Megan Conrow-Graham, MD, PhD
she/her/hers
Clinical FellowAbout
Research
Publications
2026
Moving Beyond Moral Outrage
Rawlins Y, Conrow-Graham M, Lo E, Riley S. Moving Beyond Moral Outrage. Psychiatric News 2026, 61 DOI: 10.1176/appi.pn.2026.07.7.6.Peer-Reviewed Original Research
2025
Synaptic Deficits in Adnp‐Mutant Mice Are Ameliorated by Histone Demethylase LSD1 Inhibition
Lin C, Ren Y, Tam K, Conrow‐Graham M, Yan Z. Synaptic Deficits in Adnp‐Mutant Mice Are Ameliorated by Histone Demethylase LSD1 Inhibition. Autism Research 2025, 18: 1342-1355. PMID: 40536108, PMCID: PMC12257630, DOI: 10.1002/aur.70069.Peer-Reviewed Original Research
2024
4.46 REVIEW: Rates of Neurodevelopmental Disorders and Access to Services for Indigenous Peoples of the United States and Canada
Conrow-Graham M, Williams J, Holmes D. 4.46 REVIEW: Rates of Neurodevelopmental Disorders and Access to Services for Indigenous Peoples of the United States and Canada. Journal Of The American Academy Of Child And Adolescent Psychiatry 2024, 63: s245. DOI: 10.1016/j.jaac.2024.08.291.Peer-Reviewed Original Research
2022
A convergent mechanism of high risk factors ADNP and POGZ in neurodevelopmental disorders
Conrow-Graham M, Williams J, Martin J, Zhong P, Cao Q, Rein B, Yan Z. A convergent mechanism of high risk factors ADNP and POGZ in neurodevelopmental disorders. Brain 2022, 145: 3250-3263. PMID: 35775424, PMCID: PMC10233273, DOI: 10.1093/brain/awac152.Peer-Reviewed Original ResearchConceptsAutism spectrum disorderPrefrontal cortexPogz deficiencySpectrum disorderNeurodevelopmental disordersIntellectual disabilityDecrease of glutamatergic transmissionMouse prefrontal cortexCognitive task performancePostsynaptic protein expressionNeurodevelopmental disorder risk factorsTop-ranked risk factorsAssociated with neurodevelopmental disordersCognitive deficitsGlutamatergic transmissionTask performanceRisk factorsAutismCortexPost-mortem tissueDisordersSynaptic functionPOGZADNPMicroglial activation
2021
Inhibition of histone deacetylase 5 ameliorates abnormalities in 16p11.2 duplication mouse model
Rein B, Conrow-Graham M, Frazier A, Cao Q, Yan Z. Inhibition of histone deacetylase 5 ameliorates abnormalities in 16p11.2 duplication mouse model. Neuropharmacology 2021, 204: 108893. PMID: 34822816, DOI: 10.1016/j.neuropharm.2021.108893.Peer-Reviewed Original ResearchConceptsPrefrontal cortexAutism spectrum disorderHistone deacetylase 5Human 16p11.2 gene locusHistone acetylationActivity-dependent transcription factorHistone deacetylase 5 expressionGABAergic synaptic functionSocial deficitsBehavioral deficitsNpas4 promoterSpectrum disorderGABAergic signalingNpas4Gene locusSocial preferencesTranscription factorsSynaptic functionTarget genesGene expressionHistoneMolecular mechanismsSynapse formationDeficitsDuplicate conditionsNeural circuits and activity dynamics underlying sex-specific effects of chronic social isolation stress
Tan T, Wang W, Liu T, Zhong P, Conrow-Graham M, Tian X, Yan Z. Neural circuits and activity dynamics underlying sex-specific effects of chronic social isolation stress. Cell Reports 2021, 34: 108874. PMID: 33761364, DOI: 10.1016/j.celrep.2021.108874.Peer-Reviewed Original ResearchConceptsPrefrontal cortexSocial isolation stressStressed malesStressed femalesIsolation stressPrefrontal cortex pyramidal neuronsChronic social isolation stressExposure to prolonged stressPyramidal neuronsEffects of stressSex-specific consequencesSociability testNeuronal hypoactivitySocial withdrawalElevated aggressionPsychiatric disordersEscalated aggressionBlunted increaseProlonged stressHeightened vulnerabilityNeural circuitsDevelopmental periodElectrophysiological evidenceBehavioral changesIncrease of discharge rateSynergistic inhibition of histone modifiers produces therapeutic effects in adult Shank3-deficient mice
Zhang F, Rein B, Zhong P, Shwani T, Conrow-Graham M, Wang Z, Yan Z. Synergistic inhibition of histone modifiers produces therapeutic effects in adult Shank3-deficient mice. Translational Psychiatry 2021, 11: 99. PMID: 33542189, PMCID: PMC7862604, DOI: 10.1038/s41398-021-01233-w.Peer-Reviewed Original ResearchConceptsAutism spectrum disorderShank3-deficient micePrefrontal cortexBehavioral abnormalitiesPrefrontal cortex pyramidal neuronsLevels of NMDA receptor subunitsSocial preference deficitsMale miceNMDA receptor subunitsExpression of NMDA receptorsPreference deficitsSocial deficitsHeightened aggressionEarly developmental periodPharmacological intervention strategiesSpectrum disorderDysregulation of epigenetic processesSHANK3 geneDevelopmental disordersASD pathologyNMDA receptorsDevelopmental periodPyramidal neuronsSynaptic functionReceptor subunits