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SARM1 functional polymorphisms and their contribution to ALS risk
Organization WASHINGTON UNIVERSITYLocation SAINT LOUIS, UNITED STATESPosted 1 Jan 2021Deadline 31 Dec 2025 ⚠️
NIHUS FederalResearch GrantFY2025ALS pathologyALS patientsAffectAllelesAllelomorphsAmino AcidsAmyotrophic Lateral SclerosisAmyotrophic Lateral Sclerosis Motor Neuron DiseaseAmyotrophic Lateral Sclerosis patientsAntimorphic mutationAssayAttenuatedAxonBioassayBiological AssayCRISPRCRISPR/Cas systemCategoriesCausalityCell DeathCessation of lifeChemicalsClustered Regularly Interspaced Short Palindromic RepeatsComplexDNA TherapyDNA mutationDPN hydrolaseDPNaseDataDeathDevelopmentDiphosphopyridine NucleotidaseDiseaseDisinhibitionDisorderDominant NegativeDominant-Negative MutantDominant-Negative MutationDysfunctionEnzyme GeneEnzymesEtiologyFaceFoundationsFunctional disorderGWA studyGWASGehrig's DiseaseGene Transfer ClinicalGene variantGeneral PopulationGeneral PublicGenesGenetic ChangeGenetic DiversityGenetic InterventionGenetic PolymorphismGenetic VariationGenetic defectGenetic mutationGenetic predisposing factorGenetic studyHumanHuman GeneticsInduced pluripotent stem cell derived human neuronInjuryInvestigationKI miceKO miceKnock-inKnock-in MouseKnock-out MiceKnockout MiceLinkLou Gehrig DiseaseMaintenanceMediatingMedulla SpinalisMessenger RNAMetabolicMethodsMiceMice MammalsModelingModern ManMolecularMotorMotor CellMotor NeuronsMurineMusMuscleMuscle TissueMutateMutationNAD+ GlycohydrolaseNAD+ NucleosidaseNADaseNerve CellsNerve DegenerationNerve UnitNervous SystemNeural CellNeurocyteNeurologic Body SystemNeurologic Organ SystemNeuron DegenerationNeuronsNeuropathyNull MousePalsyParalysedPathogenesisPathogenicityPathologyPathway interactionsPhenotypePhysiopathologyPlegiaProcessProtein TruncationProteinsRiskRoleRouteSOD-1SOD-1 proteinSOD1SOD1 geneSOD1 gene productSpinal CordStructureSymptomsTAR DNA-binding protein 43TDP-43TDP-43 aggregateTDP-43 aggregationTDP43TDP43 aggregateTDP43 aggregationTestingTherapeuticTraumaVariantVariationViralallelic variantaminoacidamyotrophic lateral sclerosis pathologyattenuateattenuatesaxon damageaxon injuryaxonal damageaxonal degenerationaxonal injurycausationcohortdegenerative axondevelopmentaldisease causationdisease modeldisease riskdisorder modeldisorder riskdruggable targetenzyme activityexperimentexperimental researchexperimental studyexperimentsfacesfacialfallsgain of functiongain of function mutationgene repair therapygene therapygene-based therapygenetic risk factorgenetic therapygenetic variantgenome mutationgenome wide associationgenome wide association scangenome wide association studygenomewide association scangenomewide association studygenomic therapygenomic variantgenotyped patientshiPSChiPSC-derived neuronshuman iPShuman iPSChuman iPSC-derived sensory neuronhuman induced pluripotent cellhuman induced pluripotent stem cell derived sensory neuronhuman induced pluripotent stem cellshuman inducible pluripotent stem cellshuman inducible stem cellsiPSC-derived human neuroninduced human pluripotent stem cellsinducible pluripotent stem cell derived human neuroninducible pluripotent stem cell derived human sensory neuroninherited factorinhibitor druginhibitor therapeuticinhibitor therapyinjuriesinnovateinnovationinnovativeknockinknockin micelife spanlifespanloss of functionmRNAmembermotoneuronmotor diseasemotor disordermotor dysfunctionmouse modelmurine modelmuscularnecrocytosisnerve cell deathnerve cell lossneural degenerationneurodegenerationneurodegenerativeneurodegenerative phenotypeneurological degenerationneuron cell deathneuron cell lossneuron deathneuron lossneuronalneuronal cell deathneuronal cell lossneuronal deathneuronal degenerationneuronal lossneurons differentiated from human induced pluripotent stem cellsneuropathicneuroprotectionneuroprotectivenoveloverexpressoverexpressionparalysisparalyticpathology in ALSpathophysiologypathwaypolymorphismprogramsprotein TDP-43protein TDP43small molecular inhibitorsmall molecule inhibitorsocial rolesuperoxide dismutase 1whole genome association analysiswhole genome association study
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Description preview
Motor axon loss is a cardinal symptom of amyotrophic lateral sclerosis (ALS). Axon loss can be driven
by a genetically encoded program in which the axon survival factors NMNAT2 and STMN2 inhibit the activity of
the axon destruction factor SARM1. Recent data suggest that this program of axon self-destruction may
contribute to pathology in ALS.…
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