Sreeganga Chandra, PhD
Associate Professor of Neurology and NeuroscienceDownloadHi-Res Photo
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Neurology
Fully Joint
Neuroscience
Fully Joint
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About
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Associate Professor of Neurology and Neuroscience
Biography
Sreeganga S. Chandra received her Ph.D. in Chemistry from Purdue University. In her postdoctoral research, she pursued her interest in neuronal cell biology and neurodegeneration in the lab of Thomas C. Südhof at UT Southwestern Medical Center at Dallas. She is currently an Associate Professor in the Departments of Neurology and Neuroscience.
Appointments
Neurology
Associate Professor TenureFully JointNeuroscience
Associate Professor TenureFully Joint
Other Departments & Organizations
- Chandra Lab
- Interdepartmental Neuroscience Program
- Kavli Institute for Neuroscience
- Movement Disorders
- Neural Disorders
- Neurology
- Neuroscience
- Neuroscience Track
- Program in Cellular Neuroscience, Neurodegeneration and Repair
- Wu Tsai Institute
- Yale Combined Program in the Biological and Biomedical Sciences (BBS)
- Yale Stem Cell Center
Education & Training
- PhD
- Purdue University (1997)
Research
Overview
- Role of the endolysosomal pathway in Parkinson's disease
- Protein palmitoylation and neuronal ceroid lipofuscinosis
- Identification of the physiological function of synucleins
- Role of CSP alpha in synapse maintenance
- Identification of novel synapse maintenance genes
Medical Research Interests
Neurodegenerative Diseases; Neurology; Neuronal Ceroid-Lipofuscinoses; Parkinson Disease; Receptors, Presynaptic; Synapses
- View Lab Website
Chandra Lab
Research at a Glance
Yale Co-Authors
Frequent collaborators of Sreeganga Chandra's published research.
Publications Timeline
A big-picture view of Sreeganga Chandra's research output by year.
Research Interests
Research topics Sreeganga Chandra is interested in exploring.
Leah Harmon
Pramod Mistry, MBBS, PhD, MA, MD
TuKiet Lam, PhD, BS
David A. Hafler, MD, FANA
Eduardo Martin-Lopez
Hongyu Zhao, PhD
17Publications
1,622Citations
Parkinson Disease
Synapses
Publications
2024
Single-cell transcriptomic and proteomic analysis of Parkinson’s disease brains
Zhu B, Park J, Coffey S, Russo A, Hsu I, Wang J, Su C, Chang R, Lam T, Gopal P, Ginsberg S, Zhao H, Hafler D, Chandra S, Zhang L. Single-cell transcriptomic and proteomic analysis of Parkinson’s disease brains. Science Translational Medicine 2024, 16: eabo1997. PMID: 39475571, DOI: 10.1126/scitranslmed.abo1997.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsProteomic analysisAlzheimer's diseasePrefrontal cortexBrain cell typesGenetics of PDParkinson's diseaseCell-cell interactionsChaperone expressionSingle-nucleus transcriptomesExpressed genesTranscriptional changesPostmortem human brainPostmortem brain tissueDiseased brainSynaptic proteinsSingle-cellDown-regulationBrain cell populationsBrain regionsCell typesNeurodegenerative disordersLate-stage PDParkinson's disease brainsDisease etiologyNeuronal vulnerabilityDecoding transcriptomic signatures of cysteine string protein alpha–mediated synapse maintenance
Wang N, Zhu B, Allnutt M, Grijalva R, Zhao H, Chandra S. Decoding transcriptomic signatures of cysteine string protein alpha–mediated synapse maintenance. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2320064121. PMID: 38833477, PMCID: PMC11181078, DOI: 10.1073/pnas.2320064121.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsSynapse maintenanceTranscriptional changesSynaptogenic adhesion moleculesGene ontology analysisKO miceKO brainMaintenance in vivoCell-cell interactionsGlial cellsSingle-nucleus transcriptomesOntology analysisCspADifferential expressionNeuron-glia interactionsAutophagy-related genesProtein AGenesCell typesNeurodegenerative diseasesInhibitory synapsesLittermate controlsSynaptic pathwaysAdhesion moleculesGlial responseSynapse
2023
Impaired pre-synaptic plasticity and visual responses in auxilin-knockout mice
Cheng X, Tang Y, Vidyadhara D, Li B, Zimmerman M, Pak A, Nareddula S, Edens P, Chandra S, Chubykin A. Impaired pre-synaptic plasticity and visual responses in auxilin-knockout mice. IScience 2023, 26: 107842. PMID: 37766983, PMCID: PMC10520332, DOI: 10.1016/j.isci.2023.107842.Peer-Reviewed Original ResearchCitationsAltmetricConceptsParkinson's diseasePyramidal cell synapsesVisual cortical functionSilicon probe recordingsPrimary visual cortexShort-term facilitationFamilial Parkinson's diseaseCortical dysfunctionMotor deficitsMotor symptomsCell synapsesCortical functionRepetitive stimulationVisual cortexOptokinetic responseReleasable poolProlonged stimulationLayer 4Visual responsesMiceSynaptic vesiclesEye movementsOrientation selectivityDysfunctionFunction mutationsα-Synuclein colocalizes with AP180 and affects the size of clathrin lattices
Vargas K, Colosi P, Girardi E, Park J, Harmon L, Chandra S. α-Synuclein colocalizes with AP180 and affects the size of clathrin lattices. Journal Of Biological Chemistry 2023, 299: 105091. PMID: 37516240, PMCID: PMC10470054, DOI: 10.1016/j.jbc.2023.105091.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsClathrin punctaClathrin assemblyEndocytic accessory proteinsΑ-synucleinPresynaptic membraneSynaptic vesicle cyclingImmuno-electron microscopyClathrin structuresAccessory proteinsClathrin latticesMembrane curvatureVesicle cyclingCell membranePresynaptic proteinsLipid monolayer systemProteinΓ-synucleinMembranePunctaAssemblyRelocalizesClathrinColocalizesVesicle sizeDeletionDopamine transporter and synaptic vesicle sorting defects underlie auxilin-associated Parkinson’s disease
Vidyadhara D, Somayaji M, Wade N, Yücel B, Zhao H, Shashaank N, Ribaudo J, Gupta J, Lam T, Sames D, Greene L, Sulzer D, Chandra S. Dopamine transporter and synaptic vesicle sorting defects underlie auxilin-associated Parkinson’s disease. Cell Reports 2023, 42: 112231. PMID: 36920906, PMCID: PMC10127800, DOI: 10.1016/j.celrep.2023.112231.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsParkinson's diseaseMotor deficitsDopamine transporterPathogenesis of PDNigral dopaminergic lossProgressive motor deficitsΑ-synuclein pathologyEarly-onset Parkinson's diseaseDopamine sequestrationDopaminergic vulnerabilityDopaminergic lossKO micePresynaptic sitesKO brainNeurochemical analysisDorsal striatumKnockout miceCardinal featuresReuptake kineticsL-DOPADiseaseSynaptic autophagyFunction mutationsDeficitsMiceα-Synuclein Pathology and Reduced Neurogenesis in the Olfactory System Affect Olfaction in a Mouse Model of Parkinson's Disease
Martin-Lopez E, Vidyadhara D, Liberia T, Meller S, Harmon L, Hsu R, Spence N, Brennan B, Han K, Yücel B, Chandra S, Greer C. α-Synuclein Pathology and Reduced Neurogenesis in the Olfactory System Affect Olfaction in a Mouse Model of Parkinson's Disease. Journal Of Neuroscience 2023, 43: 1051-1071. PMID: 36596700, PMCID: PMC9908323, DOI: 10.1523/jneurosci.1526-22.2022.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsΑ-syn tg miceΑ-Syn pathologyOlfactory bulb neurogenesisProjection neuronsParkinson's diseaseOlfactory dysfunctionMutant α-synucleinOlfactory deficitsOlfactory pathwaySyn pathologyBehavioral deficitsMouse modelΑ-synucleinOB granule cellsΑ-synuclein pathologyOlfactory systemMonths of ageReduced neurogenesisFunctional deficitsPeriglomerular cellsMotor progressionPathologic changesMultiple symptomsSynaptic terminalsGranule cells
2022
Pharmacological Mechanism of the Non-hallucinogenic 5‑HT2A Agonist Ariadne and Analogs
Cunningham M, Bock H, Serrano I, Bechand B, Vidyadhara D, Bonniwell E, Lankri D, Duggan P, Nazarova A, Cao A, Calkins M, Khirsariya P, Hwu C, Katritch V, Chandra S, McCorvy J, Sames D. Pharmacological Mechanism of the Non-hallucinogenic 5‑HT2A Agonist Ariadne and Analogs. ACS Chemical Neuroscience 2022, 14: 119-135. PMID: 36521179, PMCID: PMC10147382, DOI: 10.1021/acschemneuro.2c00597.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHead-twitch responseParkinson's diseaseHallucinogenic effectsTherapeutic effectTherapeutic potentialClinical therapeutic effectSevere motor deficitsNew drug classesRemarkable therapeutic effectsConsiderable therapeutic potentialComplete remissionRapid remissionMotor deficitsNeurological indicationsTwitch responseClinical resultsReceptor agonistClinical trialsPharmacological mechanismsDrug classesDopamine receptorsMembrane monoamine transporterPreclinical resultsPlasma membrane monoamine transporterGeriatric subjectsSubcellular Fractionation for the Isolation of Synaptic Components from the Murine Brain
Massaro Tieze S, Chandra S, Vidyadhara D. Subcellular Fractionation for the Isolation of Synaptic Components from the Murine Brain. Journal Of Visualized Experiments 2022 DOI: 10.3791/64574-v.Peer-Reviewed Original Research
2017
Glucosylsphingosine Promotes α-Synuclein Pathology in Mutant GBA-Associated Parkinson's Disease
Taguchi YV, Liu J, Ruan J, Pacheco J, Zhang X, Abbasi J, Keutzer J, Mistry PK, Chandra SS. Glucosylsphingosine Promotes α-Synuclein Pathology in Mutant GBA-Associated Parkinson's Disease. Journal Of Neuroscience 2017, 37: 9617-9631. PMID: 28847804, PMCID: PMC5628407, DOI: 10.1523/jneurosci.1525-17.2017.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsΑ-synuclein pathologyParkinson's diseaseCommon genetic risk factorGenetic risk factorsGaucher diseaseRisk factorsPD pathologyOligomeric α-synuclein speciesPD mouse brainPathological aggregationΑ-synuclein speciesHuman cellsAttractive therapeutic targetΑ-synuclein aggregationPrevalent neurodegenerative disorderGD patientsFunction mechanismPD riskMouse linesMutantsTherapeutic targetMutationsMouse brainNeurodegenerative disordersDiseaseGlucosylsphingosine accelerates α-synuclein pathology in GBA-associated Parkinson disease
Taguchi Y, Liu J, Ruan J, Pacheco J, Zhang X, Abbasi J, Keutzer J, Mistry P, Chandra S. Glucosylsphingosine accelerates α-synuclein pathology in GBA-associated Parkinson disease. Molecular Genetics And Metabolism 2017, 120: s129. DOI: 10.1016/j.ymgme.2016.11.338.Peer-Reviewed Original Research
News & Links
Media
- Many genes in the endolysosomal pathway are genetically linked to Parkinson's disease. We are investigating several genes that function in synaptic vesicle endocytosis.
- Synuclein null synapses showing a deficit in HRP-cholera toxin positive vesicles (black vesicles). This experiment in synuclein null neurons supports a physiological role for alpha-synuclein in synaptic vesicle endocytosis.
News
- December 15, 2024
Kavli Institute at Yale: 20 Years of Innovation
- November 07, 2024
Parkinson’s Disease Associated With Neuroinflammation in the Brain, New Analyses Reveal
- October 14, 2024
Precision Medicine for Parkinson’s: New Yale Center for Advanced Research
- August 30, 2024
Kavli Institute for Neuroscience Celebrates 20 Years with Symposium on Sept. 20
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