简介：Thequestforneuroprotectivedrugstoslowtheprogressionofneurodegenerativediseases(NDDs),includingAlzheimer'sdisease(AD),Parkinson'sdisease(PD),andHuntington'sdisease(HD),hasbeenlargelyunrewarding.Preclinicalevidencesuggeststhatrepurposingquetiapine,lithium,valproate,fluoxetine,donepezil,andmemantineforearlyandpre-symptomaticdisease-modificationinNDDsmaybepromisingandcanspareregulatorybarriers.Theliteratureofthesepsychotropicsinearlystageandpre-symptomaticAD,PD,andHDisreviewedandpropitiousfindingsfollow.Mildcognitiveimpairment(MCI)phaseofAD:salutaryhumanrandomizedcontrolledtrialfindingsforlow-doselithiumand,inselectedpatients,donepezilawaitreplication.Pre-symptomaticAD:humanepidemiologicaldataindicatethatlithiumreducesADrisk.Animalmodelstudies(AMS)revealencouragingresultsforquetiapine,lithium,donepezil,andmemantine.EarlyPD:valproateAMSfindingsshowpromise.Pre-symptomaticPD:lithiumandvalproateAMSfindingsareencouraging.EarlyHD:uncontrolledclinicaldataindicatenon-progressionwithlithium,fluoxetine,donepezil,andmemantine.Pre-symptomaticHD:lithiumandvalproateareauspiciousinAMS.Manyotherpromisingfindingsawaitingreplication(valproateinMCI;lithium,valproate,fluoxetineinpre-symptomaticAD;lithiuminearlyPD;lithium,valproate,fluoxetineinpre-symptomaticPD;donepezilinearlyHD;lithium,fluoxetine,memantineinpre-symptomaticHD)arereviewed.Dose-andstage-dependenteffectsareconsidered.Suggestionsforsignal-enhancementinhumantrialsareprovidedforeachNDDstage.

简介：Neurotrophicfactorscompriseessentialsecretedproteinsthathaveseveralfunctionsinneuralandnon-neuraltissues,mediatingthedevelopment,survivalandmaintenanceofperipheralandcentralnervoussystem.Therefore,neurotrophicfactorissuehasbeenextensivelyinvestigatedintothecontextofneurodegenerativediseases.Alzheimer'sdiseaseandParkinson'sdiseaseshowchangesintheregulationofspecificneurotrophicfactorsandtheirreceptors,whichappeartobecriticalforneuronaldegeneration.Indeed,neurotrophicfactorspreventcelldeathindegenerativeprocessesandcanenhancethegrowthandfunctionofaffectedneuronsinthesedisorders.Basedonrecentreports,thisreviewdiscussesthemainfindingsrelatedtotheneurotrophicfactorsupport–mainlybrain-derivedneurotrophicfactorandglialcellline-derivedneurotrophicfactor–inthesurvival,proliferationandmaturationofaffectedneuronsinAlzheimer'sdiseaseandParkinson'sdiseaseaswellastheirputativeapplicationasnewtherapeuticapproachforthesediseasesmanagement.

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简介：BACKGROUND:Itisdifficulttoattractinterestinnon-compulsory,preventive,medicalcare,andpersonsdiagnosedwithcertaindiseasesoftenignoretheexistenceofthesediseases.However,Huntington'sdisease(HD)isanexception.OBJECTIVE:ToqualitativelyanalyzefactorsmotivatingHDpatientstoparticipateinastudy,namelytheEuropeanHuntington'sDiseaseNetwork(EHDN)REGISTRY.DESIGN,TIMEANDSETTING:AnobservationalsurveywasconductedintheEHDNStudySiteinPoznan,Polandbetween2007and2008.PARTICIPANTS:Thestudyinvolved22personsaffectedwithHDand3pre-symptomaticindividuals,totaling9malesand16females.The24participantsinthisstudyhad24differentcaregivers.Atotalof25symptomaticorpre-symptomaticsubjectsparticipatedintheinitialREGISTRYvisit,aswellas6inthesecond,and1inthethird.Allsubjectsdidnotknoweachotherpriortothevisit.METHODS:AmutationintheIT15genewasconfirmedineachpatientorpre-symptomaticmutationcarrier.Anin-depthinterviewproduceddetailedinformationontheHDpatients,aswellasthecaregivers,fortheREGISTRYstudy.MAINOUTCOMEMEASURES:AqualitativeanalysisofthefactorsmotivatingHDpatientsandthepre-symptomaticmutationcarrierstoparticipateintheREGISTRYlongitudinal,observational,researchprojectwasperformed.RESULTS:TheprimarymotivatingfactorforinvolvementofHDpatientsandthecaregiversintheREGISTRYstudywasthehopethataneffectiveHDtherapywouldsoonbediscovered.InHDpatientsandthepre-symptomaticgroup,theresponsetoparticipateintheREGISTRYprojectreached100%,despitethefactthattheyknewtheprojectwasonlyanobservationalstudy.CONCLUSION:Patienthopeisthoughttobeafactorforengaginginpreventive,therapeuticactivities.However,thisisrarelymentionedinmedicalpapersandclinicaltextbooks,andisusuallyoverlookedinmedicalteaching.Clearly,effortsshouldbemadetoincludethisinclinicalpractice.

简介：Parkinsonsdisease(PD)isacommon,progressiveneurodegenerativediseasecharacterisedbydegenerationofnigrostriataldopaminergicneurons,aggregationofα-synucleinandmotorsymptoms.Currentdopamine-replacementstrategiesprovidesymptomaticrelief,howevertheireffectivenesswearoffovertimeandtheirprolongeduseleadstodisablingside-effectsinPDpatients.ThereisthereforeacriticalneedtodevelopnewdrugsanddrugtargetstoprotectdopaminergicneuronsandtheiraxonsfromdegenerationinPD.Overrecentyears,therehasbeenrobustevidencegeneratedshowingthatepigeneticdysregulationoccursinPDpatients,andthatepigeneticmodulationisapromisingtherapeuticapproachforPD.Thisarticlefirstdiscussesthepresentevidenceimplicatingglobal,anddopaminergicneuron-specific,alterationsinthemethylomeinPD,andthetherapeuticpotentialofpharmacologicallytargetingthemethylome.Itthenfocusesonanothermechanismofepigeneticregulation,histoneacetylation,anddescribeshowthehistoneacetyltransferase(HAT)andhistonedeacetylase(HDAC)enzymesthatmediatethisprocessareattractivetherapeutictargetsforPD.Itdiscussestheuseofactivatorsand/orinhibitorsofHDACsandHATsinmodelsofPD,andhowtheseapproachesfortheselectivemodulationofhistoneacetylationelicitneuroprotectiveeffects.Finally,itoutlinesthepotentialofemployingsmallmoleculeepigeneticmodulatorsasneuroprotectivetherapiesforPD,andthefutureresearchthatwillberequiredtodetermineandrealisethistherapeuticpotential.

简介：Propofolcaninhibittheinflammatoryresponseandreducethesecretionandharmfuleffectsofastrocyte-derivedproinflammatorycytokines.Inthisstudy,afterpropofolwasinjectedintotheinjuredsciaticnerveofmice,nuclearfactorkappaBexpressionintheL4-6segmentsofthespinalcordintheinjuredsidewasreduced,apoptosiswasdecreased,nervemyelindefectswerealleviated,andthenerveconductionblockwaslessened.Theexperimentalfindingsindicatethatpropofolinhibitstheinflammatoryandimmuneresponses,decreasestheexpressionofnuclearfactorkappaB,andreducesapoptosis.Theseeffectsofpropofolpromoteregenerationfollowingsciaticnerveinjury.

简介：Demyelinationofthecentralnervoussystem(CNS)isahallmarkofmultiplesclerosis(MS),chronicinflammatoryandneurodegenerativedisease.Chronicdemyelinationfavorsneurodegenerationofdenudedaxons,whichisamajorcauseofirreversibleneuronaldeficitsanddisabilityinMSpatients(Lucchinettietal.,2000).MSremainsanincurabledisease,despiteformida-

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简介：BACKGROUND:ToevaluatethequalityoftheliteratureaddressingtraditionalChinesemedicinefortreatingParkinson'sdisease.DATASOURCE:Acomputer-basedonlinesearchofChinesepublicationsfromJanuary2001toJuly2008wasconductedinChineseBiologyMedicalDiscDatabaseandChinaNationalKnowledgeInfrastructure.SearchkeywordswereParkinson'sdisease,integratedtraditionalChineseandWesternmedicine,traditionalChinesemedicinetherapy,andChineseherbtherapy.DATASELECTION:Articlesdescribingrandomized,controlledtrialsandquasi-randomized,controlledtrialswereincluded.Literaturequalitywasassessedusingthecriteria-SystematicevaluationofclinicalliteraturerelatedtotreatmentofParkinson'sdiseasewithtraditionalChinesemedicine.Thisincludedmethodology,interventionsinthetreatment/controlgroup,evaluationcriterionofoutcomes,andfrequency.MAINOUTCOMEMEASURES:Evaluationcriterionofoutcomes(variousscoremethodsandevaluationscales),methodologicalquality,andfrequencydistributionwereallmeasured.RESULTS:Atotalof33articleswithrandomized,controlledtrialswereincluded.Ofthese,sixdescribedarandommethod,andtheremainingdidnotdescriberandomallocationmethodsorrandomsequencegenerationmethods.Noneofthestudiesestimatedsamplesize.Casedescriptionsofwithdrawalandlosstofollow-upwereunclear.BoththeUnifiedParkinson'sDiseaseRatingScaleandWebsterscalewereusedintheeligiblestudiesasevaluationcriteria.CONCLUSION:Therearenohigh-qualitystudiesthataddresstraditionalChinesemedicinetherapyandintegratedtraditionalChineseandWesternmedicinefortreatingParkinson'sdiseaseinChina.EligiblestudieswerenotperformedinaccordancewithConsolidatedStandardsofReportingTrialsstatementorStandardsforReportingInterventionsinControlledTrialsofAcupuncturecriteria,andtheliteraturequalitywaslow.ThepresentlyusedcriteriaforevaluatingtherapeuticeffectsdonotcompletelyassessoutcomesoftraditionalCh

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简介：2010年7月23～25日，首届全国心理健康管理论坛暨北京军区提高班在京举办。会上，中国心理卫生协会理事长蔡焯基教授提出中国人心理健康的6条标准，即：①情绪稳定，有安全感。②认识自我，接纳自我。③自我学习，独立生活。④人际关系和谐良好。⑤角色功能协调统一。⑥适应环境，应对挫折。据悉，这是中国心理卫生协会经过文献调研、专家调查与讨论，

简介：目的研究真核细胞中细胞分裂周期蛋6（CDC6）与颅咽管瘤（CP）的相关性，探讨其对CP细胞的生物学作用。方法免疫组化法检测CP标本中CDC6的表达情况，并合成CDC6小的干涉核糖核酸（siRNA）片段，转染CP细胞。用四甲基偶氮唑盐（MTT）法检测干扰CDC6表达后CP细胞生长水平，绘制细胞生长曲线。同时应用流式细胞仪（FCM）检测细胞周期。结果免疫组化结果显示在正常脑组织与CP组织中CDC6表达存在明显差异，而生长曲线显示下调CDC6的表达之后，CP细胞增殖变慢，曲线变缓，与未转染的细胞相比细胞生长被明显抑制。流式细胞仪分析细胞周期发现细胞的脱氧核糖核酸合成后期（G2）明显缩短，提前进入合成（M）期。结论CDC6在CP细胞中表达量较正常细胞高，而且参与了CP细胞的增殖调控。

简介：Parkinson’sdisease(PD)isanage-relatedneurodegenerativedisordercharacterizedbytypicalmotorsignsandsymptomsthatareduetodopamine(DA)depletioninthebasalganglia.ThetreatmentofPDissymptomatic,andaimsatreplacingthelostDAinputusingeitherL-DOPAorDAagonists.ThecausesofPDareunknownin

简介：SubthalamicnucleusdeepbrainstimulationhasbecomeastandardneurosurgicaltherapyforadvancedParkinson’sdisease.Subthalamicnucleusdeepbrainstimulationcandramaticallyimprovethemotorsymptomsofcarefullyselectedpatientswiththisdisease.Surprisingly,somespecificdimensionsofqualityoflife,"psychological"aspectsandsocialadjustmentdonotalwaysimprove,andtheycouldsometimesbeevenworse.Patientsandtheirfamiliesshouldfullyunderstandthatsubthalamicnucleusdeepbrainstimulationcanalterthemotorstatusandtimeisneededtoreadapttotheirnewpostoperativestateandlifestyles.Thispaperreviewstheliteraturesregardingeffectsofbilateralsubthalamicnucleusdeepbrainstimulationonsocialadjustment,qualityoflifeandcopingstrategiesinpatientswithParkinson’sdisease.ThefindingsmayhelptounderstandthepsychosocialmaladjustmentandpoorimprovementinqualityoflifeinsomeParkinson’sdiseasepatients.

简介：Genisteiniseffectiveagainstamyloid-βtoxicity,buttheunderlyingmechanismsareunclear.Wehypothesizedthatgenisteinmayprotectneuronsbyinhibitingthemitochondrialapoptoticpathway,andtherebyplayaroleinthepreventionofAlzheimer'sdisease.AratmodelofAlzheimer'sdiseasewasestablishedbyintraperitonealinjectionofD-galactoseandintracerebralinjectionofamyloid-βpeptide(25–35).Inthegenisteintreatmentgroups,a7-daypretreatmentwithgenistein(10,30,90mg/kg)wasgivenpriortoestablishingAlzheimer'sdiseasemodel,for49consecutivedays.Terminaldeoxyribonucleotidyltransferase-mediateddUTPnickendlabelingassaydemonstratedareductioninapoptosisinthehippocampusofratstreatedwithgenistein.Westernblotanalysisshowedthatexpressionlevelsofcapase-3,Baxandcytochromecweredecreasedcomparedwiththemodelgroup.Furthermore,immunohistochemicalstainingrevealedreductionsincytochromecandBaximmunoreactivityintheserats.MorriswatermazerevealedasubstantialshorteningofescapelatencybygenisteininAlzheimer'sdiseaserats.Thesefindingssuggestthatgenisteindecreasesneuronallossinthehippocampus,andimproveslearningandmemoryability.Theneuroprotectiveeffectsofgenisteinareassociatedwiththeinhibitionofthemitochondrialapoptoticpathway,asshownbyitsabilitytoreducelevelsofcaspase-3,Baxandcytochromec.

简介：目的通过随机分组研究急性创伤昏迷大鼠中脑钙蛋白酶Ⅱ（CalpainⅡ）及电压门控钠通道亚型（Nach6）的早期表达变化。方法雄性sD大鼠12只，随机分为两组：假手术对照组（n=6）；急性创伤昏迷组（n=6）。建立急性创伤昏迷大鼠模型，1h后通过实时定量PCR法检测中脑钙蛋白酶Ⅱ及电压门控钠通道亚型（Nach6）变化。结果逆转录酶-多聚酶链反应（RT-PCR）法结果显示钙蛋白酶Ⅱ在创伤昏迷组的中脑表达相对含量增加（P〈0．01），电压门控钠通道亚型（Nach6）在创伤昏迷组的中脑组织表达相对含量增加（P〈0．05）。结论急性创伤昏迷早期钙蛋白酶Ⅱ激活、钠离子内流导致中脑神经细胞及胶质细胞损伤可能为急性创伤昏迷早期分子生物学机制之一。

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简介：Labbe＇s静脉是连接大脑中浅静脉和横窦之间的吻合静脉,又称下吻合静脉,在脑的静脉回流中起着重要的作用[1,2]。重型颅脑损伤合并Labbe＇s静脉损伤时常可导致严重后果,由于颅脑损伤的复杂性,如同时合并Labbe＇s静脉损伤使治疗更为困难。本文通过对榆林市北方医院自2006年3月至2012年2月采用手术治疗的36例重型颅脑损伤同时合并Labbe＇s静脉损伤病例分析，探讨最佳的治疗方案，现报告如下。

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