 2006.Among these patients,9 were male and 3 were female.The meam(SD)age was 69(5.3)years(range 56 to 81 years).The mean(SD)stenosis degree was 84.2%(3.7)(range 50% to 99%).All patients were successfully treated with balloon-expanded stents.and there was not any severe complications.Results:The rate of residual stenosis after the procedures was≤20%.No cerebral ischemic symptoms recurred in the patients over a 6-to 18-month follow-up period.Conclusions:Endovascular stenting is a safe and effective approach in the treatment of symptomatic middle cerebral artery stenosis,and its short-term effect is significant.

The severity of ischemic brain injury was closely associated with the mortality and disability of stroke. How to limit ischemic brain injm-y to the greatest extent and promote the recovery of neurological function is one of the most concerned hotspots at present in the field of neuroscience. A large number of studies have shown that a variety of factors involve in the pathological process of ischemic brain injury, in which, the role of T lymphocyte-mediated immune inflammatory response in ischemic brain injury has received increasing attention. This article mainly reviews the role of T cells in ischemic brain injury.