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Modulation of Somatic Repeat Expansion as a Therapeutic Approach to Huntington's Disease
Organization UNIV OF MASSACHUSETTS MED SCH WORCESTERLocation WORCESTER, UNITED STATESPosted 1 Apr 2023Deadline 2 Apr 2025 ⚠️
NIHUS FederalResearch GrantFY2025Adverse effectsAntisense AgentAntisense OligonucleotidesAssayBAC cloneBACsBacterial Artificial ChromosomesBindingBinding ProteinsBioassayBioinformaticsBiological AssayCAG repeatCAG trinucleotide repeatCOCA1Cell BodyCellsChemistryClinicalCognitive DisturbanceCognitive ImpairmentCognitive declineCognitive function abnormalComplexCorpus StriatumCorpus striatum structureDNADNA Mismatch Repair Gene HomologueDNA mutationDNA-Protein InteractionDUC1 GeneDUG GeneDUP GeneDegenerative Neurologic DisordersDeoxyribonucleic AcidDiseaseDisease OutcomeDisease ProgressionDisorderDisturbance in cognitionDrugsEventExonsFCC1FibroblastsFrequenciesGaitGene AlterationGene MutationGene TranscriptionGeneral RadiologyGenesGeneticGenetic ChangeGenetic PolymorphismGenetic TranscriptionGenetic defectGenetic mutationGrip strengthHD GeneHD proteinHNPCC3HNPCC4H_DJ0042M02.9Hand StrengthHarvestHereditaryHistologyHumanHuntingtinHuntingtin ProteinHuntington ChoreaHuntington DiseaseHuntington geneHuntington proteinHuntington'sHuntington's DiseaseHuntington's disease gene productHuntingtons DiseaseIT15 geneImmunohistochemistryImmunohistochemistry Cell/TissueImmunohistochemistry Staining MethodImpaired cognitionInheritedInjectionsInterphase CellKnock-outKnockoutLeadLengthLigand Binding ProteinLigand Binding Protein GeneLinkMLH1MLH1 geneMRP1 GeneMSH2MSH2 geneMSH3MSH3 geneMeasuresMediatingMediatorMedicationMental DepressionMessenger RNAMiceMice MammalsMismatch RepairModern ManMolecular InteractionMotorMurineMusMutL E Coli Homolog 1MutL E. Coli Homolog 1MutationNerve CellsNerve DegenerationNerve UnitNervous System Degenerative DiseasesNervous System DiseasesNervous System DisorderNeural CellNeural Degenerative DiseasesNeural degenerative DisordersNeurobiologyNeurocyteNeurodegenerative DiseasesNeurodegenerative DisordersNeurologic Degenerative ConditionsNeurologic DisordersNeurological DisordersNeuron DegenerationNeuronsNon-dividing CellNondividing CellNucleotidesOligoOligonucleotidesOnset of illnessPMS1PMS1 genePMS2PMS2 genePMSL1PMSL2PathogenicityPathologyPatientsPb elementPharmaceutical PreparationsPost-Replication Mismatch RepairProcessProtein BindingProteinsRNA ExpressionRNA SeqRNA sequencingRNAseqRadiologyRadiology SpecialtyRepair ComplexResting CellSeveritiesSeverity of illnessShort interfering RNASmall Interfering RNASmall RNAStriate BodyStriatumSymptomsSystemTherapeuticTimeTrainingTranscriptionTrinucleotide Repeat ExpansionVentricularWalkingWorkantisense oligoautosomebound proteinclinical relevanceclinically relevantcognitive dysfunctioncognitive losscurative interventioncurative therapeuticcurative therapycurative treatmentsdegenerative diseases of motor and sensory neuronsdegenerative neurological diseasesdepressiondesigndesigningdisease modeldisease onsetdisease phenotypedisease severitydisorder modeldisorder onsetdrug/agentearly onsetefficacy validationendonucleasegene defectgene repairgenome mutationhPMS1heavy metal Pbheavy metal leadimprovedin vivoin vivo Modelinteresting transcript 15intervention designmRNAmotor behaviormotor diseasemotor disordermotor dysfunctionmouse modelmurine modelmutantmutant alleleneural degenerationneurobiologicalneurodegenerationneurodegenerativeneurodegenerative illnessneurological degenerationneurological diseaseneuronalneuronal degenerationnovelnucleasenucleic acid binding proteinoligospolymorphismpre-clinicalpreclinicalpreventpreventingrational designrecruitrepair endonucleaserepair enzymesiRNAstriatalsuccesstherapeutic agent developmenttherapeutic developmenttherapy designtranscriptome sequencingtranscriptomic sequencingtreatment designvalidate efficacy
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Description preview
PROJECT SUMMARY
Huntington’s disease (HD) is caused by expanded trinucleotide repeats (CAG) in exon 1 of the huntingtin (HTT)
gene. Therapies lowering the downstream mutant HTT protein show limited clinical success. New evidence
reveals that repeat tract length in the HTT locus, not mutant HTT protein, correlates to disease onset/severity.
CAG…
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