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| First Name: | Stephen D. | | Last Name: | Ginsberg | | Title: | Associate Professor | | Advanced Degrees: | Ph.D. | | Affiliation: | Nathan Kline Institute/NYU Langone School of Medicine | | Department: | Center for Dementia Research and Depts. of Psychiatry and Physiology & Neuroscience | | Street Address 1: | 140 Old Orangeburg Road | | City: | Orangeburg | | State/Province: | NY | | Zip/Postal Code: | 10962 | Country/Territory: | U.S.A. | | Phone: | 845-398-2170 | | Fax: | 845-398-5422 | | Email Address: |  |
Disclosure:
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Member reports no financial or other potential conflicts of interest. [Last Modified: 14 September 2010]
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View all comments by Stephen D. Ginsberg
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Aging Process, Neurodevelopmental Disorders (Down syndrome, etc.), Alzheimer Disease, Parkinson Disease, Tauopathies
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Neurobiology, Tau/Cytoskeleton, Molecular and Cell biology, DNA microarrays, Apoptosis/Cell cycle, Neuropathology, Oxidative Stress, Bioinformatics/Statistics, Animal Models, A-beta PP/A-beta, Microscopy, Genetics
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University, Research institute
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My interests include neurodegeneration, single cell RNA analysis, and lesion-induced synaptic plasticity.
The principal focus of the Ginsberg laboratory is to delineate cellular and molecular mechanisms underlying synaptic and dendritic reorganization following various brain injuries, including excitotoxicity, specific lesions, and neurodegeneration. The hippocampal formation, a brain region critical for learning and memory, is the main region analyzed, with particular emphasis on identifying mechanisms that govern synaptic reorganization within dentate gyrus granule cells and dendrites. We conduct experiments on animal models of synaptic plasticity and neurodegeneration. Mice are used as experimental subjects because of a similar cellular organization of the dorsal hippocampal formation to humans; genetically altered mice are used to analyze specific gene/protein products. In addition, the laboratory studies human brain tissues obtained from patients with no cognitive impairment (NCI), mild cognitive impairment (MCI), and Alzheimer''''s disease (AD). A multidisciplinary approach of surgical, state-of-the-art molecular biology, immunohistochemical, and imaging techniques are utilized as part of the experimental design. Particular emphasis is placed upon analyzing single neurons in vivo as a means of understanding cellular events occurring locally at synaptic and somatodendritic sites. For example, lesion paradigms in mice are combined with regional and single cell mRNA amplification techniques and cDNA microarray "DNA chip" technology; we then assess several classes of transcripts simultaneously, including glutamate receptors, dopamine receptors, synaptic proteins, cytoskeletal elements, neurotrophins, cell death genes, and transcription factors from individ
ual neurons and their processes. These studies enable a "molecular fingerprint" of the hippocampus as well as specific neurons within the region following the initial injury, denervation, and reactive synaptogenesis. Furthermore, these studies aim to elucidate markers for early cell-specific synaptic and neurodegenerative changes that can be applied to other models of activity dependence and neurodegenerative disorders. |
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. 2010 Jul 22. [Epub ahead of print]. PMID: 20655510.
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 up regulation in mild cognitive impairment and Alzheimer’s disease. J. Alzheimers Dis., in press.
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.
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. NIHMSID: 93536.
Altar, C.A., Vawter, M., and Ginsberg, S.D.: Target identification for CNS diseases by transcriptional profiling. Neuropsychopharmacology, 34: 18-54, 2008. PMID: 18923405. NIHMSID: 76513.
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.
Ginsberg, S.D.: Transcriptional profiling of small samples in the central nervous system. Methods Mol. Biol., 439: 147-158, 2008. PMID: 18370101. NIHMSID: 94064.
Ginsberg, S.D., Che, S., Wuu, J., Counts, S.E., and Mufson, E.J.: Down regulation of trk but not p75NTR gene expression in single cholinergic basal forebrain neurons mark the progression of Alzheimer’s disease. J. Neurochem., 97: 475-487, 2006. PMID: 16539663.
Ginsberg, S.D., Che, S., Counts, S.E., and Mufson, E.J.: Single cell gene expression profiling in Alzheimer’s disease. NeuroRx, 3: 302-318, 2006. PMID: 16815214.
Ginsberg, S.D., Che, S., Counts, S.E., and Mufson, E.J.: Shift in the ratio of 3-repeat tau and 4-repeat tau mRNAs in individual cholinergic basal forebrain neurons in mild cognitive impairment and Alzheimer’s disease. J. Neurochem., 96: 1401-1408, 2006. PMID: 16478530. |
The selective vulnerability and underlying mechanism(s) for the deposition of pathologic hallmarks, and their subsequent function(s) that lead to dementia. |
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