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      Pluripotent stem cells in neuropsychiatric disorders

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          Abstract

          Neuropsychiatric disorders place an enormous medical burden on patients across all social and economic ranks. The current understanding of the molecular and cellular causes of neuropsychiatric disease remains limited, which leads to a lack of targeted therapies. Human-induced pluripotent stem cell (iPSC) technology offers a novel platform for modeling the genetic contribution to mental disorders and yields access to patient-specific cells for drug discovery and personalized medicine. Here, we review recent progress in using iPSC technology to model and potentially treat neuropsychiatric disorders by focusing on the most prevalent conditions in psychiatry, including depression, anxiety disorders, bipolar disorder and schizophrenia.

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          Direct conversion of fibroblasts to functional neurons by defined factors

          Thomas Vierbuchen, Austin Ostermeier, Zhiping Pang … (2010)
          Cellular differentiation and lineage commitment are considered robust and irreversible processes during development. Recent work has shown that mouse and human fibroblasts can be reprogrammed to a pluripotent state with a combination of four transcription factors. This raised the question of whether transcription factors could directly induce other defined somatic cell fates, and not only an undifferentiated state. We hypothesized that combinatorial expression of neural lineage-specific transcription factors could directly convert fibroblasts into neurons. Starting from a pool of nineteen candidate genes, we identified a combination of only three factors, Ascl1, Brn2, and Myt1l, that suffice to rapidly and efficiently convert mouse embryonic and postnatal fibroblasts into functional neurons in vitro. These induced neuronal (iN) cells express multiple neuron-specific proteins, generate action potentials, and form functional synapses. Generation of iN cells from non-neural lineages could have important implications for studies of neural development, neurological disease modeling, and regenerative medicine.
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            Differentiation of embryonic stem cells to clinically relevant populations: lessons from embryonic development.

            Charles E. Murry, Gordon Keller (2008)
            The potential to generate virtually any differentiated cell type from embryonic stem cells (ESCs) offers the possibility to establish new models of mammalian development and to create new sources of cells for regenerative medicine. To realize this potential, it is essential to be able to control ESC differentiation and to direct the development of these cells along specific pathways. Embryology has offered important insights into key pathways regulating ESC differentiation, resulting in advances in modeling gastrulation in culture and in the efficient induction of endoderm, mesoderm, and ectoderm and many of their downstream derivatives. This has led to the identification of new multipotential progenitors for the hematopoietic, neural, and cardiovascular lineages and to the development of protocols for the efficient generation of a broad spectrum of cell types including hematopoietic cells, cardiomyocytes, oligodendrocytes, dopamine neurons, and immature pancreatic beta cells. The next challenge will be to demonstrate the functional utility of these cells, both in vitro and in preclinical models of human disease.
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              A model for neural development and treatment of Rett syndrome using human induced pluripotent stem cells.

              Maria C. N. Marchetto, Cassiano Carromeu, Allan Acab … (2010)
              Autism spectrum disorders (ASD) are complex neurodevelopmental diseases in which different combinations of genetic mutations may contribute to the phenotype. Using Rett syndrome (RTT) as an ASD genetic model, we developed a culture system using induced pluripotent stem cells (iPSCs) from RTT patients' fibroblasts. RTT patients' iPSCs are able to undergo X-inactivation and generate functional neurons. Neurons derived from RTT-iPSCs had fewer synapses, reduced spine density, smaller soma size, altered calcium signaling and electrophysiological defects when compared to controls. Our data uncovered early alterations in developing human RTT neurons. Finally, we used RTT neurons to test the effects of drugs in rescuing synaptic defects. Our data provide evidence of an unexplored developmental window, before disease onset, in RTT syndrome where potential therapies could be successfully employed. Our model recapitulates early stages of a human neurodevelopmental disease and represents a promising cellular tool for drug screening, diagnosis and personalized treatment. Copyright © 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Psychiatry
                Journal ID (iso-abbrev): Mol. Psychiatry
                Title: Molecular Psychiatry
                Publisher: Nature Publishing Group
                ISSN (Print): 1359-4184
                ISSN (Electronic): 1476-5578
                Publication date (Print): September 2017
                Publication date (Electronic): 21 March 2017
                Volume: 22
                Issue: 9
                Pages: 1241-1249
                Affiliations
                [1 ]Weill Cornell Medical College, Cornell University , New York, NY, USA
                [2 ]Developmental Biology and Center of Stem Cell Biology, Sloan-Kettering Cancer Center , New York, NY, USA
                [3 ]Rockefeller University , New York, NY, USA
                Author notes
                [* ], Developmental Biology, Sloan-Kettering Cancer Center , 1275 York Avenue, Box 256, New York, NY 10065, US. E-mail: mos2028@ 123456med.cornell.edu or studerl@ 123456mskcc.org
                [4]

                These authors contributed equally to this work.

                Article
                Publisher Item ID: mp201740
                DOI: 10.1038/mp.2017.40
                PMC ID: 5582162
                PubMed ID: 28322279
                SO-VID: 675e250b-cfc1-4ca6-a7e3-2331ecb18ae8
                Copyright © Copyright © 2017 The Author(s)
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                Date received : 14 October 2016
                Date revision received : 19 December 2016
                Date accepted : 09 January 2017
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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