Vanitha Nithianandam
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Research Scientist
Biography
Dr. Nithianandam was recruited to the Adams Center from Harvard in 2025. She is a Research Scientist focusing on the Parkinson’s progression locus RIMS2 and protein clearance pathway, autophagy.
Dr. Nithianandam’s journey in neuroscience began at the National Brain Research Centre in India, supported by a prestigious national scholarship from the Indian Academy of Sciences, and was further solidified through clinical exposure during her internship at PGIMER Hospital, Chandigarh. She earned her PhD in Molecular and Cell Biology from Academia Sinica and the National Defense Medical Center in Taiwan, where she discovered and provided the first in vivo evidence of a novel dynamic form of neuronal actin, termed actin blobs. As a postdoctoral researcher with Professor Mel Feany at Harvard Medical School, she investigated the role of proteins implicated in Alzheimer’s and Parkinson’s disease in the regulation of autophagy, with key findings published in Nature Communications. Her integrative work across Drosophila, mice models, and iPSC-derived neurons has advanced our understanding of neuronal development and degeneration.
At Yale, Dr. Nithianandam continues to explore autophagy and RIMS2 as a therapeutic target in Parkinson’s disease, driven by her enduring commitment to uncovering mechanisms of neurodegeneration and identifying novel avenues for intervention.
Departments & Organizations
- Adams Center for Parkinson's Disease Research
Education & Training
- Postdoctoral Researcher
- BWH, Harvard Medical School
- PhD
- Academia Sinica, Molecular and Cell Biology (2018)
Research
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Medical Research Interests
ORCID
0000-0002-0740-0758
Publications
Featured Publications
Integrative analysis reveals a conserved role for the amyloid precursor protein in proteostasis during aging
Nithianandam V, Bukhari H, Leventhal M, Battaglia R, Dong X, Fraenkel E, Feany M. Integrative analysis reveals a conserved role for the amyloid precursor protein in proteostasis during aging. Nature Communications 2023, 14: 7034. PMID: 37923712, PMCID: PMC10624868, DOI: 10.1038/s41467-023-42822-1.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAmyloid precursor proteinPrecursor proteinNormal function of APPFunction of amyloid precursor proteinPathogenesis of Alzheimer's diseaseRelevant to Alzheimer's diseaseAlzheimer's diseaseDrosophila orthologMutant fliesTauopathy modelGenetic screeningAB peptideCellular signalingCellular pathwaysProteomic studiesMitochondrial functionProteostasisNeurodegenerative diseasesIntegrated analysisLipid metabolismRegulating autophagyNucleic acidsSingle cellsAmyloidTGFB signalingActin blobs prefigure dendrite branching sites
Nithianandam V, Chien C. Actin blobs prefigure dendrite branching sites. Journal Of Cell Biology 2018, 217: 3731-3746. PMID: 30042190, PMCID: PMC6168249, DOI: 10.1083/jcb.201711136.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsPathways controlling neurotoxicity and proteostasis in mitochondrial complex I deficiency
Nithianandam V, Sarkar S, Feany M. Pathways controlling neurotoxicity and proteostasis in mitochondrial complex I deficiency. Human Molecular Genetics 2024, 33: 860-871. PMID: 38324746, PMCID: PMC11070137, DOI: 10.1093/hmg/ddae018.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsComplex I deficiencyI deficiencyElectron transport chain componentsMitochondrial complex I deficiencyMitochondrial respiratory chainProteostasis failureMitochondrial genesProteostasis machineryDrosophila retinaProteostasis dysfunctionGenetic screeningProteostasisRespiratory chainAge-related neurodegenerationProtein degradationMitochondrial encephalomyopathyComplex IKinome screenGenetic modelsChain componentsNeurodegenerationProteinPathwayOxidative stressDrosophilaA Drosophila model relevant to chemotherapy-related cognitive impairment
Torre M, Bukhari H, Nithianandam V, Zanella C, Mata D, Feany M. A Drosophila model relevant to chemotherapy-related cognitive impairment. Scientific Reports 2023, 13: 19290. PMID: 37935827, PMCID: PMC10630312, DOI: 10.1038/s41598-023-46616-9.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsChemotherapy-related cognitive impairmentAdverse effects of treatmentDrosophila modelChemotherapeutic agent cisplatinDisease-modifying therapiesTesting chemotherapyEffects of treatmentNeurological deficitsImmunohistochemical analysisDissection of pathwaysChemotherapy patientsAgent cisplatinHistological alterationsDrosophila tissuesAdult DrosophilaChemotherapyDrosophilaAdverse effectsGenetic approachesMemory deficitsOxidative stressCisplatinCancer survivorsDoxorubicinMechanistic dissectionThe putative Neuronatin imprint control region is an enhancer that also regulates the Blcap gene
Thamban T, Sowpati D, Pai V, Nithianandam V, Abe T, Shioi G, Mishra R, Khosla S. The putative Neuronatin imprint control region is an enhancer that also regulates the Blcap gene. Epigenomics 2019, 11: 251-266. PMID: 30672333, DOI: 10.2217/epi-2018-0060.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsImprinting control regionControl regionAllele-specific DNA methylationNnat expressionActive paternal alleleAbstractText Label="MATERIALS &AbstractText Label="AIM">Histone modificationsTranscriptional regulationPaternal alleleDNA methylationIntronRegulatory potentialEpigenetic profilesBLCAPNnatGenesExpressionHistoneAllelesDeletionTranscriptionNeuronatinMiceDomainTranscriptional programs mediating neuronal toxicity and altered glial-neuronal signaling in a Drosophila knock-in tauopathy model
Bukhari H, Nithianadam V, Battaglia R, Cicalo A, Sarkar S, Comjean A, Hu Y, Leventhal M, Dong X, Feany M. Transcriptional programs mediating neuronal toxicity and altered glial-neuronal signaling in a Drosophila knock-in tauopathy model. Genome Research 2024, 34: gr.278576.123. PMID: 38599684, PMCID: PMC11146598, DOI: 10.1101/gr.278576.123.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsGenetic contextNon-cell-autonomous regulationMicrotubule-associated protein tauHuman diseasesGlial-neuronal signalingGene regulatory programsKnock-in fliesTau P301L mutationFrontotemporal dementiaProtein interaction networkModel of tauopathyAge-dependent neurodegenerationSingle-cell RNA sequencingCell signaling pathwaysExperimental model organismAccumulate DNA damageModel of frontotemporal dementiaAutosomal dominant formSingle-cell sequencing analysisPathways of neurotoxicityProtein tauP301L mutationTauopathy modelNeuronal cell typesSequence analysis
2017
Cofilin dependent dynamic actin clusters promote dendrite branching
Nithianandam V, Chien C. Cofilin dependent dynamic actin clusters promote dendrite branching. Cells And Development 2017, 145: s127. DOI: 10.1016/j.mod.2017.04.349.Peer-Reviewed Original Research
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