Isabella J. Perone
About
Biography
Isabella received her B.S. in neuroscience from the Johns Hopkins University, where she studied working memory in the Visual Learning Laboratory, as well as age-related cognitive decline in the Laboratory of Neurosciences at the National Institute on Aging at the NIH. Following her graduation, Isabella studied the age-related changes in mitochondrial metabolism associated with Alzheimer's disease at the Laboratory of Genetics and Genomics, at the National Institute on Aging, NIH. At Yale, she is a Gruber Science Fellow and she is a member of the Arnsten lab where she studies the effects of calcium dysregulation on age-related cognitive decline and Alzheimer's pathology in rhesus macaques.
Education & Training
- MPhil
- Yale University, Interdepartmental Neuroscience Program
- Post-Baccalaureate IRTA
- National Institutes of Health
- BS
- The Johns Hopkins University, Neuroscience
Research
Research at a Glance
Yale Co-Authors
Frequent collaborators of Isabella J. Perone's published research.
Publications Timeline
A big-picture view of Isabella J. Perone's research output by year.
Alvaro Duque, PhD
Christopher van Dyck, MD
Juan Arellano, PhD
Pasko Rakic, MD, PhD
Yury M. Morozov, PhD
Amy Arnsten, PhD
5Publications
6Citations
Publications
Featured Publications
Key Roles of CACNA1C/Cav1.2 and CALB1/Calbindin in Prefrontal Neurons Altered in Cognitive Disorders
Datta D, Yang S, Joyce M, Woo E, McCarroll S, Gonzalez-Burgos G, Perone I, Uchendu S, Ling E, Goldman M, Berretta S, Murray J, Morozov Y, Arellano J, Duque A, Rakic P, O’Dell R, van Dyck C, Lewis D, Wang M, Krienen F, Arnsten A. Key Roles of CACNA1C/Cav1.2 and CALB1/Calbindin in Prefrontal Neurons Altered in Cognitive Disorders. JAMA Psychiatry 2024, 81 PMID: 38776078, PMCID: PMC11112502, DOI: 10.1001/jamapsychiatry.2024.1112.Peer-Reviewed Original ResearchCitationsAltmetricConceptsDorsolateral prefrontal cortexPrefrontal cortexLayer III pyramidal cellsWorking memoryCognitive disordersNeuronal firingPrimate dorsolateral prefrontal cortexPyramidal cellsSpatial working memoryWorking memory performanceRisk of mental disordersCalcium-related proteinsReduced neuronal firingL-type calcium channel Cav1.2GluN2B-NMDA receptorsL-type calcium channel activityPrefrontal neuronsL-type calcium channel blockerMemory performanceL-type calcium channelsMental disordersRisk of cognitive disordersCognitive behaviorProtein expressionAssociated with increased riskNanoscale imaging of pT217-tau in aged rhesus macaque entorhinal and dorsolateral prefrontal cortex: Evidence of interneuronal trafficking and early-stage neurodegeneration.
Datta D, Perone I, Wijegunawardana D, Liang F, Morozov YM, Arellano J, Duque A, Xie Z, van Dyck CH, Arnsten AFT. Nanoscale imaging of pT217-tau in aged rhesus macaque entorhinal and dorsolateral prefrontal cortex: Evidence of interneuronal trafficking and early-stage neurodegeneration. BioRxiv 2023 PMID: 37986900, DOI: 10.1101/2023.11.07.566046.Peer-Reviewed Original ResearchLocalization of PDE4D, HCN1 channels, and mGluR3 in rhesus macaque entorhinal cortex may confer vulnerability in Alzheimer’s disease
Datta D, Perone I, Morozov Y, Arellano J, Duque A, Rakic P, van Dyck C, Arnsten A. Localization of PDE4D, HCN1 channels, and mGluR3 in rhesus macaque entorhinal cortex may confer vulnerability in Alzheimer’s disease. Cerebral Cortex 2023, 33: 11501-11516. PMID: 37874022, PMCID: PMC10724870, DOI: 10.1093/cercor/bhad382.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHCN1 channelsTau pathologyGlutamate synapsesEntorhinal cortexCalcium actionInternal calcium releaseEntorhinal cortex stellate cellsDorsolateral prefrontal cortexSusceptible neuronsInitial pathologySelective vulnerabilityEtiological factorsTau phosphorylationStellate cellsAlzheimer's diseaseSpecific neuronsCalcium releasePrefrontal cortexCortexSynapse strengthPathologyCalcium signalingCalbindinDiseaseNeuronsMitochondrial SIRT3 Deficiency Results in Neuronal Network Hyperexcitability, Accelerates Age-Related Aβ Pathology, and Renders Neurons Vulnerable to Aβ Toxicity.
Perone I, Ghena N, Wang J, Mackey C, Wan R, Malla S, Gorospe M, Cheng A, Mattson MP. Mitochondrial SIRT3 Deficiency Results in Neuronal Network Hyperexcitability, Accelerates Age-Related Aβ Pathology, and Renders Neurons Vulnerable to Aβ Toxicity. Neuromolecular Medicine 2022 PMID: 35749057, DOI: 10.1007/s12017-022-08713-2.Peer-Reviewed Original ResearchSIRT3 Haploinsufficiency Aggravates Loss of GABAergic Interneurons and Neuronal Network Hyperexcitability in an Alzheimer's Disease Model.
Cheng A, Wang J, Ghena N, Zhao Q, Perone I, King TM, Veech RL, Gorospe M, Wan R, Mattson MP. SIRT3 Haploinsufficiency Aggravates Loss of GABAergic Interneurons and Neuronal Network Hyperexcitability in an Alzheimer's Disease Model. The Journal Of Neuroscience : The Official Journal Of The Society For Neuroscience 2020, 40: 694-709. PMID: 31818974, PMCID: PMC6961992, DOI: 10.1523/JNEUROSCI.1446-19.2019.Peer-Reviewed Original Research
Academic Achievements and Community Involvement
honor Gruber Science Fellowship
Yale University AwardThe Gruber FoundationDetails03/10/2020United States