The incidence of vascular cognitive impairment is increasing year by year.Its medical burden is getting worse, therefore, there is an urgent need to delay and prevent its occurrence and development.Active symptomatic treatment and targeted intervention of vascular risk factors may alleviate the progress of disease to a certain extent.This article reviews the advances in the treatment and prevention of vascular cognitive impairment.

OBJECTIVETo investigate STK11 gene mutation in a pedigree with Peutz-Jeghers syndrome (PJS).

METHODSA pedigree of PJS was investigated. DNA was extracted from peripheral blood samples from affected and unaffected members of the pedigree and 100 unrelated healthy controls. PCR was performed to amplify all of the 9 coding exons of STK11 gene. PCR products were directly sequenced to detect mutation.

RESULTSA missense mutation p.F354L (c.1062C>G) in exon 8 of the STK11 gene has been identified in all patients with PJS, but was not found in normal individuals from the pedigree and 100 unrelated controls.

CONCLUSIONA missense mutation p.F354L of STK11 gene probably underlies the disease in this pedigree.

Adult ; Asian Continental Ancestry Group ; genetics ; Base Sequence ; DNA Mutational Analysis ; Exons ; Female ; Humans ; Male ; Molecular Sequence Data ; Pedigree ; Peutz-Jeghers Syndrome ; diagnosis ; enzymology ; genetics ; Protein-Serine-Threonine Kinases ; genetics

Objective To investigate the neuroproteetive effect of Rhubarb extract (RE) on cerebral ischemia-reperfusion injury in mice and its mechanism.Methods Twenty-eight male ICR mice were randomly divided into sham operation,ischemia-reperfusion,low-dose RE (100 mg/kg),and high-dose RE (100 mg/kg) groups.A model of middle cerebral artery occlusion and reperfusion in mice was induced by the suture method.The drug intervention groups were given intragastric RE administration (once a day) on the third day before model preparation,and the same volume of normal saline was injected into mice of the cerebral ischemia-reperfusion group.The volume of cerebral infarction was detected by triphenyltetrazolium chloride staining.The neuron-specific nuclear protein (NeuN),glial fibrillary acidic protein (GFAP),and ionized calcium binding adapter 1 (IBA-1) were used as markers of the ischemic cortical neurons,astrocytes,and microglial cells,respectively,and detected by inmunohistochemistry.The expression levels ofsuperoxide dismutase (SOD)-1,SOD-2,and catalase (CAT) in ischemic cortex were detected by Western blot analysis.Results Compared with the cerebral ischemia-reperfusion group,the neurological function score of the high-dose RE group was significantly reduced,the infarct volume was significantly reduced,and the number of neurons in the ischemic cortex was increased significantly,and the activation degree of astrocytes and microglia was decreased significantly (all P ＜0.05),the expression levels of SOD-1,SOD-2,and CAT were increased significantly (all P＜ 0.05);in contrast,there was no significant difference between the low-dose RE group and the cerebral ischemia-reperfusion group.Conclusions High-dose RE may play a protective role for cerebral ischemia-reperfusion mice through anti-oxidative mechanism.

The extract of Alpinia katsumadai, a member of the family Zingiberaceae, shows anti-inflammatory effects and antioxidant activity. We observed the neuroprotective effects of the extract from Alpinia katsumadai seed (EAKS) against ischemic damage in gerbils administered oral EAKS (25, and 50 mg/kg) once a day for 7 days before transient cerebral ischemia. In the 50 mg/kg EAKS-treated ischemia group, about 67% of neurons in the hippocampal CA1 region (CA1) survived after ischemia/reperfusion (I/R) based on cresyl violet staining. We observed that EAKS treatment significantly maintained brain-derived neurotrophic factor (BDNF) immunoreactivity in the ischemic CA1 region after I/R. In addition, protein levels of BDNF in the 50 mg/kg EAKS-treated ischemia group were much higher than those in the vehicle-treated ischemia group after I/R. These findings indicate that repeated supplementation of EAKS protects neurons from ischemic damage, such that BDNF is distinctively maintained in ischemic areas.
Alpinia ; Benzoxazines ; Brain-Derived Neurotrophic Factor ; CA1 Region, Hippocampal ; Gerbillinae ; Hippocampus ; Humans ; Ischemia ; Ischemic Attack, Transient ; Neurons ; Neuroprotective Agents ; Seeds ; Viola ; Zingiberaceae

Cyclooxygenase-2 (COX-2) is believed to be a multifunctional neural modulator that affects synaptic plasticity in the hippocampus. In the present study, we investigated the differential effects of treadmill exercise on COX-2 immunoreactivity in the dentate gyrus in early and chronic diabetic stages in Zucker diabetic fatty (ZDF) rats and lean control (ZLC) rats. To this end, ZLC and ZDF rats at 6 or 23 weeks of age were put on a treadmill with or without running for 1 h/day for 5 consecutive days at 16-22 m/min for 5 weeks or 12-16 m/min for 7 weeks, respectively. Treadmill exercise in prediabetic and chronic diabetic rats significantly reduced blood glucose levels. In particular, exercise in the prediabetic rat blocked the onset of diabetes. COX-2 immunoreactivity was mainly detected in the granule cell layer of the dentate gyrus and stratum pyramidale of the CA3 region in all groups. COX-2 immunoreactivity was significantly increased in these regions of ZLC and ZDF rats after treadmill exercise in the early diabetic stage. However, COX-2 immunoreactivity was not changed in these regions in ZDF rats after treadmill exercise in the chronic stage. These results suggest that treadmill exercise in diabetic animals in the chronic stage has limited ability to cause plasticity in the dentate gyrus.
Animals ; Blood Glucose ; Cyclooxygenase 2 ; Dentate Gyrus ; Hippocampus ; Plastics ; Rats ; Running

BACKGROUNDDanshen (Radix Salvia miltiorrhizae) has been used as a traditional medicine in Asia for treatment of various microcirculatory disturbance related diseases. Tanshinones are mainly hydrophobic active components, which have been isolated from Danshen and show various biological functions. In this study, we observed the neuroprotective effect of tanshinone I (TsI) against ischemic damage in the gerbil hippocampal CA1 region (CA1) after transient cerebral ischemia and examined its neuroprotective mechanism.

METHODSThe gerbils were divided into vehicle-treated-sham-group, vehicle-treated-ischemia-group, TsI-treated-sham-group, and TsI-treated-ischemia-group. TsI was administrated intraperitoneally three times (once a day for three days) before ischemia-reperfusion. The neuroprotective effect of TsI was examined using H&E staining, neuronal nuclei (NeuN) immunohistochemistry and Fluoro-Jade B staining. To investigate the neuroprotective mechanism of TsI after ischemia-reperfusion, immunohistochemical (IHC) and Western blotting analyses for Cu, Zn-superoxide dismutase (SOD1), Mn-superoxide dismutase (SOD2), brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-I (IGF-I) were performed.

RESULTSTreatment with TsI protected pyramidal neurons from ischemia-induced neuronal death in the CA1 after ischemia-reperfusion. In addition, treatment with TsI maintained the levels of SOD1 and SOD2 as determined by IHC and Western blotting in the CA1 after ischemia-reperfusion compared with the vehicle-ischemia-group. In addition, treatment with TsI increased the levels of BDNF and IGF-I determined by IHC and Western blotting in the TsI-treated-sham-group compared with the vehicle-treated-sham-group, and their levels were maintained in the stratum pyramidale of the ischemic CA1 in the TsI-treated-ischemia-group.

CONCLUSIONTreatment with TsI protects pyramidal neurons of the CA1 from ischemic damage induced by transient cerebral ischemia via the maintenance of antioxidants and the increase of neurotrophic factors.

Animals ; Antioxidants ; metabolism ; Blotting, Western ; Brain Ischemia ; drug therapy ; metabolism ; Brain-Derived Neurotrophic Factor ; metabolism ; Diterpenes, Abietane ; therapeutic use ; Gerbillinae ; Hippocampus ; metabolism ; Immunohistochemistry ; Insulin-Like Growth Factor I ; metabolism ; Male ; Nerve Growth Factors ; metabolism ; Superoxide Dismutase ; metabolism ; Superoxide Dismutase-1