- 1976 - 1977 Research Associate, Department of Neurology, Albert Einstein College of Medicine, Bronx, NY
- 1980 - 1985 Assistant Professor of Pathology, Albert Einstein College of Medicine, Bronx, NY
- 1985 - 1987 Associate Professor of Pathology, Albert Einstein College of Medicine, Bronx, NY
- 1987 - 1992 Associate Professor of Pathology (in Psychiatry), Columbia University College of Physicians & Surgeons, NY, NY
- 1992 - 2015 Professor of Pathology & Cell Biology (in Psychiatry) and Director, Division of Neuropathology, Columbia University College of Physicians & Surgeons, NY, NY
- 2015 - present Professor of Pathology & Cell Biology (in Psychiatry) and Director, Residency Training in Neuropathology, Columbia University College of Physicians & Surgeons, NY, NY
Areas of Expertise / Conditions Treated
- Professor of Pathology and Cell Biology (in Psychiatry)
- Director, Neuropathology Fellowship Program
- NewYork-Presbyterian / Columbia University Irving Medical Center
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- Great West (National)
- Medicare Managed Care
- Essential Plan
- Medicaid Managed Care
- Medicare Managed Care
- Select Care (Exchange)
- Local 1199
- Traditional Medicare
- Special Needs
- Columbia University Employee Plan
- Compass (Exchange)
- Empire Plan
- Medicare Managed Care
Credentials & Experience
Education & Training
- MD, PhD, 1976 Neurobiology (PhD), New York University School of Medicine
- Residency: Albert Einstein Medical Center
- Fellowship: 1980 Albert Einstein Medical Center
Committees, Societies, Councils
Association for the Advancement of Science
Society for Neuroscience
American Assocation of Neuropathologists
American Association for Neurochemistry
Our lab is interested in CNS glial cell development, function, and pathology. We study how astrocytes react to the presence of pathological changes and how pathological changes in astrocytes affect the other cells of the CNS.
In collaboration with Osama Al Dalahmah in Pathology and Vilas Menon in Neurology, we are using single nucleus RNASeq, a recent and powerful technique that allows us to explore gene expression of single cells of patients with neurological diseases. We have begun with Huntington disease, an inherited disorder characterized clinically by abnormal, involuntary movements and genetically by an expansion of CAG repeats in the huntingtin gene. We use fresh frozen brain specimens taken from the NY Brain Bank here at the Columbia Medical Center. In comparision to brain tissues of patients without neurological disease, we have found many significant alterations in neurons, glia, and microglia. The studies have also revealed substantial heterogeneity in transcription within individual cell types in both normal and diseased brain tissues. We are also studying transcriptional differences in the brains of individuals with Parkinson’s disease and comparing those to gene expressions in other neurological disorders.
In collaboration with Guomei Tang and David Sulzer of Neurology, Guy McKhann, Alexander Sosunov, and Xiaoping Wu of Neurosurgery, and Peter Sims of Systems Biology, we are studying the cellular and molecular changes in astrocytes and neurons that take place during the evolution of epilepsy and in the evolution of autistic-like behavior. Our collaborative group uses mouse models of Tuberous Sclerosis (TS), a disease characterized by seizures and commonly by autism-spectrum disorders, in which cells have constitutively activated mTOR. The mouse model replicates the formation of greatly enlarged neurons that are characteristic of TS and of focal cortical dysplasias. We find that these neurons are highly active and likely represent the cellular substrate of seizures. We also have performed RNASeq and ribosomal profiling and footprinting, which show us that many genes are transcriptionally regulated and also allow us to discover translationally-regulated gene expression.
As part of our studies on the neuropathology in autopsies of individuals who have died of SARS-CoV-2 infections, we discovered the deposition of amyloid protein, similar to that one sees in the brains of Alzheimer's patients. However, these individuals had no clinical or pathological signs of Alzheimer’s disease. Furthermore, we found similar deposits in the brains of people who had suffered severe hypoxia toward the ends of their lives, including children with heart anomalies.Thus, we think that these amyloid deposits are likely caused by hypoxia. We are studying what protein fragments are present in these deposits and what effects the deposits may have on brain structures in their vicinities.
- Cell Specification and Differentiation
- Glial Development and Pathology
- Tuberous Sclerosis/Epilepsy/Autism Spectrum Disorders
- Amyloid Deposition in the Central Nervous System
- Thompson Family Foundation Program for Accelerated Medicines Exploration in Alzheimer’s Disease and Related Disorders of The Nervous System (TAME-AD)
(PI: JE Goldman) "Deposition in the COVID-19 Brain"
- R21 AG075754 NIH/NINDS (OA Dalahmah, V Menon, JE Goldman, Co-PIs)
"Identifying shared and distinct cell type vulnerability across neurological diseases"
- R01NS118179 NIH/NINDS (PI: Kuo; JE Goldman, Co-I)
"Targeting cerebellar excitatory synapses for tremor progression"
07/01/2020 - 06/30/2025
- ASAP (Aligning Science Across Parkinson's).(D Sulzer, PI; JE Goldman, Collaborator)
"Adaptive Immunity in the Etiology and Progression of Parkinson's Disease"
- 3R25NS070697 NIH/NINDS; (M Elkind, PI; JE Goldman, Co-PI)
"Neurology Research Education and Mentorship Program"
- Lim RG, Al Dalahmah O, Wu Jie, Gold MP, Reidling JC, Tang G, Adam M, Dansu DK, Park H-J, Casaccia P, Miramontes R, Reyer-Ortiz AM, Lau A, Hickman R, Khan F, Paryani, Tang A, Ofori K, Miyoshi E, Michael N, Geller N, Flowers X, Vonsattel JP, Davidson S, Menon V, Swarup V, Fraenkel E, Goldman JE**, Thompson L** Single nuclei RNAseq analysis of HD mouse models and human brain reveals impaired oligodendrocyte maturation and potential role for thiamine metabolism. (**Co-senior authors). Nature Commun. 13:7791, 2022; doi: 10.1038/s41467-022-35388-x.
- Priemer DS, Rhodes C Harker, Karlovich E, Goldman JE. Aβ deposits in the neocortex of adult and infant hypoxic brains, including in cases of COVID-19. J Neuropathol Exp Neurol, 81:988-995, 2022. doi: 10.1093/jnen/nlac095
- Wu, X, Sosunov AA, Lado W, Teoh JJ, Ham A, Li H, Al Dalahmah O, Gill BJA, Arancio O, Schevon C, Frankel W, McKhann GM II, Sulzer D, Goldman JE, Tang G. Synaptic Hyperexcitability of Cytomegalic Pyramidal Neurons Contributes to Epileptogenesis in Tuberous Sclerosis?Complex. Cell Reports, 40:111085, 2022. doi: 10.1016/j.celrep.2022.111085.
- Thakur KT*, Miller EH*, Glendinning MD* ……. Agalliu D**, Uhlemann A-C**, Goldman JE**, Canoll PD** COVID-19 Neuropathology at Columbia University Irving Medical Center/New York Presbyterian Hospital (**Co-Senior authors). Brain, April 15, 2021. https://doi.org/10.1093/brain/awab148.
- Al-Dalahmah O, Thakur K, Nordvig A, Prust M, Roth W, Lignelli A, Uhlemann A-C, Miller EH, Kunnath-Velayudhan S, Del Portillo A, Liu Y, Lin C-C, Hargus G, Teich AF, Hickman R, Tanji K, Vonsattel JP, Goldman JE, Faust P, Canoll P. Vasculopathy, neuronophagia, and microglial nodules in a SARS-CoV-2 patient with cerebellar hemorrhage. Acta Neuropathol Commun, 8, 147 (2020). https://doi.org/10.1186/s40478-020-01024-2
- Sosunov A, Wu X,McGovern R, Mikell C, McKhann II GM*, Goldman JE* (2020) Abnormal mitosis in reactive astrocytes. Acta Neuropathologica Comm 8:47 https://doi.org/10.1186/s40478-020-00919-4 (*Co-Senior authors).
- Al-Dalahmah O, Sosunov AA,l Shaik A, Ofori K, Liu Y, Vonsattel JP, Adorjan I, Menon V, Goldman JE. Single-nucleus RNA-seq identifies Huntington disease astrocyte states. Acta Neuropathol Comm. 8:19, 2020 DOI: 10.1186/s40470-020-0880-]
- Sapi E, Kasliwala R, Ismail H, Torres JP, Oldakowski M, Markland S, Gaur G, Melillo A, Eisendle K, Liegner KB, Libien J, Goldman JE. Long-term Persistence of Borrelia burgdorferi Antigens and DNA in Tissues of a Patient with Lyme Disease. Antibiotics. 8.pil: E183. doi:10.3390/antibiotics8040183, 2019