Clemens Scherzer, MD
Stephen and Denise Adams Professor of Neurology & Director of the Stephen & Denise Adams Center for Parkinson’s Disease Research and Professor of Genetics and of NeuroscienceCards
Appointments
Additional Titles
Academic Chief, Division of Movement Disorders, Neurology
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Yale School of Medicine
101 College Street, Floor 10
New Haven, CT 06510
United States
Appointments
Additional Titles
Academic Chief, Division of Movement Disorders, Neurology
Contact Info
Yale School of Medicine
101 College Street, Floor 10
New Haven, CT 06510
United States
Appointments
Additional Titles
Academic Chief, Division of Movement Disorders, Neurology
Contact Info
Yale School of Medicine
101 College Street, Floor 10
New Haven, CT 06510
United States
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Titles
Stephen and Denise Adams Professor of Neurology & Director of the Stephen & Denise Adams Center for Parkinson’s Disease Research and Professor of Genetics and of Neuroscience
Academic Chief, Division of Movement Disorders, Neurology
Biography
Clemens Scherzer, M.D. is a physician-scientist and the Stephen & Denise Adams Professor of Neurology, and Professor of Genetics and Neuroscience at Yale School of Medicine. He heads the Stephen & Denise Adams Center for Parkinson’s Disease Research of Yale School of Medicine, an inter- departmental center building the future of precision medicine for Parkinson’s through genomics and AI, and the American Parkinson Disease Association Center for Advanced Research. In his clinical practice he is the Academic Chief of the Division of Movement Disorders and directs the Yale Harvard Biomarkers Study (YHBS). Prior to his recruitment to Yale in 2024, Scherzer was Professor of Neurology at Harvard Medical School, where he headed the Neurogenomics Lab (2003-2023) and developed the inter-divisional Brigham & Women’s Hospital Precision Neurology Program (2017-2023). Under his leadership, two US institutions – first Brigham & Women’s Hospital (since 2017-) and then Yale (2024- ) – were nationally recognized for the first time in their histories as research centers of excellence by the American Parkinson Disease Association.
Scherzer uses genomics and big data to develop a new, predictive, preventive precison medicine for Parkinson's disease. His interdisciplinary lab includes bioinformatics engineers, geneticists, biologists, and clinicians. The lab's goal is to build a Parkinson AI engine that matches drugs and tests to a patient based on a search of his entire biology. This transformative research is powered by the Yale Harvard Biomarkers Study, with more than 4,000 participants one of the largest longitudinal biobanks for Parkinson's in the world. To understand how the human genome encodes human brain cells in health and disease, Scherzer is leading the $15 million Parkinson Cell Atlas in 5D with two awards from the ASAP Foundation. This initiative is decoding the genetic software of millions of brain cells and searches for glitches that cause disease. He is a pioneer in precision neurology, whose research led to the discovery of genetic drivers, biomarkers, and therapeutic targets, and clinical trials.
Scherzer, a graduate of the University of Vienna Medical School, completed internship and neurology residency at Emory University (under Lasker Laurate Mahlon DeLong, MD, PhD and Allan Levey, MD, PhD), and movement disorders and genomics fellowship training at Harvard. He received the Dr. Paul Beeson and the George C. Cotzias Memorial Awards, and was awarded an honorary master degree from Harvard University. He contributed to the launch of a foundational network of Parkinson’s biobanks and the Accelerating Medicines Partnership-PD in the US, which form the national backbone for precision neurology research for PD. He co-founded the Harvard Biomarkers Study (HBS) in 2008 and contributed to the launch of the Michael J. Fox Foundation’s PPMI (on the founding Advisory Committee), and the NIH’s PDBP (as inaugural Co-Chair). He served on the Parkinson Vision Setting Panel of the U.S. Department of Defense, and is on the Steering Committee of the NINDS Parkinson's Disease Biomarkers Program and the Scientific Advisory Board of the American Parkinson Disease Foundation. He serves on the Editorial Boards of Neurogenetics and Biomarkers in Medicine. His research has been featured in international and national news media such as Scientific American, Washington Post, Bloomberg, US News & World Reports, and NOVA Next.
Research from the Scherzer laboratory has led to the discovery of genetic drivers (e.g. distinct types of GBA mutations in 10% of patients; Annals of Neurology, 2016; Lancet Neurology, 2017), biomarkers, and therapeutic mechanisms (e.g. beta2-adrenoreceptor as regulator of the alpha-synuclein gene; Science, 2017), and is inspiring clinical trials. Scherzer revealed that the genetics of disease progression --- the main driver of patients’ wellbeing and clinical trials --- and the genetics of susceptibility importantly differ (Nature Genetics, 2021). His landmark systems transcriptomics study on defects in PGC1alpha-regulated bioenergetics genes in prodromal Parkinson's neuropathology (Science Translational Medicine, 2010) was highlighted as “a glimpse into the future of biomedicine”. To decode how the human genome codes our brain cells in health and disease, Scherzer is mapping a Parkinson Cell Atlas in 5D (PD5D) using high-resolution spatial, multiome, sub-cellular, and single-cell genomics combined with single-cell expression Quantitative Trait Locus analysis in millions of brain cells and thousand brains. While virtually everything we know about the human brain is based on just the 1.2% of the human genome that encodes proteins, his group found that actually as much as 64% of the genome are actively transcribed in our brain cells. Scherzer believes that this massive, hidden RNA software underlies the complexity of the human brain and neuropsychiatric disease (e.g. Nature Neuroscience, 2018; Nature Communications, 2023). For Alzheimer’s disease, he made the seminal discovery of SORL1 (LR11, SORLA) gene activity changes (Archives of Neurology, 2004), which is widely recognized as a top Alzheimer’s gene and “Amyloid-beta traffic cop.”
Appointments
Neurology
ProfessorPrimaryGenetics
ProfessorSecondaryNeuroscience
ProfessorSecondary
Other Departments & Organizations
- Center for RNA Science and Medicine
- Computational Biology and Biomedical Informatics
- Genetics
- Human Genome Sciences
- Neurology
- Neuroscience
- Yale Combined Program in the Biological and Biomedical Sciences (BBS)
- Yale Medicine
- Yale New Haven Health System
Education & Training
- MD
- Medical University of Vienna (1995)
Research
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Research Projects
Polygenic Score for Dementia in Parkinson's Disease
Neurology / , parent organization of Movement Disorders Division
ORCID
0000-0002-0567-9193- View Lab Website
Neurogenomics Laboratory
Research at a Glance
Yale Co-Authors
Publications Timeline
Xianjun Dong, PhD
Beatrice Weykopf, PhD
Jesse M. Cedarbaum, MD, FAAN (Neurology), FANA
Publications
2026
Postmortem Associations Between Alzheimer Disease Pathology and Plasma pTau217, GFAP, and NfL in AD and AD-Related Dementias
Kivisäkk P, Fatima H, Wu C, Padmanabhan N, Romero D, Gorham T, Weik M, Dodge H, Scherzer C, Das S, Chibnik L, Blacker D, Gomez-Isla T, Oakley D, Frosch M, Hyman B, Demos C, Sigal G, Wohlstadter J, Serrano-Pozo A, Arnold S. Postmortem Associations Between Alzheimer Disease Pathology and Plasma pTau217, GFAP, and NfL in AD and AD-Related Dementias. Neurology 2026, 106: e214351. PMID: 41610380, PMCID: PMC12857747, DOI: 10.1212/wnl.0000000000214351.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMassachusetts Alzheimer's Disease Research CenterGlial fibrillary acidic proteinNon-AD dementiaAD neuropathologic changeAlzheimer's Disease Research CenterBrain autopsyCross-sectional associationsYears of follow-upGlial fibrillary acidic protein levelsAlzheimer's diseaseBanked plasma samplesFibrillary acidic proteinLinear regression modelsAD-related dementiaCohort studyMeso Scale DiscoveryNormal cognitionFollow-upGroups of participantsDementiaNeurological diagnosisAlzheimer's disease pathologyBiomarker levelsADRDTDP-43 proteinopathy
2025
Phosphorylated Ubiquitin as a Clinical Biomarker for Mitochondrial Damage in Neurodegenerative Diseases.
Fiesel F, Watzlawik J, Heckman M, Blumenfeld S, Rigby M, Kehili M, Lohmann K, Klein C, Narendra D, Scherzer C, Ertekin-Taner N, Graff-Radford N, Wszolek Z, Ross O, Springer W. Phosphorylated Ubiquitin as a Clinical Biomarker for Mitochondrial Damage in Neurodegenerative Diseases. Aging And Disease 2025 PMID: 41400571, DOI: 10.14336/ad.2025.1220.Peer-Reviewed Original ResearchCitationsAltmetricConceptsPhosphorylated ubiquitinAssociated with disease statusAutophagy-lysosome systemPINK1-ParkinDamaged mitochondriaHuman autopsy brainsMitochondrial damageAlzheimer's diseaseNeurodegenerative diseasesLysosomal dysfunctionUbiquitinCase-control seriesDiscovery platformSpectrum of mild cognitive impairmentMesoScale discovery platformParkinson's diseasePotential resilience factorsClinical biomarkersAlzheimerDisease riskAutopsy brainsNeurologically normal controlsDiagnostic markerMild cognitive impairmentMitophagyAssociation of Medication Use and 8-Year Mortality Risk in Patients With Parkinson Disease
Tuominen J, Riise T, Romanowska J, Flores-Torres M, Cortese M, Scherzer C, Bjornevik K, Igland J. Association of Medication Use and 8-Year Mortality Risk in Patients With Parkinson Disease. Neurology 2025, 105: e213783. PMID: 40644656, PMCID: PMC12264975, DOI: 10.1212/wnl.0000000000213783.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMortality riskInverse probabilityLevel 1 groupTarget trial designIntention-to-treat effectRisk of deathObservational cohort studyHealth registriesInverse probability of treatment weightingProbability of treatment weightingHistamine-2 blockersPotential confoundersCohort studyObservational analogsProgression of Parkinson's diseasePrescription drugsTrial designTreatment weightingTarget trialsParkinson's diseaseClinical trialsNonsteroidal anti-inflammatory drugsSleep aidsTargeted drugsOpioid analgesicsGenetic Analysis of the X Chromosome Associates Loci with Progression of Parkinson's Disease
Liao Y, Wu H, Wang J, Corvol J, Maple‐Grødem J, Campbell M, Elbaz A, Brice A, Schwarzschild M, Taba P, Kõks S, Beach T, Alves G, Tysnes O, Perlmutter J, Maiti B, van Hilten J, Barker R, Williams‐Gray C, Scherzer C, Liu G, Consortium I. Genetic Analysis of the X Chromosome Associates Loci with Progression of Parkinson's Disease. Movement Disorders 2025, 40: 1908-1918. PMID: 40459076, PMCID: PMC12353966, DOI: 10.1002/mds.30252.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsExpression quantitative trait lociHoehn and Yahr stage 3Cognitive declineMotor impairmentGenetic colocalization analysisGenome-wide significanceX chromosome variantsP-valueQuantitative trait lociYahr stage 3Associated with cognitive declineMale-only analysisAssociation lociLongitudinal cognitive declineTrait lociX chromosomeLewy body dementiaGenetic analysisGenetic variantsGenetic underpinningsColocalization analysisGlobal cognitive impairmentParkinson's diseaseLociMotor progressionImpact of Y chromosome loss on the risk of Parkinson's disease and progression
Wang J, Chen X, Du W, Lin C, Liao Y, Corvol J, Maple-Grødem J, Campbell M, Elbaz A, Lesage S, Brice A, Schwarzschild M, Taba P, Kõks S, Alves G, Tysnes O, Perlmutter J, Maiti B, van Hilten J, Barker R, Williams-Gray C, Scherzer C, Liu G, Consortium I, Liu G, Valentino R, Liao Z, Locascio J, Corvol J, Dong X, Maple-Grødem J, Campbell M, Elbaz A, Lesage S, Brice A, Mangone G, Growdon J, Hung A, Schwarzchild M, Hayes M, Wills A, Herrington T, Ravian B, Shoulson I, Taba P, Kõks S, Beach T, Cormier-Dequaire F, Alves G, Tysnes O, Perlmutter J, Heutink P, van Hilten J, Kasten M, Mollenhauer B, Trenkwalder C, Klein C, Barker R, Williams-Gray C, Marinus J, Scherzer C. Impact of Y chromosome loss on the risk of Parkinson's disease and progression. EBioMedicine 2025, 117: 105769. PMID: 40446401, PMCID: PMC12159889, DOI: 10.1016/j.ebiom.2025.105769.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsLoss of Y chromosomeSingle-nucleusWhole-genome sequencing dataGenome sequence dataDynamic gene expression analysisGenome-wide arraySingle-nucleus RNA sequencingY chromosome lossGene expression analysisChip genotypesAge-related somatic mutationSequence dataY chromosomeSingle-nucleus transcriptomesSnRNA-seqMale participantsRNA sequencingExpression analysisProgression of Parkinson's diseaseSomatic mutationsAge-related diseasesMagnetic resonance imagingNIHR Cambridge Biomedical Research CentreProgression of PDClinical phenotypeAn integrative systems-biology approach defines mechanisms of Alzheimer’s disease neurodegeneration
Leventhal M, Zanella C, Kang B, Peng J, Gritsch D, Liao Z, Bukhari H, Wang T, Pao P, Danquah S, Benetatos J, Nehme R, Farhi S, Tsai L, Dong X, Scherzer C, Feany M, Fraenkel E. An integrative systems-biology approach defines mechanisms of Alzheimer’s disease neurodegeneration. Nature Communications 2025, 16: 4441. PMID: 40393985, PMCID: PMC12092734, DOI: 10.1038/s41467-025-59654-w.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsDisease proteomicsDrosophila model of Alzheimer's diseaseAlzheimer's diseaseDisease neurodegenerationSystems-biology approachAlzheimer's disease neurodegenerationModel of Alzheimer's diseaseModify gene expressionAge-associated neurodegenerationDrosophila modelTau proteinGenetic screeningGenetic variantsGene expressionRelevant pathwaysDNA damageAmeliorate neurodegenerationDrosophilaYears of intensive investigationNeural progenitor cellsProteomicsNeurodegenerationNeuronal deathAlzheimerProgenitor cells
2024
Investigation of the genetic aetiology of Lewy body diseases with and without dementia
Wu L, Real R, Martinez-Carrasco A, Chia R, Lawton M, Shoai M, Bresner C, Blauwendraat C, Singleton A, Ryten M, Abramzon Y, Ahmed S, Alba C, Albert M, Bacikova D, Barrett M, Beach T, Bennett D, Besser L, Bigio E, Boeve B, Bohannan R, Caraway C, Palma J, Chia R, Dalgard C, Dickson D, Ding J, Faber K, Ferman T, Ferrucci L, Flanagan M, Foroud T, Ghetti B, Gibbs J, Goate A, Goldstein D, Graff-Radford N, Hu H, Hupalo D, Kaiser S, Kaufmann H, Kim R, Klein G, Kukull W, Kuzma A, Leverenz J, Lopez G, Mao Q, Martinez-McGrath E, Masliah E, Monuki E, Newell K, Norcliffe-Kaufmann L, Perkins M, Pletnikova O, Renton A, Resnick S, Ross O, Sabir M, Scherzer C, Scholz S, Serrano G, Shakkotai V, Sidransky E, Singleton A, Tanaka T, Tayebi N, Traynor B, Troncoso J, Viollet C, Walton R, Woltjer R, Wszolek Z, Black S, Gan-Or Z, Keith J, Masellis M, Rogaeva E, Aarsland D, Al-Sarraj S, Attems J, Ferrari R, Gentleman S, Hardy J, Hodges A, Love S, McKeith I, Morris C, Morris H, Palmer L, Pickering-Brown S, Reynolds R, Ryten M, Thomas A, Tilley B, Troakes C, Brett F, Brice A, Duyckaerts C, Lesage S, Brunetti M, Calvo A, Canosa A, Chiò A, Floris G, Logroscino G, Zecca C, Clarimon J, Diez-Fairen M, Fortea J, González-Aramburu I, Infante J, Lage C, Lleó A, Pastor P, Porcel-Molina L, Rodríguez-Rodríguez E, Sanchez-Juan P, Krüger R, May P, Xiromerisiou G, Scholz S, Traynor B, Williams N, Hu M, Ben-Shlomo Y, Grosset D, Hardy J, Morris H. Investigation of the genetic aetiology of Lewy body diseases with and without dementia. Brain Communications 2024, 6: fcae190. PMID: 38978726, PMCID: PMC11228432, DOI: 10.1093/braincomms/fcae190.Peer-Reviewed Original ResearchCitationsAltmetricConceptsGenome-wide association studiesParkinson's disease dementiaPhenotypic genome-wide association studiesAssociation studiesAccelerating Medicines Partnership - Parkinson’s disease initiativeLewy bodies/Parkinson's disease dementiaGenetic driversGenetic aetiologyDevelopment of dementiaLewy body diseasePatients of European ancestryRisk lociMotor symptom onsetEuropean ancestryDementiaBody diseaseMotor onsetDisease heterogeneityDisease pathwaysCognitive impairmentLewy bodiesSymptom onsetDisease initiationParkinson's disease patientsBiological mechanismsDisease progression strikingly differs in research and real-world Parkinson’s populations
Beaulieu-Jones B, Frau F, Bozzi S, Chandross K, Peterschmitt M, Cohen C, Coulovrat C, Kumar D, Kruger M, Lipnick S, Fitzsimmons L, Kohane I, Scherzer C. Disease progression strikingly differs in research and real-world Parkinson’s populations. Npj Parkinson's Disease 2024, 10: 58. PMID: 38480700, PMCID: PMC10937726, DOI: 10.1038/s41531-024-00667-5.Peer-Reviewed Original ResearchCitationsAltmetricConceptsNatural language processingLanguage modelLanguage processingGranular comparisonElectronic health record dataReal-world dataAvailability of real-world dataDownstream tasksHealth record dataAcademic hospital systemCharacterization of Parkinson's diseaseMass General BrighamReal worldData sourcesFox InsightHealth recordsMultiple data sourcesCombination of selection biasBiomarkers Cohort StudyResearch populationHospital systemIn-personParkinson's populationCohort studyRecord dataVenglustat in GBA1-related Parkinson's disease – Authors' reply
Sardi S, authors M, Giladi N, Alcalay R, Cuer G, Gasser T, Gurevich T, Höglinger G, Marek K, PaccheE C, Schapira A, Scherzer C, Simuni T, Minini P, Peterschmi M. Venglustat in GBA1-related Parkinson's disease – Authors' reply. The Lancet Neurology 2024, 23: 137-138. PMID: 38267178, DOI: 10.1016/s1474-4422(23)00470-2.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsAuthor replies
2023
Utilizing low‐volume PBMC samples from Alzheimer’s disease clinical research cohorts for immune cell RNA‐sequencing
Viera A, Bellier J, Runnels A, Touil H, Fitzpatrick C, Tuncali I, Greco G, Liu L, Chhatwal J, Johnson K, Scherzer C, Selkoe D, De Jager P, Sperling R, Yang H. Utilizing low‐volume PBMC samples from Alzheimer’s disease clinical research cohorts for immune cell RNA‐sequencing. Alzheimer's & Dementia 2023, 19 DOI: 10.1002/alz.082614.Peer-Reviewed Original ResearchConceptsPeripheral blood mononuclear cellsCell preparation tubesPeripheral immune systemT cellsPBMC samplesCD20+ B cellsCD8+ T cellsCD4+ T cellsPeripheral blood mononuclear cell samplesImmune systemPeripheral blood mononuclear cell collectionCD14+ monocytesBlood mononuclear cellsCD20 antibodyAnti-CD4B cellsRNeasy Micro KitMononuclear cellsFlow cytometryCell RNA sequencingPreparation tubesCell-type-specific proteomicsBlood samplesRNA sequencingCell number
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News
- November 12, 2025Source: American Parkinson Disease Association
Precision Medicine for Parkinson’s Disease: Inside Yale University’s APDA Research
- November 21, 2024
Three Yale School of Medicine-led Teams Awarded $18 Million to Advance Parkinson’s Disease Research
- November 07, 2024Source: For Humanity: The Yale Campaign
Stopping Parkinson’s—Even Before It Starts
- October 14, 2024
Precision Medicine for Parkinson’s: New Yale Center for Advanced Research
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Yale School of Medicine
101 College Street, Floor 10
New Haven, CT 06510
United States
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Adams Center for Parkinson's Disease Research
Academic Office
101 College Street, Fl 10, Rm Room 1029H
New Haven, CT 06510