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  1. AU="Van Gorp, Sebastiaan"
  2. AU="Nakatani, Fumihiko"
  3. AU="Júnior, José Dias Correa"
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  5. AU=Barton Michael C
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  1. Article ; Online: A First-in-Human, Phase I Study of Neural Stem Cell Transplantation for Chronic Spinal Cord Injury.

    Curtis, Erik / Martin, Joel R / Gabel, Brandon / Sidhu, Nikki / Rzesiewicz, Teresa K / Mandeville, Ross / Van Gorp, Sebastiaan / Leerink, Marjolein / Tadokoro, Takahiro / Marsala, Silvia / Jamieson, Catriona / Marsala, Martin / Ciacci, Joseph D

    Cell stem cell

    2018  Volume 22, Issue 6, Page(s) 941–950.e6

    Abstract: We tested the feasibility and safety of human-spinal-cord-derived neural stem cell (NSI-566) transplantation for the treatment of chronic spinal cord injury (SCI). In this clinical trial, four subjects with T2-T12 SCI received treatment consisting of ... ...

    Abstract We tested the feasibility and safety of human-spinal-cord-derived neural stem cell (NSI-566) transplantation for the treatment of chronic spinal cord injury (SCI). In this clinical trial, four subjects with T2-T12 SCI received treatment consisting of removal of spinal instrumentation, laminectomy, and durotomy, followed by six midline bilateral stereotactic injections of NSI-566 cells. All subjects tolerated the procedure well and there have been no serious adverse events to date (18-27 months post-grafting). In two subjects, one to two levels of neurological improvement were detected using ISNCSCI motor and sensory scores. Our results support the safety of NSI-566 transplantation into the SCI site and early signs of potential efficacy in three of the subjects warrant further exploration of NSI-566 cells in dose escalation studies. Despite these encouraging secondary data, we emphasize that this safety trial lacks statistical power or a control group needed to evaluate functional changes resulting from cell grafting.
    MeSH term(s) Adult ; Animals ; Cell Line ; Chronic Disease ; Female ; Humans ; Male ; Neural Stem Cells/cytology ; Neural Stem Cells/transplantation ; Rats ; Rats, Nude ; Spinal Cord Injuries/pathology ; Spinal Cord Injuries/surgery ; Spinal Cord Injuries/therapy ; Stem Cell Transplantation/adverse effects ; Young Adult
    Language English
    Publishing date 2018-06-01
    Publishing country United States
    Document type Case Reports ; Clinical Trial, Phase I ; Journal Article
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2018.05.014
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  2. Article ; Online: Amelioration of motor/sensory dysfunction and spasticity in a rat model of acute lumbar spinal cord injury by human neural stem cell transplantation.

    van Gorp, Sebastiaan / Leerink, Marjolein / Kakinohana, Osamu / Platoshyn, Oleksandr / Santucci, Camila / Galik, Jan / Joosten, Elbert A / Hruska-Plochan, Marian / Goldberg, Danielle / Marsala, Silvia / Johe, Karl / Ciacci, Joseph D / Marsala, Martin

    Stem cell research & therapy

    2013  Volume 4, Issue 3, Page(s) 57

    Abstract: Introduction: Intraspinal grafting of human neural stem cells represents a promising approach to promote recovery of function after spinal trauma. Such a treatment may serve to: I) provide trophic support to improve survival of host neurons; II) improve ...

    Abstract Introduction: Intraspinal grafting of human neural stem cells represents a promising approach to promote recovery of function after spinal trauma. Such a treatment may serve to: I) provide trophic support to improve survival of host neurons; II) improve the structural integrity of the spinal parenchyma by reducing syringomyelia and scarring in trauma-injured regions; and III) provide neuronal populations to potentially form relays with host axons, segmental interneurons, and/or α-motoneurons. Here we characterized the effect of intraspinal grafting of clinical grade human fetal spinal cord-derived neural stem cells (HSSC) on the recovery of neurological function in a rat model of acute lumbar (L3) compression injury.
    Methods: Three-month-old female Sprague-Dawley rats received L3 spinal compression injury. Three days post-injury, animals were randomized and received intraspinal injections of either HSSC, media-only, or no injections. All animals were immunosuppressed with tacrolimus, mycophenolate mofetil, and methylprednisolone acetate from the day of cell grafting and survived for eight weeks. Motor and sensory dysfunction were periodically assessed using open field locomotion scoring, thermal/tactile pain/escape thresholds and myogenic motor evoked potentials. The presence of spasticity was measured by gastrocnemius muscle resistance and electromyography response during computer-controlled ankle rotation. At the end-point, gait (CatWalk), ladder climbing, and single frame analyses were also assessed. Syrinx size, spinal cord dimensions, and extent of scarring were measured by magnetic resonance imaging. Differentiation and integration of grafted cells in the host tissue were validated with immunofluorescence staining using human-specific antibodies.
    Results: Intraspinal grafting of HSSC led to a progressive and significant improvement in lower extremity paw placement, amelioration of spasticity, and normalization in thermal and tactile pain/escape thresholds at eight weeks post-grafting. No significant differences were detected in other CatWalk parameters, motor evoked potentials, open field locomotor (Basso, Beattie, and Bresnahan locomotion score (BBB)) score or ladder climbing test. Magnetic resonance imaging volume reconstruction and immunofluorescence analysis of grafted cell survival showed near complete injury-cavity-filling by grafted cells and development of putative GABA-ergic synapses between grafted and host neurons.
    Conclusions: Peri-acute intraspinal grafting of HSSC can represent an effective therapy which ameliorates motor and sensory deficits after traumatic spinal cord injury.
    MeSH term(s) Animals ; Disease Models, Animal ; Female ; Graft Survival/drug effects ; Humans ; Immunosuppressive Agents/pharmacology ; Magnetic Resonance Imaging ; Motor Activity ; Muscle Spasticity/therapy ; Neural Stem Cells/cytology ; Neural Stem Cells/transplantation ; Rats ; Rats, Sprague-Dawley ; Recovery of Function ; Spinal Cord Injuries/therapy ; Tacrolimus/pharmacology ; Transplantation, Heterologous
    Chemical Substances Immunosuppressive Agents ; Tacrolimus (WM0HAQ4WNM)
    Language English
    Publishing date 2013-05-28
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2548671-8
    ISSN 1757-6512 ; 1757-6512
    ISSN (online) 1757-6512
    ISSN 1757-6512
    DOI 10.1186/scrt209
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Neuropathy-induced spinal GAP-43 expression is not a main player in the onset of mechanical pain hypersensitivity.

    Jaken, Robby J / van Gorp, Sebastiaan / Joosten, Elbert A / Losen, Mario / Martínez-Martínez, Pilar / De Baets, Marc / Marcus, Marco A / Deumens, Ronald

    Journal of neurotrauma

    2011  Volume 28, Issue 12, Page(s) 2463–2473

    Abstract: Structural plasticity within the spinal nociceptive network may be fundamental to the chronic nature of neuropathic pain. In the present study, the spatiotemporal expression of growth-associated protein-43 (GAP-43), a protein which has been traditionally ...

    Abstract Structural plasticity within the spinal nociceptive network may be fundamental to the chronic nature of neuropathic pain. In the present study, the spatiotemporal expression of growth-associated protein-43 (GAP-43), a protein which has been traditionally implicated in nerve fiber growth and sprouting, was investigated in relation to mechanical pain hypersensitivity. An L5 spinal nerve transection model was validated by the presence of mechanical pain hypersensitivity and an increase in the early neuronal activation marker cFos within the superficial spinal dorsal horn upon innocuous hindpaw stimulation. Spinal GAP-43 was found to be upregulated in the superficial L5 dorsal horn from 5 up to 10 days after injury. GAP-43 was co-localized with calcitonin-gene related peptide (CGRP), but not vesicular glutamate transporter-1 (VGLUT-1), IB4, or protein kinase-γ (PKC-γ), suggesting the regulation of GAP-43 in peptidergic nociceptive afferents. These GAP-43/CGRP fibers may be indicative of sprouting peptidergic fibers. Fiber sprouting largely depends on growth factors, which are typically associated with neuro-inflammatory processes. The putative role of neuropathy-induced GAP-43 expression in the development of mechanical pain hypersensitivity was investigated using the immune modulator propentofylline. Propentofylline treatment strongly attenuated the development of mechanical pain hypersensitivity and glial responses to nerve injury as measured by microglial and astroglial markers, but did not affect neuropathy-induced levels of spinal GAP-43 or GAP-43 regulation in CGRP fibers. We conclude that nerve injury induces structural plasticity in fibers expressing CGRP, which is regarded as a main player in central sensitization. Our data do not, however, support a major role of these structural changes in the onset of mechanical pain hypersensitivity.
    MeSH term(s) Animals ; Female ; GAP-43 Protein/biosynthesis ; Hyperalgesia/metabolism ; Hyperalgesia/pathology ; Pain/metabolism ; Pain/pathology ; Peptide Biosynthesis/physiology ; Physical Stimulation/methods ; Rats ; Rats, Sprague-Dawley ; Spinal Cord/metabolism ; Spinal Cord/pathology ; Up-Regulation/genetics
    Chemical Substances GAP-43 Protein
    Language English
    Publishing date 2011-10-20
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 645092-1
    ISSN 1557-9042 ; 0897-7151
    ISSN (online) 1557-9042
    ISSN 0897-7151
    DOI 10.1089/neu.2011.1833
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  4. Article ; Online: Effective long-term immunosuppression in rats by subcutaneously implanted sustained-release tacrolimus pellet: effect on spinally grafted human neural precursor survival.

    Sevc, Juraj / Goldberg, Danielle / van Gorp, Sebastiaan / Leerink, Marjolein / Juhas, Stefan / Juhasova, Jana / Marsala, Silvia / Hruska-Plochan, Marian / Hefferan, Michael P / Motlik, Jan / Rypacek, Frantisek / Machova, Ludka / Kakinohana, Osamu / Santucci, Camila / Johe, Karl / Lukacova, Nadezda / Yamada, Kazuhiko / Bui, Jack D / Marsala, Martin

    Experimental neurology

    2013  Volume 248, Page(s) 85–99

    Abstract: Achievement of effective, safe and long-term immunosuppression represents one of the challenges in experimental allogeneic and xenogeneic cell and organ transplantation. The goal of the present study was to develop a reliable, long-term immunosuppression ...

    Abstract Achievement of effective, safe and long-term immunosuppression represents one of the challenges in experimental allogeneic and xenogeneic cell and organ transplantation. The goal of the present study was to develop a reliable, long-term immunosuppression protocol in Sprague-Dawley (SD) rats by: 1) comparing the pharmacokinetics of four different subcutaneously delivered/implanted tacrolimus (TAC) formulations, including: i) caster oil/saline solution, ii) unilamellar or multilamellar liposomes, iii) biodegradable microspheres, and iv) biodegradable 3-month lasting pellets; and 2) defining the survival and immune response in animals receiving spinal injections of human neural precursors at 6 weeks to 3 months after cell grafting. In animals implanted with TAC pellets (3.4 mg/kg/day), a stable 3-month lasting plasma concentration of TAC averaging 19.1 ± 4.9 ng/ml was measured. Analysis of grafted cell survival in SOD+ or spinal trauma-injured SD rats immunosuppressed with 3-month lasting TAC pellets (3.4-5.1 mg/kg/day) showed the consistent presence of implanted human neurons with minimal or no local T-cell infiltration. These data demonstrate that the use of TAC pellets can represent an effective, long-lasting immunosuppressive drug delivery system that is safe, simple to implement and is associated with a long-term human neural precursor survival after grafting into the spinal cord of SOD+ or spinal trauma-injured SD rats.
    MeSH term(s) Animals ; Delayed-Action Preparations/administration & dosage ; Delayed-Action Preparations/pharmacokinetics ; Drug Implants ; Graft Survival/drug effects ; Graft Survival/immunology ; Humans ; Immunosuppression/methods ; Immunosuppressive Agents/administration & dosage ; Immunosuppressive Agents/pharmacokinetics ; Neural Stem Cells/immunology ; Neural Stem Cells/transplantation ; Neurons/immunology ; Neurons/transplantation ; Rats ; Rats, Sprague-Dawley ; Spinal Cord/drug effects ; Spinal Cord/immunology ; Spinal Cord Injuries/immunology ; Tacrolimus/administration & dosage ; Tacrolimus/pharmacokinetics
    Chemical Substances Delayed-Action Preparations ; Drug Implants ; Immunosuppressive Agents ; Tacrolimus (WM0HAQ4WNM)
    Language English
    Publishing date 2013-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 207148-4
    ISSN 1090-2430 ; 0014-4886
    ISSN (online) 1090-2430
    ISSN 0014-4886
    DOI 10.1016/j.expneurol.2013.05.017
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    Zs.A 184: Show issues Location:
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  5. Article ; Online: Probing sporadic and familial Alzheimer's disease using induced pluripotent stem cells.

    Israel, Mason A / Yuan, Shauna H / Bardy, Cedric / Reyna, Sol M / Mu, Yangling / Herrera, Cheryl / Hefferan, Michael P / Van Gorp, Sebastiaan / Nazor, Kristopher L / Boscolo, Francesca S / Carson, Christian T / Laurent, Louise C / Marsala, Martin / Gage, Fred H / Remes, Anne M / Koo, Edward H / Goldstein, Lawrence S B

    Nature

    2012  Volume 482, Issue 7384, Page(s) 216–220

    Abstract: Our understanding of Alzheimer's disease pathogenesis is currently limited by difficulties in obtaining live neurons from patients and the inability to model the sporadic form of the disease. It may be possible to overcome these challenges by ... ...

    Abstract Our understanding of Alzheimer's disease pathogenesis is currently limited by difficulties in obtaining live neurons from patients and the inability to model the sporadic form of the disease. It may be possible to overcome these challenges by reprogramming primary cells from patients into induced pluripotent stem cells (iPSCs). Here we reprogrammed primary fibroblasts from two patients with familial Alzheimer's disease, both caused by a duplication of the amyloid-β precursor protein gene (APP; termed APP(Dp)), two with sporadic Alzheimer's disease (termed sAD1, sAD2) and two non-demented control individuals into iPSC lines. Neurons from differentiated cultures were purified with fluorescence-activated cell sorting and characterized. Purified cultures contained more than 90% neurons, clustered with fetal brain messenger RNA samples by microarray criteria, and could form functional synaptic contacts. Virtually all cells exhibited normal electrophysiological activity. Relative to controls, iPSC-derived, purified neurons from the two APP(Dp) patients and patient sAD2 exhibited significantly higher levels of the pathological markers amyloid-β(1-40), phospho-tau(Thr 231) and active glycogen synthase kinase-3β (aGSK-3β). Neurons from APP(Dp) and sAD2 patients also accumulated large RAB5-positive early endosomes compared to controls. Treatment of purified neurons with β-secretase inhibitors, but not γ-secretase inhibitors, caused significant reductions in phospho-Tau(Thr 231) and aGSK-3β levels. These results suggest a direct relationship between APP proteolytic processing, but not amyloid-β, in GSK-3β activation and tau phosphorylation in human neurons. Additionally, we observed that neurons with the genome of one sAD patient exhibited the phenotypes seen in familial Alzheimer's disease samples. More generally, we demonstrate that iPSC technology can be used to observe phenotypes relevant to Alzheimer's disease, even though it can take decades for overt disease to manifest in patients.
    MeSH term(s) Aged, 80 and over ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid Precursor Protein Secretases/antagonists & inhibitors ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Astrocytes/cytology ; Biomarkers/metabolism ; Cells, Cultured ; Cellular Reprogramming ; Coculture Techniques ; Endosomes/metabolism ; Enzyme Activation ; Female ; Fibroblasts/cytology ; Fibroblasts/metabolism ; Glycogen Synthase Kinase 3/metabolism ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Induced Pluripotent Stem Cells/pathology ; Male ; Middle Aged ; Models, Biological ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Peptide Fragments/metabolism ; Phosphoproteins/metabolism ; Phosphorylation/drug effects ; Protease Inhibitors/pharmacology ; Proteolysis ; Synapsins/metabolism ; tau Proteins/metabolism
    Chemical Substances Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Biomarkers ; Peptide Fragments ; Phosphoproteins ; Protease Inhibitors ; Synapsins ; amyloid beta-protein (1-40) ; tau Proteins ; Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; Amyloid Precursor Protein Secretases (EC 3.4.-)
    Language English
    Publishing date 2012-01-25
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/nature10821
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