grant
Nicotinamide Adenine Dinucleotide Augmentation to Prevent or Reverse the Progression of Alzheimer's Disease in People with Down Syndrome
Organization BRIGHAM AND WOMEN'S HOSPITALLocation BOSTON, UNITED STATESPosted 15 Sept 2025Deadline 31 Aug 2028
NIHUS FederalResearch GrantFY20252(lH)-pyridinone2-hydroxypyridine2-pyridinone2-pyridone21+ years old3-Pyridinecarboxamide3-Pyridinecarboxylic AcidAD dementiaAD modelAD pathologyAPP processingAbeta synthesisAcidsAdultAdult HumanAffectAgeAlzheimer Type DementiaAlzheimer beta-ProteinAlzheimer disease dementiaAlzheimer sclerosisAlzheimer syndromeAlzheimer'sAlzheimer's Amyloid beta-ProteinAlzheimer's DiseaseAlzheimer's amyloidAlzheimer's biomarkerAlzheimer's disease biological markerAlzheimer's disease modelAlzheimer's disease pathologyAlzheimer's disease patientAlzheimer's pathologyAlzheimer's patientAlzheimers DementiaAlzheimer’s biological markerAlzheimer’s disease biomarkerAmentiaAmyloid A4 Protein PrecursorAmyloid Alzheimer's Dementia Amyloid ProteinAmyloid Beta-PeptideAmyloid Protein A4Amyloid Protein PrecursorAmyloid beta-ProteinAmyloid beta-Protein PrecursorAmyloid βAmyloid β oligomerAmyloid β productionAmyloid β synthesisAmyloid β toxicityAmyloid β-PeptideAmyloid β-ProteinAmyloid β-Protein PrecursorAttenuatedAβAβ productionAβ synthesisAβOBioenergeticsBiogenesisBiological MarkersBloodBlood PlasmaBlood PressureBlood Reticuloendothelial SystemBody TissuesBrainBrain Nervous SystemCerebrospinal FluidChemistryChromosome 21ClinicalClottingCoagulationCoagulation ProcessDementiaDevelopmentDiagnostic FindingsDihydronicotinamide Adenine DinucleotideDiphosphopyridine NucleotideDoseDown SyndromeDrug KineticsDrug TargetingDrugsECGEKGElectrocardiogramElectrocardiographyEncephalonExhibitsFamilyGene Copy NumberGene DosageGene ProteinsHumanImageIndividuals with down syndromeIntellectual disabilityIntellectual functioning disabilityIntellectual limitationLaboratoriesLangdon Down syndromeLifeMR SpectroscopyMagnetic Resonance SpectroscopyMaximal Tolerated DoseMaximally Tolerated DoseMaximum Tolerated DoseMeasurementMeasuresMediatingMedicationMethodsMiceMice MammalsMitochondriaModern ManMongolismMorbidityMorbidity - disease rateMurineMusMuscleMuscle TissueNadideNerve DegenerationNeuron DegenerationNeuropsychologiesNeuropsychologyNiacinNiacinamideNicotinamideNicotinamide MononucleotideNicotinamide adenine dinucleotideNicotinamide-Adenine DinucleotideNicotinamidumNicotinic AcidsNicotinic acid amideNicotylamideOralOral AdministrationOral Drug AdministrationOrigin of LifeOutcomeOxidative PhosphorylationOxidative Phosphorylation PathwayPK/PDParalysis AgitansParkinsonParkinson DiseasePathway interactionsPellagra-Preventing FactorPeptidesPerformancePersonsPharmaceutical AgentPharmaceutical PreparationsPharmaceuticalsPharmacodynamicsPharmacokineticsPharmacologic SubstancePharmacological SubstancePhasePhase I StudyPhysical FunctionPlacebo ControlPlasmaPlasma SerumPopulationPre-Clinical ModelPreclinical ModelsPreventionPrimary ParkinsonismPrimary Senile Degenerative DementiaProtein Gene ProductsProteinsPyridinonesPyridonesRandomization trialRandomizedRecommendationRepressionReticuloendothelial System, Serum, PlasmaRunningSafetySigns and SymptomsStructureTauopathiesTestingTherapeuticTimeTissuesTrisomy 21UrineVitamin B 3Vitamin B3Vitamin PPa beta peptideabetaabeta accumulationabeta aggregationabeta oligomerabeta productionabeta toxicityadulthoodadverse event monitoringagesalpha secretasealzheimer modelamyloid betaamyloid beta accumulationamyloid beta aggregationamyloid beta oligomeramyloid beta productionamyloid beta synthesisamyloid beta toxicityamyloid pathologyamyloid precursor proteinamyloid precursor protein processingamyloid β accumulationamyloid β aggregationamyloid-b proteinattenuateattenuatesaβ accumulationaβ aggregationaβ oligomeraβ toxicitybeta amyloid fibrilbio-markersbiologic markerbiological adaptation to stressbiomarkerblood lipidcerebral spinal fluidchromosome 21 trisomychromosome 21 trisomy syndromecognitive functioncongenital acromicria syndromedetermine efficacydevelopmentaldown syndrome individualsdown syndrome patientsdrug candidatedrug/agentefficacy analysisefficacy assessmentefficacy determinationefficacy evaluationefficacy examinationefficacy trialevaluate efficacyexamine efficacyexperienceimagingimprovedinnovateinnovationinnovativeintellectual and developmental disabilityintraoral drug deliverylimited intellectual functioningmitochondrialmorbus Downmortalitymouse modelmurine modelmuscularnerve cell deathnerve cell lossneural degenerationneural inflammationneurodegenerationneurodegenerativeneuroinflammationneuroinflammatoryneurological degenerationneuron cell deathneuron cell lossneuron deathneuron lossneuron regenerationneuron toxicityneuronal cell deathneuronal cell lossneuronal deathneuronal degenerationneuronal lossneuronal regenerationneuronal toxicityneuropathologicneuropathologic tauneuropathologicalneuropathological tauneuropathologyneuropsychologicneurotoxicitynicotinamide ribonucleosidenicotinamide ribosenicotinamide ribosidenicotinamide-beta-ribosideoAβoligomeric amyloid betaoligomeric amyloid-βp-taup-τpathwaypatient living with Alzheimer's diseasepatient suffering from Alzheimer's diseasepatient with Alzheimer'spatient with Alzheimer's diseasepatients with down syndromepeople with down syndromepharmaceuticalpharmacokinetics and pharmacodynamicsphase 1 studyphase 1 trialphase I trialphospho-tauphospho-τphosphorylated tauplacebo controlledpost-translational modification of tauposttranslational modification of taupreventpreventingprimary degenerative dementiaproteotoxicproteotoxicitypseudohypertrophic progressive muscular dystrophyrandomisationrandomizationrandomized trialrandomly assignedreaction; crisisresponsesenile dementia of the Alzheimer typesoluble amyloid precursor proteinspinal fluidstress responsestress; reactiontau associated neurodegenerationtau associated neurodegenerative processtau driven neurodegenerationtau induced degenerationtau induced neurodegenerationtau mediated neurodegenerationtau neurodegenerative diseasetau neuropathologytau pathologytau pathophysiologytau phosphorylationtau posttranslational modificationtau proteinopathytau related neurodegenerationtau-1tau-induced pathologytauopathic neurodegenerative disordertauopathytrial designtrisomy 21 syndromeα-secretaseτ phosphorylation
Description preview
A large proportion of people with Down syndrome (DS) will exhibit Alzheimer's Disease (AD) neuropathology
and will eventually develop dementia by age 60. The prevention and treatment of dementia is a high priority for
people with DS and their families. Thus, there is an unmet need for strategies that can prevent, treat, or slow
the progression of…
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