Stephen D. Ginsberg, PhD
Nathan S. Kline Institute for Psychiatric Research Ginsberg Lab Page
Associate Professor; Department of Psychiatry, Department of Physiology & Neuroscience
NYU Langone Medical Center Ginsberg NYU Page
P: (845)398-2170 (office)
P: (845)398-XXXX (lab)
Click for publications
BA, College of Arts and Sciences, Cornell University, Ithaca, NY
PhD, Mount Sinai Medical Center, New York, NY
Fellow, The Johns Hopkins University School of Medicine, Baltimore, MD
Fellow, University of Pennsylvania School of Medicine, Philadelphia, PA
Awards and Honors
Graduated cum laude in Psychology, Cornell University
Dr. Ginsberg’s editorial responsibilities include serving as Academic Editor for PLoS One and Associate Editor for Translational Neuroscience. Steve also currently serves on the Editorial Board of 8 journals, and acted as Guest Editor/Section Editor for 3 journal issues.
Dr. Ginsberg sits on Advisory Boards for the Autism Tissue Program (ATP) tissue advisory board (TAB) and the Rett syndrome International Rett Syndrome Foundation (IRSF).
Dr. Ginsberg is the Chairman of the Institutional Animal Care and Use Committee (IACUC) at the Nathan Kline Institute (NKI). Steve is a member of the Department of Psychiatry Appointments and Promotions Committee (DAPC) at the New York University Langone Medical Center (NYULMC), and is on Steering Committee for the Center for Excellence (CoE) on Brain Aging at NYULMC.
The principal focus of the Ginsberg laboratory in the Center for Dementia Research (CDR) is to delineate cellular and molecular mechanisms underlying cellular, synaptic, and dendritic reorganization following neurodevelopmental and neurodegenerative brain insults. The Ginsberg laboratory employs the use of animal and cellular models of neurodegeneration as well as human postmortem brain tissues for functional genomic and proteomic based studies. Steve’s underlying hypothesis is that individual cell types are likely to have unique patterns of gene and protein expression under normative conditions that are altered in pathological states, which drives subsequent neurodegeneration. Indeed, the molecular and cellular basis of why certain neuronal populations are vulnerable to neurodegeneration, often termed “selective vulnerability”, can be elucidated by discrete cell analysis more readily than by utilizing regional and total brain preparations. The hippocampal formation and cholinergic basal forebrain, brain regions critical for learning and memory, are the main structures analyzed, with particular emphasis given to identifying mechanisms that underlie changes within specific cell types, including cholinergic basal forebrain (CBF) neurons, dentate gyrus granule cells, CA1 & CA3 pyramidal neurons, and entorhinal cortex stellate cells. Experiments are conducted on animal and cellular models of neurodegeneration, including mouse models of amyloid overexpression, Down syndrome (DS), and tauopathy. The Ginsberg lab also conducts parallel studies on postmortem human brain tissues accrued from subjects diagnosed with Alzheimer’s disease (AD), DS, mild cognitive impairment (MCI), and nondemented controls with no cognitive impairment (NCI). Dr. Ginsberg is also spearheading a program to investigate selective vulnerability of specific pyramidal neurons and GABAergic interneurons in schizophrenia (SZ) and major depressive disorder (MDD).
The Ginsberg Laboratory has provided essential data in human and relevant mouse models that compare and contrast cells that degenerate (e.g., CBF neurons, CA1 hippocampal pyramidal neurons, and glutamatergic neocortical pyramidal neurons) versus cells that are relatively spared within these specific paradigms (e.g., dentate gyrus granule cells). Dr. Ginsberg is one of the relatively few neuroscientists that conduct expression profiling research at the single cell level consistently. Dr. Ginsberg developed his own RNA amplification technology termed terminal continuation (TC) RNA amplification which is employed in conjunction with microarray and qPCR based investigations of gene expression at the single cell level. The Ginsberg laboratory has just developed a new technology for the amplification of microRNAs termed miRNA signature sequence amplification (SSAM) for biomarker discovery science. miRNAs are a short 17-25 nucleotide class of non-protein coding RNAs (ncRNAs) that have been shown to have critical functions in a wide variety of biological processes. One major obstacle when profiling miRNAs is their low expression level. miRNAs are estimated to constitute only 0.01% of total RNA. As a result, large quantities of starting materials were required for miRNA profiling until the advent of the developing SSAM technology.
Selected publications since 2008(from a total of 75 peer-reviewed manuscripts and 23 book chapters)
Ginsberg, S.D.: Transcriptional profiling of small samples in the central nervous system. Methods Mol. Biol., 439: 147-158, 2008. PMID: 18370101. PMCID: PMC2648843.
Levine, S., Saltzman, A., and Ginsberg, S.D.: Different inflammatory reactions to vitamin D(3) among the lateral, third and fourth ventricular choroid plexuses of the rat. Exp. Mol. Pathol., 85: 117-121, 2008. PMID: 18675267.
Mufson, E.J., Counts, S.E., Perez, S., and Ginsberg, S.D.: Cholinergic system during the progression of Alzheimer’s disease: therapeutic implications. Expert Rev. Neurother., 8: 1703-1718, 2008. PMID: 18986241. PMCID: PMC2631573.
Alldred, M.J., Che, S., and Ginsberg, S.D.: Terminal continuation (TC) RNA amplification enables expression profiling using minute RNA input obtained from mouse brain. Int. J. Mol. Sci., 9: 2091-2104, 2008. PMID: 19165351. PMCID: PMC2629436.
Ginsberg, S.D., Che, S., Counts, S.E., and Mufson, E.J.: Gene expression abnormalities mark the progression of Alzheimer's disease. In Sun, M.K. (ed): Research Progress in Alzheimer's Disease and Dementia, Volume 3, Hauppauge: Nova Science Publishing, pp. 25-58, 2008. ISBN-13: 978-1-60021-960-3.
Ginsberg, S.D.: Single and rare cell analysis-amplification methods. T7 based amplification protocols. In Bosio, A. and Gerstmayer, B. (eds): Microarrays in Inflammation. Progress in Inflammation Research, Basel: Birkhäuser-Verlag, pp. 81-94, 2008. ISBN-13: 978-3-7643-8333-6.
Altar, C.A., Vawter, M., and Ginsberg, S.D.: Target identification for CNS diseases by transcriptional profiling. Neuropsychopharmacology, 34: 18-54, 2009. PMID: 18923405. PMCID: PMC2675576.
Alldred, M.J., Che, S., and Ginsberg, S.D.: Terminal continuation (TC) RNA amplification without second strand synthesis. J. Neurosci. Meth., 177: 381-385, 2009. PMID: 19026688. PMCID: PMC2659495.
Levine, S., Saltzman, A., Levy, E., and Ginsberg, S.D.: Systemic pathology in aged mouse models of Down's syndrome and Alzheimer's disease. Exp. Mol. Pathol., 86: 18-22, 2009. PMID: 19041304. PMCID: PMC2659493.
Choi, J.H.K., Berger, J.D., Mazzella, M.J., Morales-Corraliza, J., Nixon, R.A., Ginsberg, S.D., Levy, E., and Mathews, P.M.: Age-dependent dysregulation of brain amyloid precursor protein in the Ts65Dn Down syndrome mouse model. J. Neurochem., 110: 1818-1827, 2009. PMID: 19619138. PMCID: PMC2744432.
Jiang, Y., Mullaney, K.A., Peterhoff, C.M., Che, S., Schmidt, S.D., Boyer-Boiteau, A., Ginsberg, S.D., Cataldo, A.M., Mathews, P.M., and Nixon, R.A.: Alzheimer’s-related endosome dysfunction in Down syndrome is Abeta-independent but requires APP and is reversed by BACE-1 inhibition. Proc. Natl. Acad. Sci. USA, 107: 1630-1635, 2010. PMID: 20080541. PMCID: PMC2824382.
Ginsberg, S.D.: Alterations in discrete glutamate receptor subunits in adult mouse dentate gyrus granule cells following perforant path transection. Anal. Bioanal. Chem., 397: 3349-3358, 2010. PMID: 20577723. PMCID: PMC3149099.
Levine, S., Saltzman, A., and Ginsberg, S.D.: Mitotic figures in the median eminence of the hypothalamus. Neurochem. Res., 35: 1743-1746, 2010. PMID: 20680457. PMCID: PMC3148030.
Haskew-Layton, R.E., Payappilly, J.B., Smirnova, N.A., Ma, T.C., Chan, K.K., Murphy, T.H., Guo, H., Langley, B., Sultana, R., Butterfield, D.A., Santagata, S., Alldred, M.J., Gazaryan, I.G., Bell, G.W., Ginsberg, S.D., and Ratan, R.R.: Controlled enzymatic production of astrocytic hydrogen peroxide protects neurons from oxidative stress via an Nrf2 independent pathway. Proc. Natl. Acad. Sci. USA, 107: 17385-17390, 2010. PMID: 20855618. PMCID: PMC2951414.
Ginsberg, S.D., Alldred, M.J., Counts, S.E., Cataldo, A.M., Neve, R.L., Jiang, Y., Wuu, J., Chao, M.V., Mufson, E.J., Nixon, R.A., and Che, S.: Microarray analysis of hippocampal CA1 neurons implicates early endosomal dysfunction during Alzheimer’s disease progression. Biol. Psychiatry, 68: 885-893, 2010. PMID: 20655510. PMCID: PMC2965820.
Kaur, G., Mohan, P., Pawlik, M., DeRosa, S., Fajiculay, J., Che, S., Grubb, A., Ginsberg, S.D., Nixon, R.A., and Levy, E: Cystatin C rescues degenerating neurons in a cystatin B-knockout mouse model of progressive myoclonus epilepsy. Am. J. Pathol., 177: 2256-2267, 2010. PMID: 20889561. PMCID: PMC2966785.
Ginsberg, S.D.: Microarray use for the analysis of the CNS. In Squire, L.R. (ed): Encyclopedia of Neuroscience, Volume 5, Oxford: Academic Press, pp. 835-841, 2009. ISBN-13: 978-0-08-045046-9.
Ginsberg, S.D.: Gene microarrays. In Kompoliti, K., and Verhagen Metman, L. (eds): Encyclopedia of Movement Disorders. Oxford: Academic Press, pp. 538-540, 2010. ISBN: 978-0-12-374101-1.
Mufson, E.J., Counts, S.E., Perez, S.E., and Ginsberg, S.D.: Cholinergic systems in aging and Alzheimer’s disease: neurotrophic and molecular analysis. In Koob, G.F., Le Moal, M., and Thompson, R.F. (eds): Encyclopedia of Behavioral Neuroscience, Volume 1, Oxford: Academic Press, pp. 249-256, 2010. ISBN-13: 978-0-08-044732-2.
Devi, L., Alldred, M.J., Ginsberg, S.D., and Ohno, M.: Sex- and brain region-specific acceleration of beta-amyloidogenesis following behavioral stress in a mouse model of Alzheimer's disease. Molecular Brain, 3: 34, 2010. PMID: 21059265. PMCID: PMC2988063.
Ginsberg, S.D., Mufson, E.J., Counts, S.E., Wuu, J., Alldred, M.J., Nixon, R.A., and Che, S.: Regional selectivity of rab5 and rab7 protein upregulation in mild cognitive impairment and Alzheimer’s disease. J. Alzheimers Dis., 22: 631-639, 2010. PMID: 20847427. PMCID: PMC3031860.
Counts, S.E., Perez, S.E., Ginsberg, S.D., and Mufson, E.J.: Neuroprotective role for galanin in Alzheimer’s disease. EXS, 102: 143-162, 2010. PMID: 21299067. PMCID: PMC3117305.
Levine, S., Saltzman, A., and Ginsberg, S.D.: Vacuolar pathology in the median eminence of the hypothalamus after hyponatremia. J. Neuropathol. Exp. Neurol., 70: 151-156, 2011. PMID: 21343884. PMCID: PMC3074179.
Ginsberg, S.D., Mufson, E.J., Alldred, M.J., Counts, S.E., Wuu, J., Nixon, R.A., and Che, S.: Upregulation of select rab GTPases in cholinergic basal forebrain neurons in mild cognitive impairment and Alzheimer's disease. J. Chem. Neuroanat., 42: 102-110, 2011. PMID: 21669283. PMCID: PMC3163754.
Counts, S.E., Che, S., Ginsberg, S.D., and Mufson, E.J.: Gender differences in neurotrophin and glutamate receptor expression in cholinergic nucleus basalis neurons during the progression of Alzheimer's disease. J. Chem. Neuroanat., 42: 111-117, 2011. PMID: 21397006. PMCID: PMC3155625.
Ginsberg, S.D., Che, S., Hashim, A., Zavadil, J., Cancro, R., Lee, S.H., Petkova, E., Sershen, H.W., and Volavka, J.: Differential regulation of catechol-O-methyltransferase expression in a mouse model of aggression. Brain Struct. Funct. 2011 Apr 22. [Epub ahead of print]. PMID: 21512897. NIHMSID: 303942.
Mufson, E.J., Perez, S., Kelley, C.M., Chu, S., Galarza, A., Blakely, S., and Ginsberg, S.D.: Fixation protocols for neurohistology: neurons to genes. In Walz, C.M., and Doucette, R. (eds): Neurohistology and Imaging: Basic Techniques, Totowa: Humana Press, in press.
Ginsberg, S.D., Alldred, M.J., and Che, S.: Gene expression profiling using the terminal continuation (TC) RNA amplification method for small input samples in neuroscience. In Karamanos, Y. (ed): Expression Profiling in Neuroscience, Neuromethods, Volume 64. New York: Humana Press, in press. ISBN 978-1-61779-447-6.
Ginsberg, S.D., Alldred, M.J., and Che, S.: Gene expression levels assessed by CA1 pyramidal neuron and regional hippocampal dissections in Alzheimer's disease. Neurobiol. Dis., in press. Jul 28. [Epub ahead of print]. PMID: 21821124. NIHMSID: 315619.