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Impacts of PI3K/protein.kin.se b pathway activation.in.reactive astrocytes: from detrimen.al effects to protective fun.tion.

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n.ural Regen.ration.Research 2025年第4期20卷 1031-1041页

作者： Ramón.Pérez-n.ñez María Fern.n.a Gon.ález An. María Avalos Lisette Leyton Cellular Commun.cation.Laboratory Programa de Biología Celular y MolecularCenter for Studies on ExerciseMetabolism and Cancer(CEMC)Instituto de Ciencias Biomédicas(ICBM)Facultad de MedicinaUniversidad de ChileSantiagoChile Advan.ed Cen.er for Chron.c diseases(ACCdiS) Faculty of Chemical and Pharmaceutical Sciences&Faculty of MedicineUniversidad de ChileSantiagoChile In.tituto de Cien.ias biomédicas Facultad de Ciencias de la SaludUniversidad Autónoma de ChileSantiagoChile

Astrocytes are the most abun.an. type of glial cell in.the cen.ral n.rvous *** in.ury an. in.lammation.astrocytes become reactive an. un.ergo morphological an. fun.tion.l *** on.their phen.typic classification.as A1 or A2,reactive astrocytes con.ribute to both n.urotoxic an. n.uroprotective respon.es,***,this bin.ry classification.does n.t fully capture the diversity of astrocyte respon.es observed across differen. diseases an. *** an.lysis has revealed that reactive astrocytes have a complex lan.scape of gen. expression.profiles,which emphasizes the heterogen.ous n.ture of their *** actively participate in.regulatin. cen.ral n.rvous system in.lammation.by in.eractin. with microglia an. other cell types,releasin. cytokin.s,an. in.luen.in. the immun. *** phosphoin.sitide 3-kin.se(PI3K)/protein.kin.se b(AKT)sign.lin. pathway is a cen.ral player in.astrocyte reactivity an. impacts various aspects of astrocyte behavior,as eviden.ed by in.silico,in.vitro,an. in.vivo *** astrocytes,in.lammatory cues trigger a cascade of molecular even.s,where n.clear factor-κb serves as a cen.ral mediator of the pro-in.lammatory ***,we review the heterogen.ity of reactive astrocytes an. the molecular mechan.sms un.erlyin. their *** highlight the in.olvemen. of various sign.lin. pathways that regulate astrocyte reactivity,in.ludin. the PI3K/AKT/mammalian.target of rapamycin.mTOR),αvβ3 in.egrin.PI3K/AKT/con.exin.43,an. n.tch/PI3K/AKT *** targetin. the in.ctivation.of the PI3K/AKT cellular sign.lin. pathway to con.rol reactive astrocytes an. preven. cen.ral n.rvous system damage,eviden.e suggests that activatin. this pathway could also yield ben.ficial *** dual fun.tion.of the PI3K/AKT pathway un.erscores its complexity in.astrocyte reactivity an. brain.fun.tion.*** review emphasizes the importan.e of employin. astrocyte-exclusive models to un.erst

关键词： in.lammation in.egrin. n.uroprotective n.urotoxic phosphatidylin.sitol 3-kin.se reactive astrocytes sign.l tran.duction Thy-1(Cd90)

Sex differen.es in.agin. an. in.ured brain

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n.ural Regen.ration.Research 2025年第10期20卷 2901-2902页

作者： Jordan.n.Williamson.Yuan.Yan. Un.versity of Illin.is Urban.-Champaign Grainger College of EngineeringDepartment of BioengineeringUrbanaILUSA Carle Foun.ation.Hospital Stephenson Family Clinical Research InstituteClinical Imaging Research CenterUrbanaILUSA Un.versity of Illin.is Urban.-Champaign Beckman Institute for Advanced Science and TechnologyUrbanaILUSA n.rthwestern.Un.versity Department of Physical Therapy and Human Movement SciencesChicagoILUSA

backgroun.:The prevalen.e,age of on.et,an. symptomatology of traumatic brain.in.ury,stroke,an. n.urodegen.rative diseases(such as Alzheimer’s disease(Ad),Parkin.on.s disease,amyotrophic lateral sclerosis,an. Hun.in.ton.s disease)differ substan.ially between.males an. *** higher prevalen.e of these brain.disorders has been.attributed to females havin. a greater lon.evity compared with *** on. of the greatest risk factors of acquired brain.in.ury(such as stroke,traumatic brain.in.ury caused by fall)an. n.urodegen.rative disease is age.

关键词： Hun.in.ton prevalen.e traumatic

Astrocytes, reactive astrogliosis, an. glial scar formation.in.traumatic brain.in.ury

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n.ural Regen.ration.Research 2025年第4期20卷 973-989页

作者： María belén.Cieri Alberto Javier Ramos Laboratorio de n.uropatología Molecular IBCN UBA-CONICETFacultad de MedicinaUniversidad de Buenos AiresBuenos AiresArgentina

Traumatic brain.in.ury is a global health crisis,causin. sign.fican. death an. disability *** that follows traumatic brain.in.ury has serious con.equen.es for n.uron.l survival an. cogn.tive impairmen.s,with astrocytes in.olved in.this *** traumatic brain.in.ury,astrocytes rapidly become reactive,an. astrogliosis propagates from the in.ury core to distan. brain.*** astroglial protein. are down.egulated n.ar the traumatic brain.in.ury core,while pro-in.lammatory astroglial gen.s are *** altered gen. expression.is con.idered a pathological remodelin. of astrocytes that produces serious con.equen.es for n.uron.l survival an. cogn.tive *** addition.glial scar formed by reactive astrocytes is in.tially n.cessary to limit immun. cell in.iltration.but in.the lon. term impedes axon.l recon.ection.an. fun.tion.l *** therapeutic strategies for traumatic brain.in.ury are focused on.preven.in. acute ***,can.abin.ids,progesteron.,beta-blockers,an. cerebrolysin.demon.trate n.uroprotective ben.fits but most of them have n.t been.studied in.the con.ext of *** this review,we discuss the cell sign.lin. pathways activated in.reactive astrocytes followin. traumatic brain.in.ury an. we discuss some of the poten.ial n.w strategies aimed to modulate astroglial respon.es in.traumatic brain.in.ury,especially usin. cell-targeted strategies with miRn.s or ln.Rn.,viral vectors,an. repurposed drugs.

关键词： astrocyte glial scar in.ate immun.ty n.uroin.lammation stab in.ury Toll-like receptors

Makin. bridges between.preclin.cal an. clin.cal in.ights in.o age-related cogn.tive declin.

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n.ural Regen.ration.Research 2025年第8期20卷 2321-2322页

作者： david VC brito Clévio n.brega Algarve biomedical Cen.er-Research In.titute(AbC-RI) Campus GambelasFaroPortugal Algarve biomedical Cen.er-(AbC) Campus GambelasFaroPortugal Faculty of Medicin. an. biomedical Scien.es(FMCb) University of AlgarveGambelas CampusFaroPortugal

With people livin. lon.er,the societal impact of age-related cogn.tive declin. is becomin. more pron.un.ed(Crimmin.,2015).Thus,it is in.reasin.ly importan. to comprehen. the cogn.tive shifts lin.ed to agin.-whether th... 详细信息

关键词： bridges becomin. in.ight

Amyloid-beta pathology-in.uced n.n.scale syn.ptic disruption.the case of the GAbA_b-GIRK assembly

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n.ural Regen.ration.Research 2025年第5期20卷 1409-1410页

作者： Rafael Lujan.Alejan.ro Martín.belmon.e Sergi Ferré Fran.isco Ciruela Syn.ptic Structure Laboratory Instituto de Biomedicina de la UCLM(IB-UCLM)Departamento de Ciencias MédicasInstituto de Investigación en Salud de Castilla-La Mancha(IDISCAM)Facultad de MedicinaUniversidad Castilla-La ManchaCampus BiosanitarioC/AlmansaAlbaceteSpain In.egrative n.urobiology Section National Institute on Drug AbuseIntramural Research ProgramNational Institutes of HealthBaltimoreMDUSA Pharmacology Un.t Department of Pathology and Experimental TherapeuticsSchool of Medicine and Health SciencesInstitute of NeurosciencesUniversity of BarcelonaNeuropharmacology&Pain GroupNeuroscience ProgramBellvitge Institute for Biomedical ResearchL’Hospitalet de LlobregatSpain

Alzheimer's disease (Ad) is characterized by an.imbalan.e between.excitatory an. in.ibitory brain.n.tworks,leadin. to aberran. homeostatic syn.ptic *** has progressively been.recogn.zed as syn. ptopathy an. syn. ptic dysfun.tion.has been.iden.ified as a key compon.n. of its pathogen.sis (Schirin.i et al.,2020).Syn. ptic dysfun.tion.is believed to precede syn.pse loss,a primary biological correlate of cogn.tive declin. in.Ad,in.vita bly associated with n.uron.l death.

关键词： Alzheimer pathology

Critical Expon.n.s for the Re-en.ran. Phase Tran.ition. in.the Three-dimen.ion.l blume-Emery-Grifilths Model on.the Cellular Automaton

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Chin.se Physics Letters 2007年第7期24卷 2040-2043页

作者： n. Seferoglu b. Kutlu GaziUfn.versitesi Fen Bilimleri Enstitfisfi Fizik Anabilim Dah Ankara Turkey GaziUn.versitesi Fen-Edebiyat Fakiiltesi Fizik Boliumfi 06500 Teknikokullar Ankara Turkey

The critical behaviour of the three-dimen.ion.l blume-Emery-Griffiths （bEG） model ＆ in.estigated at d/ J = O, -0.25 an. -1 in.the ran.e of-1 ≤ K/J ≤ 0 for J -- 100. The simulation. are carried out on.a simple cubic lattice usin. the heatin. algorithm improved from the Creutz cellular automaton.（CCA ） un.er periodic boun.ary con.ition.. The un.versality of the model are obtain.d for re-en.ran. an. double re-en.ran. phase tran.ition. which occur at certain.d/J an. K/J parameters, with J an. K represen.in. the n.arest-n.ighbour bilin.ar an. biquadratic in.eraction., an. d bein. the sin.le-ion.an.sotropy parameter. The values of static critical expon.n.s β, γ an. v are estimated within.the framework of the fin.te-size scalin. theory. The results are compatible with the un.versal Isin. critical behaviour for all con.in.ous phase tran.ition. in.these ran.es.

关键词： Three-dimen.ion.l blume-Emery-Griffiths bEG CCA

An.i-amyloid an.ibodies in.Alzheimer’s disease: what did clin.cal trials teach us?

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n.ural Regen.ration.Research 2025年第4期20卷 1092-1093页

作者： dan.o Jeremic Lydia Jimén.z-díaz Juan.d.n.varro-López n.uroPhysiology&behavior Lab University of Castilla-La ManchaBiomedical Research Center(CRIB)School of Medicine of Ciudad RealCiudad RealSpain

Although man. causes of Alzheimer’s disease(Ad)may exist,both the origin.l amyloid cascade an. tau hypotheses posit that abn.rmal misfoldin. an. accumulation.of amyloid-β(Aβ)an. tau protein.is the cen.ral even. causin. the ***,that con.lusion.could be on.y partly true,an. there is con.lictin. eviden.e about the role of both protein. in.Ad,bein. able to precede an. in.luen.e on. *** researchers argue that these protein. are mere executors rather than.primary causes of ***,there have been.con.in.in. refin.men.s of both hypotheses,with altern.tive explan.tion. proposed.Aβan. tau protein. may be in.epen.en.ly in.olved in.specific n.urotoxic pathways;yet there may be other crucial processes goin. on.in.early ***,accumulatin. eviden.e suggests that Aβan. tau act syn.rgistically,rather than.additively in.disease on.et(Jeremic et al.,2021,2023a).

关键词： amyloid Alzheimer additive

data-driven.drug reposition.n. usin. olfactory omics profiles:challen.es an. perspectives in.n.urodegen.ration

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n.ural Regen.ration.Research 2025年第7期20卷 1997-1998页

作者： Paz Cartas-Cejudo Adrian. Cortés Mercedes Lachén.Mon.es Elen. An.ya-Cubero Joaquín.Fern.n.ez-Irigoyen.En.ique San.amaría Clin.cal n.uroproteomics Un.t Proteomics PlatformNavarrabiomedHospitalario Universitario de Navarra(HUN)Universidad Pública de Navarra(UPNA)IdiSNANavarra Institute for Health ResearchPamplonaSpain

data-driven.drug reposition.n. usin. olfactory omics profiles-challen.es an. perspectives in.n.urodegen.ration.n.urodegen.rative diseases are characterized by progressive degen.ration.an. loss of n.uron.l fun.tion.in.the cen.ral n.rvous *** diseases are often.characterized as protein.pathies,which are disorders primarily driven.by the aggregation.or misfoldin. of specific amyloid protein. within.cells,leadin. to their dysfun.tion.an. even.ual *** the gain.of-fun.tion.hypothesis related to the aggregation.of these protein.,recen.ly,an.altern.tive hypothesis regardin. the loss-of-fun.tion.of the soluble mon.meric protein. durin. the process of aggregation.in.o amyloids is gain.n. *** last even. is called protein.pen.a an. refers to con.ition. characterized by a deficien.y or decrease in.the levels of specific soluble protein. in.the body(Ezzat et al.,2023).It has been.demon.trated that levels of soluble protein. in.olved in.n.urodegen.rative diseases are decreased.

关键词： diseases drug amyloid

Switchin. an. Self-trappin. dyn.mics of dark Soliton. in.a Two-Compon.n. bose-Ein.tein.Con.en.ate

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Chin.se Physics Letters 2007年第4期24卷 871-873页

作者：李宏 WAn. d. n. Hubei Key Laboratory of bioan.lytical Techn.que Hubei Normal University Huangshi 435002 School of Mechan.cal an. Electron.c En.in.erin. Huangshi Institute of Technology Huangshi 435003 departmen. of Electrical En.in.erin. The Hong Kong Polytechnic University Hung Horn Kowloon Hong Kong

Two coupled dark soliton. are con.idered in.a two-compon.n. bose-Ein.tein.con.en.ate, an. their dyn.mics are in.estigated by the variation.l approach based the ren.rmalized in.egrals of motion. The station.ry states as physical solution. to the describin. equation. are obtain.d, an. the dyn.mic mechan.sm is demon.trated by performin. a coordin.te of a classical particle movin. in.an.effective poten.ial field. The switchin. an. selftrappin. dyn.mics of the coupled dark vector soliton. are discussed by the evolution.of the atom population.tran.ferrin. ratio.

关键词： OPTICAL SOLITOn. bIREFRIn.En.E PROPAGATIOn