Voluntary Faculty
Voluntary faculty are typically clinicians or others who are employed outside of the School but make significant contributions to department programs at the medical center or at affiliate institutions.
Voluntary rank detailsDavid S. Russell, MD, PhD
Assistant Clinical ProfessorDownloadHi-Res Photo
About
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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.
Last Updated on December 20, 2024.
Appointments
Psychiatry
Assistant Clinical ProfessorPrimary
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
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Overview
Medical Research Interests
Alzheimer Disease; Huntington Disease; Movement Disorders; Neurodegenerative Diseases; Parkinson Disease
ORCID
0000-0002-9105-2943
Research at a Glance
Yale Co-Authors
Frequent collaborators of David S. Russell's published research.
Publications Timeline
A big-picture view of David S. Russell's research output by year.
Research Interests
Research topics David S. Russell is interested in exploring.
John Seibyl, MD
Catharine Duman, PhD
Gilles Tamagnan, PhD
Stephen Strittmatter, MD, PhD, AB
27Publications
2,685Citations
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 ResearchCitationsAltmetricMeSH 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.Commentaries, Editorials and LettersQuantifying 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, 50: 1093-1101. PMID: 39757283, PMCID: PMC12089418, DOI: 10.1038/s41386-024-02046-3.Peer-Reviewed Original ResearchCitationsAltmetricConceptsVesicular 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 ResearchCitationsAltmetricMeSH 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 ResearchCitationsAltmetricConceptsReduced 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 approach
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 ResearchCitationsAltmetricMeSH 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 ResearchCitationsAltmetricMeSH 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
2021
Binding characteristics of [18F]PI-2620 distinguish the clinically predicted tau isoform in different tauopathies by PET
Song M, Beyer L, Kaiser L, Barthel H, van Eimeren T, Marek K, Nitschmann A, Scheifele M, Palleis C, Respondek G, Kern M, Biechele G, Hammes J, Bischof G, Barbe M, Onur Ö, Jessen F, Saur D, Schroeter M, Rumpf J, Rullmann M, Schildan A, Patt M, Neumaier B, Barret O, Madonia J, Russell D, Stephens A, Mueller A, Roeber S, Herms J, Bötzel K, Danek A, Levin J, Classen J, Höglinger G, Bartenstein P, Villemagne V, Drzezga A, Seibyl J, Sabri O, Boening G, Ziegler S, Brendel M. Binding characteristics of [18F]PI-2620 distinguish the clinically predicted tau isoform in different tauopathies by PET. Journal Of Cerebral Blood Flow And Metabolism : Official Journal Of The International Society Of Cerebral Blood Flow And Metabolism 2021, 41: 2957-2972. PMID: 34044665, PMCID: PMC8545042, DOI: 10.1177/0271678x211018904.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and Concepts
2018
Immunohistochemical Method and Histopathology Judging for the Systemic Synuclein Sampling Study (S4)
Beach T, Serrano G, Kremer T, Canamero M, Dziadek S, Sade H, Derkinderen P, Corbillé A, Letournel F, Munoz D, White C, Schneider J, Crary J, Sue L, Adler C, Glass M, Intorcia A, Walker J, Foroud T, Coffey C, Ecklund D, Riss H, Goßmann J, König F, Kopil C, Arnedo V, Riley L, Linder C, Dave K, Jennings D, Seibyl J, Mollenhauer B, Chahine L, Guilmette L, Russell D, Noyes-Lloyd C, Mitchell C, Smith D, Potter M, Case R, Lott D, Duffy A, Hogarth P, Cresswell M, Akhtar R, Purri R, Amara A, Blair C, Keshavarzian A, Marras C, Visanji N, Rothberg B, Oza V. Immunohistochemical Method and Histopathology Judging for the Systemic Synuclein Sampling Study (S4). Journal Of Neuropathology & Experimental Neurology 2018, 77: 793-802. PMID: 30107604, PMCID: PMC6097838, DOI: 10.1093/jnen/nly056.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsParkinson's diseaseASyn pathologyΑ-synuclein pathologySubmandibular gland biopsyPeripheral biopsiesControl subjectsGland biopsyBlinded panelImmunohistochemical methodsImmunoperoxidase methodMonoclonal antibodiesScore agreementNeuropathologistsPathologyBiopsySkinSubsequent testingSampling study
2015
O4‐07‐06: Approaches to quantitative analysis of the PET tau radiotracer [18F]AV1451
Seibyl J, Barret O, Alagille D, Jennings D, Russell D, Marek K, Tamagnan G. O4‐07‐06: Approaches to quantitative analysis of the PET tau radiotracer [18F]AV1451. Alzheimer's & Dementia 2015, 11: p285-p285. DOI: 10.1016/j.jalz.2015.07.386.Peer-Reviewed Original Research