Altered Regulation of Akt Signaling with Murine Cerebral Malaria, Effects on Long-Term Neuro-Cognitive Function, Restoration with Lithium Treatment 英文参考文献.docVIP
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Altered Regulation of Akt Signaling with Murine Cerebral Malaria, Effects on Long-Term Neuro-Cognitive Function, Restoration with Lithium Treatment 英文参考文献
AlteredRegulationofAktSignalingwithMurineCerebral
Malaria,EffectsonLong-TermNeuro-CognitiveFunction,
RestorationwithLithiumTreatment
MinxianDai1,2.,BrandiFreeman2.,HenryJ.Shikani2.,FernandoPereiraBruno2,J.EliasCollado3,
RolandoMacias4,SandraE.Reznik1,PeterDavies2,5,6,DavidConoverSpray5,7 ,Herbert
BernardTanowitz2,7,LouisMartinWeiss2,7,MahaliaSabrinaDesruisseaux2,7
*
1Department of Pharmaceutical Sciences, College of Pharmacy and Allied Health Professions, St John’s University, Queens, New York, United States of America,
2DepartmentofPathology,AlbertEinsteinCollegeofMedicine,Bronx,NewYork,UnitedStatesofAmerica,3PontificiaUniversidadCatolicaMadreyMaestra,Santiago,
DominicanRepublic,4MeharryMedicalCollege,Nashville,Tennessee,UnitedStatesofAmerica,5TheDominickP.PurpuraDepartmentofNeuroscience,AlbertEinstein
CollegeofMedicine,Bronx,NewYork,UnitedStatesofAmerica,6Litwin-ZuckerCenterfortheStudyofAlzheimer’sDiseaseandMemoryDisorders,FeinsteinInstitutefor
Medical Research, Manhasset,New York, United States ofAmerica, 7Department ofMedicine,Albert Einstein CollegeofMedicine,Bronx, New York, United States of
America
Abstract
Neurologicalandcognitiveimpairmentpersistinmorethan20%ofcerebralmalaria(CM)patientslongaftersuccessfulanti-
parasitictreatment.Werecentlyreportedthatlongtermmemoryandmotorcoordinationdeficitsarealsopresentinour
experimental cerebral malaria model (ECM). We also documented, in a murine model, a lack of obvious pathology or
inflammation after parasite elimination, suggesting that the long-term negative neurological outcomes result from
potentially reversible biochemical and physiological changes in brains of ECM mice, subsequent to acute ischemic and
inflammatoryprocesses.Here,wedemonstrateforthefirsttimethatacuteECMresultsinsignificantlyreducedactivationof
protein kinase B (PKB or Akt) leading to decreased Akt phosphorylation and inhibition of the glycogen kinase synthase
(GSK3b)inthebrainsofmiceinfectedwithPlasmodiumbergheiANKA(PbA)comparedtouninfectedco
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