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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：Objective:Toobservetheclinicalefficacyofacupuncture-moxibustionintreatingAlzheimer’sdisease(AD).Methods:Forty-eighteligibleADpatientswereenrolledtoreceiveacupunctureplusherb-partitionedmoxibustion.Mini-mentalstateexamination(MMSE)wasadoptedforevaluationbeforeandafterintervention,andthetherapeuticefficacywasobserved.Results:Afterintervention,theMMSEscorechangedsignificantly(P<0.01),andthetotaleffectiveratewas83.3%.Conclusion:Acupuncture-moxibustioncansignificantlyimprovethecognitivefunctionofADpatients,beneficialtothegeneralpromotionofthequalityoflife.

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：MemorylossandmentalconfusionarethefirstovertsignsofAlzheimer'sDisease,anincurableandfatalbrainailment.Butscientistsarestartingtofindevidenceofthediseaselongbeforesymptomsappear.

简介：AbstractTraumatic brain injury (TBI), a growing public health problem, is a leading cause of death and disability worldwide, although its prevention measures and clinical cares are substantially improved. Increasing evidence shows that TBI may increase the risk of mood disorders and neurodegenerative diseases, including Alzheimer's disease (AD). However, the complex relationship between TBI and AD remains elusive. Metabolic dysfunction has been the common pathology in both TBI and AD. On the one hand, TBI perturbs the glucose metabolism of the brain, and causes energy crisis and subsequent hyperglycolysis. On the other hand, glucose deprivation promotes amyloidogenesis via β-site APP cleaving enzyme-1 dependent mechanism, and triggers tau pathology and synaptic function. Recent findings suggest that TBI might facilitate Alzheimer's pathogenesis by altering metabolism, which provides clues to metabolic link between TBI and AD. In this review, we will explore how TBI-induced metabolic changes contribute to the development of AD.

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简介：AIM:ToexaminetheprotectiveeffectsofGinkgobilobaextract(GbE)onthelearningandmemoryintheAlzheimerdisease(AD)modelinducedbyaluminumsaltinrats,andtoexaminethepotentialmechanisms.METHODS.TheADmodelofratswasinducedbyadministrationanddrinkingofaluminumchloridesolution.Theabilitiesofspatialleafingand

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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.

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简介：采取评估石杉碱甲片治疗阿尔采木病的疗效及其安全性。采用多中心、前瞻性、双盲、平行、空白对照和随机方法，给8例阿尔采木病一日两次口服石杉碱甲片4片（每片含50微克），并给8例阿尔采木病一日两次口服安慰剂4片，共8wk，所有病人都用韦氏智力量表、简易精神状态量表、长谷川痴呆量表、日常生活能力量表、副反应量表和其它实验室检查。结果发现石杉碱甲片服用者记忆、认知和行为能力均有改善，疗效明显优于对照组，而两组均无严重副反应。我们认为石杉碱甲片是治疗阿尔采木病的一个有前景的药物。

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简介：Alzheimer’sdisease(AD)isoneofthemostdevastatingdiseasesaffectingthelifeandhealthofagingpopulation.TwohallmarksofADaresenileplaquesandneurofibrillarytangles,andADiswellknownforthemassivelossofneuronsandimpairedcognitivefunctionsespeciallymemoryloss.Despiteextensivesearchforeffectivetreatment,available