grant

Deciphering the role of CD44 astrocytes in Alzheimer's disease

Organization COLUMBIA UNIVERSITY HEALTH SCIENCESLocation NEW YORK, UNITED STATESPosted 15 Sept 2025Deadline 31 Aug 2029
NIHUS FederalResearch GrantFY2025AD dementiaAD modelAD pathologyAbeta clearanceActive Follow-upAddressAdhesion MoleculeAffectAge of OnsetAlzheimer Type DementiaAlzheimer beta-ProteinAlzheimer disease dementiaAlzheimer sclerosisAlzheimer syndromeAlzheimer'sAlzheimer's Amyloid beta-ProteinAlzheimer's DiseaseAlzheimer's amyloidAlzheimer's brainAlzheimer's disease brainAlzheimer's disease modelAlzheimer's disease pathologyAlzheimer's disease patientAlzheimer's disease therapeuticAlzheimer's disease therapyAlzheimer's pathologyAlzheimer's patientAlzheimer's therapeuticAlzheimer's therapyAlzheimers DementiaAmyloidAmyloid (Aβ) plaquesAmyloid Alzheimer's Dementia Amyloid ProteinAmyloid Beta-PeptideAmyloid PlaquesAmyloid Protein A4Amyloid SubstanceAmyloid beta-ProteinAmyloid βAmyloid β clearanceAmyloid β-PeptideAmyloid β-ProteinAstrocytesAstrocytusAstrogliaAutopsyAβ clearanceBehavioral AssayBindingBiologyBody TissuesBrainBrain Nervous SystemCD44CD44 geneCancersCause of DeathCell Adhesion Molecule GeneCell Adhesion MoleculesCell Communication and SignalingCell Growth in NumberCell MultiplicationCell NucleusCell ProliferationCell SignalingCell modelCell-Extracellular MatrixCellular ProliferationCellular modelCharacteristicsCo-cultureCocultivationCocultureCoculture TechniquesCognitive DisturbanceCognitive ImpairmentCognitive declineCognitive function abnormalDataDegenerative Neurologic DisordersDiseaseDisease ProgressionDisorderDisturbance in cognitionDysfunctionECMElderlyEncephalonEventExperimental DesignsExtracellular MatrixFoundationsFunctional disorderGene ExpressionGene TranscriptionGenesGeneticGenetic TranscriptionHumanHypertrophyHypoxiaHypoxicImmunofluorescenceImmunofluorescence ImmunologicImpaired cognitionImpairmentIn VitroInduced pluripotent stem cell derived neuronsInflammationInflammatoryIntracellular Communication and SignalingInvestigationJ20J20 mouseKO miceKnock-out MiceKnockout MiceLiteratureMDU3Malignant NeoplasmsMalignant TumorMediatingMiceMice MammalsModelingModern ManMolecularMolecular InteractionMorphologyMurineMusNerve CellsNerve DegenerationNerve UnitNervous System Degenerative DiseasesNeural CellNeural Degenerative DiseasesNeural degenerative DisordersNeuritic PlaquesNeurocyteNeurodegenerative DiseasesNeurodegenerative DisordersNeurofibrillary TanglesNeurologic Degenerative ConditionsNeuron DegenerationNeuron from iPSCNeuron from induced pluripotent stem cellsNeuronal DysfunctionNeuronsNucleusNull MouseOutcomeOxygen DeficiencyPaperPathogenesisPathologyPatientsPgp1PhenotypePhysiopathologyPlayPopulationPrimary Senile Degenerative DementiaProcessProliferatingProtein CleavageProteolysisRNA ExpressionRNA SeqRNA sequencingRNAseqReceptor ProteinRoleSeizuresSenile PlaquesSignal PathwaySignal TransductionSignal Transduction SystemsSignalingSingle-Nucleus SequencingTestingTimeTissuesTranscriptionUpregulationViralVirusa beta peptidea-beta peptide clearanceabetaabeta peptide clearanceactive followupadvanced agealzheimer modelamyloid betaamyloid beta clearanceamyloid beta peptide clearanceamyloid beta plaqueamyloid-b plaqueamyloid-b proteinastrocytic gliaastrogliosisaβ plaquesbeta amyloid associated pathologybeta amyloid fibrilbeta amyloid pathologybiological signal transductioncell adhesion proteincell typecognitive dysfunctioncognitive losscored plaquedegenerative diseases of motor and sensory neuronsdegenerative neurological diseasesdiffuse plaquedisease phenotypeexperimentexperimental researchexperimental studyexperimentsextracellularfollow upfollow-upfollowed upfollowupgeriatriciPSiPS neuronsiPSCiPSC derived-neuronsiPSCsimproved outcomein vivoin vivo Modelinduced pluripotent cellinduced pluripotent stem cellinduced pluripotent stem cell neuronsinducible pluripotent cellinducible pluripotent stem cellknock-downknockdownmalignancymouse modelmurine modelnecropsyneoplasm/cancernerve cell deathnerve cell lossneural degenerationneural dysfunctionneural inflammationneurodegenerationneurodegenerativeneurodegenerative illnessneurofibrillary degenerationneurofibrillary lesionneurofibrillary pathologyneuroinflammationneuroinflammatoryneurological degenerationneuron cell deathneuron cell lossneuron deathneuron lossneuronalneuronal cell deathneuronal cell lossneuronal deathneuronal degenerationneuronal lossneurons derived from induced pluripotent stem cellsneurons differentiated from induced pluripotent stem cellsneuropathologicneuropathologicalneuropathologyneuroprotectionneuroprotectivenew drug targetnew druggable targetnew pharmacotherapy targetnew therapeutic targetnew therapy targetnovelnovel drug targetnovel druggable targetnovel pharmacotherapy targetnovel therapeutic targetnovel therapy targetoverexpressoverexpressionpathophysiologypatient living with Alzheimer's diseasepatient suffering from Alzheimer's diseasepatient with Alzheimer'spatient with Alzheimer's diseasepharmacologicpostmortemprimary degenerative dementiareceptorresponsesNuc-Seqsenile dementia of the Alzheimer typesenior citizensingle nucleus RNA-sequencingsingle nucleus seqsingle-nucleus RNA-seqsnRNA sequencingsnRNA-seqsocial rolesoluble amyloid precursor proteinspatial RNA sequencingspatial gene expression analysisspatial gene expression profilingspatial resolved transcriptome sequencingspatial transcriptome analysisspatial transcriptome profilingspatial transcriptome sequencingspatial transcriptomicsspatially resolved transcriptomicsspatio transcriptomicssynapse functionsynaptic functiontangletargeted drug therapytargeted drug treatmentstargeted therapeutictargeted therapeutic agentstargeted therapytargeted treatmenttherapeutic targettranscriptome sequencingtranscriptomic sequencingtranscriptomicsβ-amyloid pathology
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Description preview

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder, characterized by
neurofibrillary tangles, β-amyloid (Aβ) plaques, and astrocyte dysfunction. Astrocytes play critical roles

in AD pathophysiology, including Aβ clearance and modulation of neuroinflammation. Thus, astrocytes

are essential in the pathogenesis of AD, yet the…

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