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      Cell transplantation therapy for spinal cord injury

      Author(s): , , , ,
      Publication date Created:
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      Journal: Nature Neuroscience
      Publisher: Springer Nature

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          Abstract

          The consequences of spinal cord injury are often severe and irreversible; cell transplantation has emerged as a potential treatment. In this Review, the authors highlight mechanisms through which cell transplantation is thought to promote functional improvements and the obstacles to making cell transplantation a viable therapy.

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          DREADDs for Neuroscientists.

          Bryan Roth (2016)
          To understand brain function, it is essential that we discover how cellular signaling specifies normal and pathological brain function. In this regard, chemogenetic technologies represent valuable platforms for manipulating neuronal and non-neuronal signal transduction in a cell-type-specific fashion in freely moving animals. Designer Receptors Exclusively Activated by Designer Drugs (DREADD)-based chemogenetic tools are now commonly used by neuroscientists to identify the circuitry and cellular signals that specify behavior, perceptions, emotions, innate drives, and motor functions in species ranging from flies to nonhuman primates. Here I provide a primer on DREADDs highlighting key technical and conceptual considerations and identify challenges for chemogenetics going forward.
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            Graded histological and locomotor outcomes after spinal cord contusion using the NYU weight-drop device versus transection.

            D Basso, M S Beattie, J C Bresnahan (1996)
            Injury reproducibility is an important characteristic of experimental models of spinal cord injuries (SCI) because it limits the variability in locomotor and anatomical outcome measures. Recently, a more sensitive locomotor rating scale, the Basso, Beattie, and Bresnahan scale (BBB), was developed but had not been tested on rats with severe SCI complete transection. Rats had a 10-g rod dropped from heights of 6.25, 12.5, 25, and 50 mm onto the exposed cord at Tl 0 using the NYU device. A subset of rats with 25 and 50 mm SCI had subsequent spinal cord transection (SCI + TX) and were compared to rats with transection only (TX) in order to ascertain the dependence of recovery on descending systems. After 7-9 weeks of locomotor testing, the percentage of white matter measured from myelin-stained cross sections through the lesion center was significantly different between all the groups with the exception of 12.5 vs 25 mm and 25 vs 50 mm groups. Locomotor recovery was greatest for the 6.25-mm group and least for the 50-mm group and was correlated positively to the amount of tissue sparing at the lesion center (p 0.05). Thus, spared descending systems appear to modify segmental systems which produce greater behavioral improvements than isolated cord systems.
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              Central nervous system injury-induced immune deficiency syndrome.

              Christian Meisel, Jan Schwab, Konstantin Prass … (2005)
              Infections are a leading cause of morbidity and mortality in patients with acute CNS injury. It has recently become clear that CNS injury significantly increases susceptibility to infection by brain-specific mechanisms: CNS injury induces a disturbance of the normally well balanced interplay between the immune system and the CNS. As a result, CNS injury leads to secondary immunodeficiency - CNS injury-induced immunodepression (CIDS) - and infection. CIDS might serve as a model for the study of the mechanisms and mediators of brain control over immunity. More importantly, understanding CIDS will allow us to work on developing effective therapeutic strategies, with which the outcome after CNS damage by a host of diseases could be improved by eliminating a major determinant of poor recovery.
              Article 0 comments Cited 300 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: Nature Neuroscience
                Abbreviated Title: Nat Neurosci
                Publisher: Springer Nature
                ISSN (Print): 1097-6256
                ISSN (Electronic): 1546-1726
                Publication date Created: April 25 2017
                Publication date (Print): April 25 2017
                Volume: 20
                Issue: 05
                Pages: 637-647
                Article
                DOI: 10.1038/nn.4541
                PubMed ID: 28440805
                SO-VID: a98ce5b3-5fa5-4290-b309-aedfc42f1fe8
                Copyright © © 2017
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