The Spinal Cord Meeting ISCORE’19 organized by the Step by Step foundation aims to bring together high profile international speakers consist of leading experts clinicians, clinical scientists and molecular biologists of international prestige in areas which have already entered, or are expected to enter shortly, in experimental therapeutic trials in patients. A major goal of The Spinal Cord Meeting ISCORE’15 in advancing the translation of research data to the clinic is to promote multi-pronged approaches for therapy of this complex problem.
The objective is for the speakers to report their progresses as well as to promote dialogue with the other researchers.
School Health Sciences Center for Neural Repair
The work of the Spinal Cord Injury Group at the Center for Neural Repair focuses on augmenting regeneration of the adult spinal cord after injury. The injured spinal cord does not regenerate because: 1) cellular “bridges” that can support axonal regeneration do not naturally form in an SCI lesion site; 2) growth factors are not produced in the injured spinal cord to stimulate regeneration; 3) injured CNS neurons do not fully express a “growth program” to recruit new regeneration; and 4) the environment of the injured adult spinal cord inhibits regeneration due to the presence of inhibitory extracellular matrix molecules that form around the injury site, and due to the presence of inhibitory proteins on adult myelin that block regeneration.
Neural stem cells exist in an intrinsically high growth state. When grafted to sites of spinal cord injury, neural stem cells survive and extend up to hundreds of thousands of axons into the injured spinal cord (Lu et al, Cell 2012; Lu et al, Neuron 2014; Kadoya et al, Nature Medicine 2016; Lu et al, J Clin Invest 2017; Poplawski et al, Science Trans Med 2017; Dulin et al, Nature Comm 2018; Rosenzweig et al, Nature Medicine 2018). Injured adult axons regenerate into neural stem cell grafts and form synapses; in turn, axons extending from grafts to the host spinal cord below the lesion site also form synapses onto host neurons. New neural relay circuits are formed that support partial functional improvement.
Building on this biology, our current research efforts are focused on a range of topics from basic discovery of genes that enable host axon regeneration, to late stage translational primate studies that are leading up to human translation. Our experimental techniques include genomic and epigenomic studies, cell biology, proteomics, bioinformatics, in vitro assays, in vivo models of SCI in rodents and primates, electrophysiology and behavior.
We are also using tools of bioengineering, nanotechnology and 3D printing to enhance and guide regenerating axons in the injured spinal cord and peripheral nerve.
Last publications related to Spinal Cord Injury
Kumamaru H, Lu P, Rosenzweig ES, Kadoya K, Tuszynski MH.
Cell Rep. 2019 Feb 26;26(9):2329-2339.e4. doi: 10.1016/j.celrep.2019.01.099.
Lien BV, Tuszynski MH, Lu P.
Exp Neurol. 2019 Apr;314:46-57. doi: 10.1016/j.expneurol.2019.01.006. Epub 2019 Jan 15.
Koffler J, Zhu W, Qu X, Platoshyn O, Dulin JN, Brock J, Graham L, Lu P, Sakamoto J, Marsala M, Chen S, Tuszynski MH.
Nat Med. 2019 Feb;25(2):263-269. doi: 10.1038/s41591-018-0296-z. Epub 2019 Jan 14.
Kumamaru H, Lu P, Rosenzweig ES, Tuszynski MH.
Stem Cell Reports. 2018 Oct 9;11(4):861-868. doi: 10.1016/j.stemcr.2018.08.009. Epub 2018 Sep 6.
Poplawski GHD, Lie R, Hunt M, Kumamaru H, Kawaguchi R, Lu P, Schäfer MKE, Woodruff G, Robinson J, Canete P, Dulin JN, Geoffroy CG, Menzel L, Zheng B, Coppola G, Tuszynski MH.
Sci Transl Med. 2018 May 23;10(442). pii: eaal2563. doi: 10.1126/scitranslmed.aal2563.
Rosenzweig ES, Brock JH, Lu P, Kumamaru H, Salegio EA, Kadoya K, Weber JL, Liang JJ, Moseanko R, Hawbecker S, Huie JR, Havton LA, Nout-Lomas YS, Ferguson AR, Beattie MS, Bresnahan JC, Tuszynski MH.
Nat Med. 2018 May;24(4):484-490. doi: 10.1038/nm.4502. Epub 2018 Feb 26.
Brock JH, Graham L, Staufenberg E, Im S, Tuszynski MH.
J Neurotrauma. 2018 May 1;35(9):1069-1078. doi: 10.1089/n
Axonal Growth and Degeneration, Neuro-degeneration/protection, Neuronal Regeneration, Neuroscience
PhD, University of Miami
Postdoc, Harvard Medical School
Neural Degeneration and Regeneration in the Mammalian Retina
We are currently recruiting motivated postdoctoral researchers and students to join our research adventures. The main research interests of my laboratory focus on the mechanistic and therapeutic studies of neurodegenerative diseases in the retina resulting in vision impairment and blindness. We study signaling pathways and gene expression network in retinal neurons in normal and diseased conditions, with an ultimate aim to save vision. Neuroprotection and neuroregeneration are the two main strategies we use to prevent the death of existing neurons or to generate new neurons. 1. For neuroprotection, we investigate molecular mechanisms underlying the degeneration of photoreceptors, the primary sensory neurons that mediate the first step in vision, and ganglion cells, the output neurons of the retina. An in-depth understanding the signaling pathways that are perturbed in a diseased retina will facilitate the design of therapeutic strategies to protect photoreceptors and ganglion cells through modulation of the components of the affected pathways. 2. For neural regeneration, we examine the intrinsic signaling pathways and transcription control in Müller glial cells, the primary glial cell type in the retina, in order to reprogram them in vivo to generate adult retinal stem cells that are capable of differentiating to retinal neurons. 3. In addition, my laboratory is also actively exploring strategies to promote axon regeneration using optic nerve crush to model CNS (central nervous system) injury.