2022
Alzheimer risk gene product Pyk2 suppresses tau phosphorylation and phenotypic effects of tauopathy
Brody AH, Nies SH, Guan F, Smith LM, Mukherjee B, Salazar SA, Lee S, Lam TKT, Strittmatter SM. Alzheimer risk gene product Pyk2 suppresses tau phosphorylation and phenotypic effects of tauopathy. Molecular Neurodegeneration 2022, 17: 32. PMID: 35501917, PMCID: PMC9063299, DOI: 10.1186/s13024-022-00526-y.Peer-Reviewed Original ResearchConceptsPS19 miceTau phosphorylationDisease riskPyk2 expressionPyk2 activityHuman neuronal culturesAlzheimer's disease riskNeuro-inflammationSynapse lossTau accumulationTau pathologyMouse survivalC1q depositionT cellsAssociated pathologyMouse modelLittermate controlsMAPK activityHuman neuronsHuman tauNeuronal culturesPyk2 inhibitionVivo modelMouse brainSynaptic function
2017
Loss of TMEM106B Ameliorates Lysosomal and Frontotemporal Dementia-Related Phenotypes in Progranulin-Deficient Mice
Klein ZA, Takahashi H, Ma M, Stagi M, Zhou M, Lam TT, Strittmatter SM. Loss of TMEM106B Ameliorates Lysosomal and Frontotemporal Dementia-Related Phenotypes in Progranulin-Deficient Mice. Neuron 2017, 95: 281-296.e6. PMID: 28728022, PMCID: PMC5558861, DOI: 10.1016/j.neuron.2017.06.026.Peer-Reviewed Original ResearchConceptsLysosomal protein levelsFrontotemporal lobar degenerationProtein levelsMultiple lysosomal enzymesLysosomal enzymesV0 subunitsTMEM106B geneProteomic analysisProgranulin-deficient miceExtent of neurodegenerationCommon neurodegenerative disorderLysosomal acidificationLysosomal enzyme levelsProtein 1Microglial accumulationRisk modificationFTLD riskBehavioral abnormalitiesRetinal degenerationNeurodegenerative disordersFrontotemporal dementiaGRNTMEM106BFunctional relationshipEnzyme levelsSilent Allosteric Modulation of mGluR5 Maintains Glutamate Signaling while Rescuing Alzheimer’s Mouse Phenotypes
Haas LT, Salazar SV, Smith LM, Zhao HR, Cox TO, Herber CS, Degnan AP, Balakrishnan A, Macor JE, Albright CF, Strittmatter SM. Silent Allosteric Modulation of mGluR5 Maintains Glutamate Signaling while Rescuing Alzheimer’s Mouse Phenotypes. Cell Reports 2017, 20: 76-88. PMID: 28683325, PMCID: PMC5547898, DOI: 10.1016/j.celrep.2017.06.023.Peer-Reviewed Original ResearchConceptsAD transgenic mouse modelDisease pathologyMetabotropic glutamate receptor 5Allosteric modulationGlutamate receptor 5Alzheimer's disease pathologyTransgenic mouse brainSilent allosteric modulatorsTransgenic mouse modelBroad therapeutic windowMouse phenotypeAD interventionSynaptic depletionBrain slicesGlutamate signalingMouse modelTherapeutic windowAD phenotypeReceptor 5Mouse brainAllosteric modulatorsMemory deficitsCellular prion proteinPathological roleMGluR5
2012
LRRTM1-deficient mice show a rare phenotype of avoiding small enclosures—A tentative mouse model for claustrophobia-like behaviour
Voikar V, Kulesskaya N, Laakso T, Lauren J, Strittmatter SM, Airaksinen MS. LRRTM1-deficient mice show a rare phenotype of avoiding small enclosures—A tentative mouse model for claustrophobia-like behaviour. Behavioural Brain Research 2012, 238: 69-78. PMID: 23089646, PMCID: PMC3784023, DOI: 10.1016/j.bbr.2012.10.013.Peer-Reviewed Original Research
2009
LGI1-associated epilepsy through altered ADAM23-dependent neuronal morphology
Owuor K, Harel NY, Englot DJ, Hisama F, Blumenfeld H, Strittmatter SM. LGI1-associated epilepsy through altered ADAM23-dependent neuronal morphology. Molecular And Cellular Neuroscience 2009, 42: 448-457. PMID: 19796686, PMCID: PMC2783222, DOI: 10.1016/j.mcn.2009.09.008.Peer-Reviewed Original ResearchConceptsNeuronal morphologyAutosomal dominant partial epilepsyCA1 pyramidal neuronsSeizure thresholdSpontaneous seizuresPartial epilepsyPyramidal neuronsDendritic arborizationLGI1PSD-95LGI1 geneEpilepsy genesADAM23ADPEAFADAM22EpilepsyNeurite outgrowthIon channelsBrain genesUnbiased screenAuditory featuresOutgrowthSeizuresArborizationRelated proteins
2007
Response to Correspondence: Kim et al., “Axon Regeneration in Young Adult Mice Lacking Nogo-A/B.” Neuron 38, 187–199
Cafferty WB, Kim JE, Lee JK, Strittmatter SM. Response to Correspondence: Kim et al., “Axon Regeneration in Young Adult Mice Lacking Nogo-A/B.” Neuron 38, 187–199. Neuron 2007, 54: 195-199. PMID: 17442242, PMCID: PMC2848952, DOI: 10.1016/j.neuron.2007.04.005.Peer-Reviewed Original Research
2003
Axon Regeneration in Young Adult Mice Lacking Nogo-A/B
Kim J, Li S, GrandPré T, Qiu D, Strittmatter SM. Axon Regeneration in Young Adult Mice Lacking Nogo-A/B. Neuron 2003, 38: 187-199. PMID: 12718854, DOI: 10.1016/s0896-6273(03)00147-8.Peer-Reviewed Original ResearchConceptsCNS axon repairAxon growth inhibitorsSpinal cord injuryAdult mammalian brainAxonal sproutingCorticospinal axonsCord segmentsCord injuryTract tracingAdult CNSLocomotor functionMice LackingAxon repairMammalian brainB expressionMiceYoung adultsInjuryNumerous fibersNormal locomotionAxonsNogoTransectionGrowth inhibitorLittle regeneration