David S. Russell, MD, PhD
Assistant Clinical ProfessorAbout
Titles
Assistant Clinical Professor
Positions outside Yale
Senior Medical Director, Clinical Research, Perceptive New Haven Clinic; Senior Director, Clinical Research, Translational Research, Invicro
Biography
Dr. Russell is a neurologist specializing in movement disorders, dementias, and other neurodegenerative disorders. He is working full-time as Senior Medical Director for a clinical research center, devoted entirely to clinical research on diseases with major unmet needs. As a former director of the Yale Movement Disorders Consultation Clinic, he continues to work closely with other area neurologists and researchers to try to help improve the future for people with these diseases. Referrals to the Perceptive New Haven Clinic for potential research participation can be made most efficiently through the patient's treating neurologist or other physician.
Appointments
Psychiatry
Assistant Clinical ProfessorPrimaryNeurology
Assistant Clinical ProfessorSecondary
Other Departments & Organizations
Education & Training
- Neurology Resident
- Yale-New Haven Hospital (1995)
- Chief Resident, Neurology
- Yale-New Haven Hospital (1995)
- Intern
- Yale-New Haven Hospital (1992)
- MD
- Cornell University (1991)
- PhD
- Cornell University (1991)
- BA
- Oberlin College, Biology (1982)
Research
Overview
Medical Research Interests
ORCID
0000-0002-9105-2943Perceptive New Haven Clinic
A 100% research-dedicated clinical research facility
View Lab Website
Research at a Glance
Yale Co-Authors
Publications Timeline
Research Interests
Gilles Tamagnan, PhD
Catharine Duman, PhD
Stephen Strittmatter, MD, PhD, AB
Parkinson Disease
Alzheimer Disease
Publications
2025
Evidence for alpha-synuclein aggregation in older individuals with hyposmia: a cross-sectional study
Marek K, Russell D, Concha-Marambio L, Choi S, Jennings D, Brumm M, Coffey C, Brown E, Seibyl J, Stern M, Soto C, Siderowf A. Evidence for alpha-synuclein aggregation in older individuals with hyposmia: a cross-sectional study. EBioMedicine 2025, 112: 105567. PMID: 39893720, PMCID: PMC11835612, DOI: 10.1016/j.ebiom.2025.105567.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsDementia with Lewy bodiesCross-sectional studyCognitive symptomsParkinson Associated Risk Syndrome StudyPrevention StudyYear follow-upOlder individualsDopamine transporter imagingHigh riskSyndrome studiesParticipantsParkinson's diseaseHyposmic individualsFollow-upSynuclein pathologySymptomsHyposmicsDepartment of DefenseU.S. Department of DefenseIndividualsRiskLewy bodiesClinical parkinsonismMichael J. Fox FoundationDementiaCorrection: Quantifying VMAT2 target occupancy at effective valbenazine doses and comparing to a novel VMAT2 inhibitor: a translational PET study
Terry-Lorenzo R, Albrecht D, Crouch S, Wong R, Loewen G, Giri N, Skor H, Lin K, Sandiego C, Pajonas M, Rabiner E, Gunn R, Russell D, Haubenberger D. Correction: Quantifying VMAT2 target occupancy at effective valbenazine doses and comparing to a novel VMAT2 inhibitor: a translational PET study. Neuropsychopharmacology 2025, 50: 719-719. PMID: 39843851, PMCID: PMC11845734, DOI: 10.1038/s41386-025-02055-w.Peer-Reviewed Original ResearchQuantifying VMAT2 target occupancy at effective valbenazine doses and comparing to a novel VMAT2 inhibitor: a translational PET study
Terry-Lorenzo R, Albrecht D, Crouch S, Wong R, Loewen G, Giri N, Skor H, Lin K, Sandiego C, Pajonas M, Rabiner E, Gunn R, Russell D, Haubenberger D. Quantifying VMAT2 target occupancy at effective valbenazine doses and comparing to a novel VMAT2 inhibitor: a translational PET study. Neuropsychopharmacology 2025, 1-9. PMID: 39757283, DOI: 10.1038/s41386-024-02046-3.Peer-Reviewed Original ResearchConceptsVesicular monoamine transporter type 2Treatment of tardive dyskinesiaPositron emission tomographyVesicular monoamine transporter type 2 inhibitorsTarget occupancyTreatment of chorea associated with Huntington's diseaseTreatment of TDChorea associated with Huntington's diseaseCentral nervous systemTardive dyskinesiaVMAT2 inhibitorsValbenazineClinical developmentEffect sizeAssociated with efficacyPET studiesEmission tomographyGold standard biomarkerDosing regimensClinical benefitDaily doseHuntington's diseaseActive metabolitePlasma concentrationsAcceptable doseIn Vivo Head-to-Head Comparison of [18F]GTP1 with [18F]MK-6240 and [18F]PI-2620 in Alzheimer Disease
Olafson E, Tonietto M, Klein G, Teng E, Stephens A, Russell D, Pickthorn K, Bohorquez S. In Vivo Head-to-Head Comparison of [18F]GTP1 with [18F]MK-6240 and [18F]PI-2620 in Alzheimer Disease. Journal Of Nuclear Medicine 2025, 66: jnumed.124.268623. PMID: 39746756, PMCID: PMC11800736, DOI: 10.2967/jnumed.124.268623.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsAlzheimer's diseaseAccumulation of tau neurofibrillary tanglesTau neurofibrillary tanglesOff-target regionsNeurofibrillary tanglesTau pathologyTau-PET signalTau PET tracersBinding profilesTau-PETMild ADNormal cognitionBraak regionsHead-to-head studiesAD patientsTauMagnitude of uptakeTracer bindingAlzheimerTarget region
2024
Discovery and clinical translation of ceperognastat, an O‐GlcNAcase (OGA) inhibitor, for the treatment of Alzheimer's disease
Kielbasa W, Goldsmith P, Donnelly K, Nuthall H, Shcherbinin S, Fleisher A, Hendle J, DuBois S, Lowe S, Zhang F, Woerly E, Dreyfus N, Evans D, Gilmore J, Mancini M, Constantinescu C, Gunn R, Russell D, Collins E, Brys M, Hutton M, Mergott D. Discovery and clinical translation of ceperognastat, an O‐GlcNAcase (OGA) inhibitor, for the treatment of Alzheimer's disease. Alzheimer's & Dementia: Translational Research & Clinical Interventions 2024, 10: e70020. PMID: 39748851, PMCID: PMC11694536, DOI: 10.1002/trc2.70020.Peer-Reviewed Original ResearchConceptsReduced tau pathologyO-GlcNAcaseOGA inhibitorsO-GlcNAcO-GlcNAcylationPost-translational modifications of tauTau pathologyAlzheimer's diseaseTau O-GlcNAcylationRemoval of O-GlcNAcModifications of tauO-GlcNAcase inhibitionPost-translational modificationsInhibitor of O-GlcNAcaseO-GlcNAcase inhibitorProgression of ADEnzyme occupancyTauopathy modelPathological tauPhase 1 clinical studyTreatment of Alzheimer's diseaseHuman brainEnzyme activityPatients relative to healthy controlsPotential therapeutic approachGlutamatergic Dysfunction in Autism Spectrum Disorder (P1-8.001)
Brasic J, Nandi A, Russell D, Jennings D, Barret O, Slifer K, Sedlak T, Seibyl J, Berry-Kravis E, Wong D, Budimirovic D. Glutamatergic Dysfunction in Autism Spectrum Disorder (P1-8.001). Neurology 2024, 102 DOI: 10.1212/wnl.0000000000204347.Peer-Reviewed Original Research
2023
The α-synuclein PET tracer [18F] ACI-12589 distinguishes multiple system atrophy from other neurodegenerative diseases
Smith R, Capotosti F, Schain M, Ohlsson T, Vokali E, Molette J, Touilloux T, Hliva V, Dimitrakopoulos I, Puschmann A, Jögi J, Svenningsson P, Andréasson M, Sandiego C, Russell D, Miranda-Azpiazu P, Halldin C, Stomrud E, Hall S, Bratteby K, Tampio L’Estrade E, Luthi-Carter R, Pfeifer A, Kosco-Vilbois M, Streffer J, Hansson O. The α-synuclein PET tracer [18F] ACI-12589 distinguishes multiple system atrophy from other neurodegenerative diseases. Nature Communications 2023, 14: 6750. PMID: 37891183, PMCID: PMC10611796, DOI: 10.1038/s41467-023-42305-3.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsMultiple-system atrophyPositron emission tomographyMultiple-system atrophy patientsDiagnostic work-upMiddle cerebellar peduncleCerebellar white matterParkinson's diseasePositron emission tomography ligandsMultiple system atrophyTarget engagement in vivoTargeted therapyMSA patientsClinical evaluationHealthy controlsIn vitro affinityEmission tomographyPET imagingPET tracersWhite matterSystem atrophyPatientsNeurodegenerative disordersDiseaseA-synucleinRelated disordersCase report of a patient with unclassified tauopathy with molecular and neuropathological features of both progressive supranuclear palsy and corticobasal degeneration
Koga S, Metrick M, Golbe L, Santambrogio A, Kim M, Soto-Beasley A, Walton R, Baker M, De Castro C, DeTure M, Russell D, Navia B, Sandiego C, Ross O, Vendruscolo M, Caughey B, Dickson D. Case report of a patient with unclassified tauopathy with molecular and neuropathological features of both progressive supranuclear palsy and corticobasal degeneration. Acta Neuropathologica Communications 2023, 11: 88. PMID: 37264457, PMCID: PMC10236843, DOI: 10.1186/s40478-023-01584-z.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsSuperior frontal gyrusFrontal gyrusConsistent with corticobasal degenerationConsistent with progressive supranuclear palsyMotor cortexCorticobasal degenerationProgressive supranuclear palsyPosterior cortical areasPresentation of corticobasal degenerationSubtype of frontotemporal lobar degenerationRichardson's syndromeBrain regionsOccipital cortexSubcortical structuresCaudate nucleusFrontotemporal lobar degenerationTau PET scansSubstantia nigraGlobus pallidusCorticobasal syndromeGyrusSupranuclear palsyCortexCortical areasClinical presentation of progressive supranuclear palsy
2022
In Vivo Head‐To‐Head Comparison of [18F]GTP1 and [18F]PI2620 in Alzheimer’s Disease
Bohorquez S, Constantinescu C, Manser P, Gunn R, Russell D, Tonietto M, Bullich S, Stephens A, Mueller A, Klein G, Teng E, Pickthorn K. In Vivo Head‐To‐Head Comparison of [18F]GTP1 and [18F]PI2620 in Alzheimer’s Disease. Alzheimer's & Dementia 2022, 18 DOI: 10.1002/alz.063517.Peer-Reviewed Original ResearchConceptsChoroid plexusAlzheimer's diseaseTau pathology distributionModerate AD subjectsTarget cortical regionsTherapeutic trialsTau pathologyHead studiesPathology distributionCentrum semiovaleCortical greyBraak regionsAD subjectsHuman studiesInferior cerebellumSubcortical regionsHead comparisonQuantification scaleCortical regionsSubcortical structuresMinute imagesCSF spaceDiseaseUnimpaired subjectsSUVRPROGRESS IN DEVELOPING A LIGHT‐STABLE 4R TAU PET IMAGING AGENT: APN‐1701 FIH
Tempest P, Lin Y, Tai C, Ono M, Russell D, Sandiego C, Carroll V, Gunn R, Margolin R, Higuchi M, Jang M. PROGRESS IN DEVELOPING A LIGHT‐STABLE 4R TAU PET IMAGING AGENT: APN‐1701 FIH. Alzheimer's & Dementia 2022, 18 DOI: 10.1002/alz.063028.Peer-Reviewed Original ResearchConceptsAD subjectsMulticenter phase 2 clinical trialAlzheimer's diseasePhase 2 clinical trialTau PET tracersPET imaging agentSimilar brain regionsCortical uptakeTest-retest studyCN subjectsClinical trialsNormal subjectsTau tracersBrain regionsSUV valuesDiverse tauopathiesPET tracersSame rank orderSUVR imagesImaging agentImaging profileDisease
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