The post-stroke depression (PSD) is one of the common complications of stroke.It can not only delay the recovery of the neurological function in patients, seriously affect the quality of life of patients, but also increase the mortality and morbidity.More and more attention has been paid to the pathogenesis of PSD.Recent studies have confirmed that brain small vessel disease is closely related to the occurrence of PSD.This article reviews relationship between brain small vessel diseases and PSD.

Objective To investigate the effects of peroxisome proliferators-activated receptorγ(PPARγ)agonist pioglitazone on the expressions of glial fibrillary acidic protein (GFAP) and cyclin D1 in the hippocampal CA1 region after cerebral ischemia in rats.Methods Fifty-four Sprague-Dawley rats were randomly divided into 3 groups:sham operation group,ischemia/reperfusion group,and pioglitazone intervention group (18 in each group).A rat middle cerebral artery occlusion and reperfusion model was induced by the modified suture method.Continuous pioglitazone rosiglitazone gavage (0.65 mg/kg once a day) was conducted for 5 days before modeling in the pioglitazone intervention group.At day 1,3,and 7 after modeling the rats (6 at each time point) were sacrificed and their brains were removed.HE staining was used to detecte the pathological changes of neurons in the hippocampal CA1 region.Immunohistochemical staining was use to detect the expressions of GFAP and cyclin D1 in the hippocampal CA1 region.Results Compared to the sham operation group,at day 3 and 7 after ischemia/reperfusion,the number of neuronal survival in the hippocarmpal CA1 region in the ischemia/reperfusion group was significantly reduced (all P ＜ 0.01).The expressions of GFAP and Cyclin D1 at all time points were significantly upregulated (all P ＜ 0.01).At day 3 and 7 after ischemia/reperfusion,the numbers of neuronal survival in the hippocampal CA1 region in the pioglitazone intervention group were significantly increased (all P ＜0.01).Compared to the ischemia/reperfusion group,the expressions of GFAP and Cyclin D1 at all time points were significantly down-regulated (all P ＜ 0.01).Conclusions PPARγagonist pioglitazone has a significant protective effect on neuron in the hippocampal CA1 region after cerebral ischemia/reperfusion in rats.Its mechanism may be associated with inhibiting GFAP and cyclin D1 expressions.

Cerebral vasospasm (CVS) is one of the serious complications of subarachnoid hemorrhage (SAH).Pathogenesis of CVS has not been fully clarified,and it may be associated with a variety of factors.With the development of molecular biology techniques,people have more understanding on SAH caused pathogenesis of CVS,and the research has also made considerable progress in the prevention of CVS.

Dyslipidemia refers to the elevated cholesterol,triacylglyceride levels and/or the reduced high density lipoprotein level.It is the important risk factor for the occurrence of atherosclerosis,and it is alsoassociated with the onset and outcome of acute cerebrovascular disease.Therefore,the highly efficient and comprehensive lipid lowering therapy has become one of the most important and effective prevention measures for cerebrovascular disease.This article reviews the recent advances in research on dyslipidemia and lipid lowering therapy in patients with cerebrovascular disease.

Thiazolidinodiones are a synthetic ligand of peroxisome proliferator-activated receptor γ(PPARγ).PPARγhas certain protective effects for several types of tissues.The research covers the areas of glucose,lipid metabolism,cancer and atherosclerosis,etc.At present,the roles of thiazolidinediones in central nervous system diseases have received much attention,such as cerebral infarction,multiple sclerosis,and Alzheimer's disease.This article reviews the effects of PPARγ ligand thiazolidinediones on inhibiting the proliferation of glial cells,promoting angiogenesis,and antagonizing neuronal apoptosis after cerebral ischemia.

Objective To investigate the significance and mechanism of intracerebroventricular injection viper venom nerve growth factor (Vngf) in rat neural plasticity after cerebral ischemia reperfusion injury.Methods Ninety Wistar male rats were randomly assigned into Vngf-25 U group (n = 18), Vngf-50 U group (n = 18), Vngf-100 U group (n = 18), ischemia reperfusion group (n = 18) and sham operated group.The expression of candidate plasticity-related gene 15(cpg-15) Mrna and nuclear factor of kappa B ( NF-Κb ) Mrna in rat brain tissues which were collection at 2,7,14 days after surgery were evaluated by the real time PCR.Results The expression of cpg-15 Mrna and NF-Κb Mrna began to increase after surgery( the F value of cpg-15:70.43, 34.11, 31.89, the F value of NF-Κb: 27.47, 34.56, 31.89,P＜0.01).At the same time, expression of cpg-15 Mrna and NF-Κb Mrna in the Vngf groups was significantly different from the I/R group and the sham operated group (the F value of cpg-15:48.18, 55.93, 78.43, the F value of NF-Κb: 45.92, 55.72, 50.49, P ＜0.01).The more Vngf were injected, the more cpg-15 Mrna and NF-Κb Mrna were expressed in Vngf groups.Conclusions The Vngf could accelerate neural plasticity and restore neurofunctional defect through up-regulated the expression of cpg-15 and NF-Κb.

S100B is a class of acid calcium-binding protein. It mainly exists in neuroglial cells in the central nervous system, and it is one of the signs of astrocyte activation. S100B may reflect the function of neuroglial cells and regulate the complex interactions between the neurons and neuroglial cells. Studies in recent years have demonstrated that S100B protein is involved in the pathological processes of acute ischemic brain injury. Serum S100B protein can be used as an important marker for identifying the severity of cerebral infarction, progress and outcome.

ObjectiveTo explore the Apolipoprotein-E （ApoE） gene polymorphism in patients with Alzheimer's disease （AD）, vascular dementia (VD) or mild cognitive impairment (MCI). MethodsPeripheral blood was taken from patient with AD, VD or MCI to determine the ApoE genotypes. ResultsThe most of the patients were ε3/ε3 genotype, while the ε2/ε2 and ε4/ε4 could not be detected. ε3/ε4 genotype （P=0.001） and ApoE ε4 allele （P=0.013） was more frequent in AD than in MCI. ApoE ε4 was more frequent in VD than in MCI （P=0.044）. ConclusionApoE ε4 allele is a risk factor in AD, and may be associated with VD and MCI.

Brain ischemic conditioning (BIP) can improve the tolerance to ischemic injury in the brain. Nuclear factor-κB (NF-κB) is an important transcriptional regulatory factor.It presents in all types of cells in the nerous system. Studies have suggested that BIP may exert neuroprotective effects by mediating NF-κB through a series of cascade reactions. This may provide a new therapeutic strategy for BIP in the prevention and treatment of ischemic cerebrovascular disease in clinical practice.

Objective To investigate the cerebral ischemia/reperfusion protection mechanism of viper venom nerve growth factor(vNGF) by the change of expression of growth associated protein-43 (GAP-43) and neurological function.Methods 45 adult male Wistar rats (weight 220～280 g) were divided randomly into 3 groups: sham group(S, n=9), balanced salt solution group (BSS, n=9) and venom nerve growth factor group (vNGF, n=27). Each group was observed for 7 days. vNGF group was divided into 25 U, 50 U and 100 U subgroups respectively. The following indexes in 3 groups were observed respectively: neurologic deficits and the expression of GAP-43 (immunohistochemistry method).Results Neurological function: The scores of neurological function was 0 in S group. The neurological deficits score was lower at the same time in vNGF group than that in BSS group (P<0.05). Immunohistochemistry: GAP-43 expressed in both BSS group and vNGF group. The expression of GAP-43 in vNGF group increased in 25 U, and to maximum in 100 U. The expression of GAP-43 in BSS group was significantly lower than in vNGF group (P<0.05). Conclusion vNGF can effectively enhance and prolong the expression of GAP-43, increase the survival rats of nerve cells, and has the protection effect on nerve cells after cerebral ischemia injured.