Journal articles: 'Neural transplantation; Parkinson's disease'

1

Mehta, V., J. Spears, and I. Mendez. "Neural Transplantation in Parkinson's Disease." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 24, no. 04 (November 1997): 292–301. http://dx.doi.org/10.1017/s0317167100032959.

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ABSTRACT:Parkinson's disease is a neurodegenerative disorder that affects about 1% of Canadians between the ages of fifty and seventy. The medical management for these patients consists of drug therapy that is initially effective but has limited long term benefits and does not alter the progressive course of the disease. The recalcitrance of longstanding Parkinson's disease to medical management has prompted the use of alternative surgical therapies. Many neurosurgical procedures have been utilized in order to improve the disabling symptoms these patients harbour. Although most of the current procedures involve making destructive lesions within various basal ganglia nuclei, neural transplantation attempts to reconstitute the normal nigrostriatal pathway and restore striatal dopamine. The initial success of neural transplantation in the rodent and primate parkinsonian models has led to its clinical application in the treatment of parkinsonian patients. Currently, well over one hundred patients throughout the world have been grafted with fetal tissue in an effort to ameliorate their parkinsonian symptoms. Although the results of neural transplantation in clinical trials are promising, a number of issues need to be resolved before this technology can become a standard treatment option. This review focuses on the current status of neural transplantation in Parkinson's disease within the context of other surgical therapies in current use.

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Lindvall, Olle. "Neural Transplantation." Cell Transplantation 4, no. 4 (July 1995): 393–400. http://dx.doi.org/10.1177/096368979500400410.

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Cell transplantation is now being explored as a new therapeutic strategy to restore function in the diseased human central nervous system. Neural grafts show long-term survival and function in patients with Parkinson's disease but the symptomatic relief needs to be increased. Cell transplantation seems justified in patients with Huntington's disease and, at a later stage, possibly also in demyelinating disorders. The further development in this research field will require systematic studies in animal experiments but also well-designed clinical trials in small groups of patients.

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Shimizu, K., M. Yamada, Y. Matsui, K. Tamura, S. Moriuchi, and H. Mogami. "Neural Transplantation in Mouse Parkinson's Disease." Stereotactic and Functional Neurosurgery 54, no. 1-8 (1990): 353–57. http://dx.doi.org/10.1159/000100234.

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Hagell, Peter, Paola Piccini, Anders Björklund, Patrik Brundin, Stig Rehncrona, Håkan Widner, Lesley Crabb, et al. "Dyskinesias following neural transplantation in Parkinson's disease." Nature Neuroscience 5, no. 7 (June 3, 2002): 627–28. http://dx.doi.org/10.1038/nn863.

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Borlongan, Cesario V., and Paul R. Sanberg. "Neural transplantation for treatment of Parkinson's disease." Drug Discovery Today 7, no. 12 (June 2002): 674–82. http://dx.doi.org/10.1016/s1359-6446(02)02297-3.

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Kupsch, Andreas, and Wolfgang H. Oertel. "Neural transplantation, trophic factors and Parkinson's disease." Life Sciences 55, no. 25-26 (January 1994): 2083–95. http://dx.doi.org/10.1016/0024-3205(94)00389-0.

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Freed, William J. "Neural Transplantation: Prospects for Clinical use." Cell Transplantation 2, no. 1 (January 1993): 13–31. http://dx.doi.org/10.1177/096368979300200105.

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Neural transplantation has been extensively applied in Parkinson's disease, including numerous clinical studies, studies in animal models, and related basic research on cell biology. There is evidence that the clinical trials of both adrenal medulla transplantation and fetal substantia nigra transplantation have produced a detectable clinical effect, although it is not yet clear whether the clinical benefit is sufficient to justify a more widespread application of these procedures. Studies of long-term outcome and quantitative tests are important in assaying the degree of benefit produced by transplantation procedures in Parkinson's disease and for developing improved and refined procedures. Other disease-related applications of neural transplantation are beginning to be developed. These include Huntington's disease, chronic pain, epilepsy, spinal cord injury, and perhaps even demyelinating diseases and cortical ischemic injury. Although most of these applications lie in the future, it is not too soon to begin to consider the scientific justification that should be required for initiation of human clinical trials.

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Madrazo, Ignacio, Rebecca Franco-Bourland, Maricarmen Aguilera, Feggy Ostrosky-Solis, Carlos Cuevas, Hugo Castrejón, Eduardo Magalloón, and Mario Madrazo. "Development of Human Neural Transplantation." Neurosurgery 29, no. 2 (August 1, 1991): 165–77. http://dx.doi.org/10.1227/00006123-199108000-00001.

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Abstract The possibility of altering the course of Parkinson's disease by brain grafting is slowly becoming a reality through the efforts of many research groups worldwide. It has been shown that this procedure, as performed in high-level medical research centers, usually produces no permanent adverse effects and can effectively ameliorate parkinsonian signs in certain patients. This progress has served to reinforce our commitment to develop neural transplantation into an effective therapy to treat such a devastating neurodegenerative disease. We have summarized the most important events that have shaped the initial phase of this research. In the course of the last 4 years, considerable knowledge has been gained in the clinical neurosciences regarding the real potential of various brain grafting procedures in treating Parkinson's disease, their shortcomings, and their usefulness in carefully selected patients. There is still no consensus regarding the various fundamental aspects of human brain grafting in Parkinson's disease. Questions concerning surgical technique, candidate selection, the optimal brain regions for implantation, the optimal tissue for implantation, and the real usefulness of brain grafting must be addressed. The importance of the quality of adrenal medulla fragments for grafting, the requirement for immunosuppressors in fetal brain grafting, and the optimal fetal age and the amount of donor tissue for effective grafting are additional areas of concern. The potential of xenografting, preserved tissues, and genetically engineered cells for human brain grafting remain unanswered. The development of human neural transplantation is the responsibility and privilege of neurosurgery.

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Rosenfeld, J. V., T. J. Kilpatrick, and P. F. Bartlett. "Neural transplantation for Parkinson's disease: a critical appraisal." Australian and New Zealand Journal of Medicine 21, no. 4 (August 1991): 477–84. http://dx.doi.org/10.1111/j.1445-5994.1991.tb01357.x.

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Björklund, Anders, Stephen B. Dunnett, Patrik Brundin, A. Jon Stoessl, Curt R. Freed, Robert E. Breeze, Marc Levivier, Marc Peschanski, Lorenz Studer, and Roger Barker. "Neural transplantation for the treatment of Parkinson's disease." Lancet Neurology 2, no. 7 (July 2003): 437–45. http://dx.doi.org/10.1016/s1474-4422(03)00442-3.

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Emerich, Dwaine F., Michael Ragozzino, Michael N. Lehman, and Paul R. Sanberg. "Behavioral Effects of Neural Transplantation." Cell Transplantation 1, no. 6 (November 1992): 401–27. http://dx.doi.org/10.1177/096368979200100604.

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Considerable evidence suggests that transplantation of fetal neural tissue ameliorates the behavioral deficits observed in a variety of animal models of CNS disorders. However, it is also becoming increasingly clear that neural transplants do not necessarily produce behavioral recovery, and in some cases have either no beneficial effects, magnify existing behavioral abnormalities, or even produce a unique constellation of deficits. Regardless, studies demonstrating the successful use of neural transplants in reducing or eliminating behavioral deficits in these animal models has led directly to their clinical application in human neurodegenerative disorders such as Parkinson's disease. This review examines the beneficial and deleterious behavioral consequences of neural transplants in different animal models of human diseases, and discusses the possible mechanisms by which neural transplants might produce behavior recovery.

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12

Bradbury, Jane. "Are dyskinesias a problem after neural transplantation for Parkinson's disease?" Lancet 359, no. 9322 (June 2002): 2007. http://dx.doi.org/10.1016/s0140-6736(02)08852-9.

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Collier, TJ, and R, Sladek John. "Neural Transplantation in Animal Models of Neurodegenerative Disesase." Physiology 3, no. 5 (October 1, 1988): 204–6. http://dx.doi.org/10.1152/physiologyonline.1988.3.5.204.

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Interest in neural transplantation research has increased greatly in the past five years. Although this procedure initially was viewed as a research tool for studying neuronal development, it is gaining attention as a potential therapeutic intervention. Indeed, replacement of chemically defined neurons in animal models of the neurodegeneration that occurs in Parkinson's disease and Alzheimer's disease indicates that grafted fetal neurons survive transplantation, integrate with the host brain, and produce a sustained improvement of motor function and memory performance.

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Fink, J. Stephen, James M. Schumacher, Samuel L. Ellias, E. Prather Palmer, Marie Saint-Hilaire, Kathleen Shannon, Richard Penn, et al. "Porcine Xenografts in Parkinson's Disease and Huntington's Disease Patients: Preliminary Results." Cell Transplantation 9, no. 2 (March 2000): 273–78. http://dx.doi.org/10.1177/096368970000900212.

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The observation that fetal neurons are able to survive and function when transplanted into the adult brain fostered the development of cellular therapy as a promising approach to achieve neuronal replacement for treatment of diseases of the adult central nervous system. This approach has been demonstrated to be efficacious in patients with Parkinson's disease after transplantation of human fetal neurons. The use of human fetal tissue is limited by ethical, infectious, regulatory, and practical concerns. Other mammalian fetal neural tissue could serve as an alternative cell source. Pigs are a reasonable source of fetal neuronal tissue because of their brain size, large litters, and the extensive experience in rearing them in captivity under controlled conditions. In Phase I studies porcine fetal neural cells grafted unilaterally into Parkinson's disease (PD) and Huntington's disease (HD) patients are being evaluated for safety and efficacy. Clinical improvement of 19% has been observed in the Unified Parkinson's Disease Rating Scale “off” state scores in 10 PD patients assessed 12 months after unilateral striatal transplantation of 12 million fetal porcine ventral mesencephalic (VM) cells. Several patients have improved more than 30%. In a single autopsied PD patient some porcine fetal VM cells were observed to survive 7 months after transplantation. Twelve HD patients have shown a favorable safety profile and no change in total functional capacity score 1 year after unilateral striatal placement of up to 24 million fetal porcine striatal cells. Xenotransplantation of fetal porcine neurons is a promising approach to delivery of healthy neurons to the CNS. The major challenges to the successful use of xenogeneic fetal neuronal cells in neurodegenerative diseases appear to be minimizing immune-mediated rejection, management of the risk of xenotic (cross-species) infections, and the accurate assessment of clinical outcome of diseases that are slowly progressive.

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Barker, Roger A., and Anne E. Rosser. "Neural transplantation therapies for Parkinson's and Huntington's diseases." Drug Discovery Today 6, no. 11 (June 2001): 575–82. http://dx.doi.org/10.1016/s1359-6446(01)01775-5.

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Kitada, Masaaki, and Mari Dezawa. "Parkinson's Disease and Mesenchymal Stem Cells: Potential for Cell-Based Therapy." Parkinson's Disease 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/873706.

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Cell transplantation is a strategy with great potential for the treatment of Parkinson's disease, and many types of stem cells, including neural stem cells and embryonic stem cells, are considered candidates for transplantation therapy. Mesenchymal stem cells are a great therapeutic cell source because they are easy accessible and can be expanded from patients or donor mesenchymal tissues without posing serious ethical and technical problems. They have trophic effects for protecting damaged tissues as well as differentiation ability to generate a broad spectrum of cells, including dopamine neurons, which contribute to the replenishment of lost cells in Parkinson's disease. This paper focuses mainly on the potential of mesenchymal stem cells as a therapeutic cell source and discusses their potential clinical application in Parkinson's disease.

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Clarkson, Edward D., and Curt R. Freed. "Development of fetal neural transplantation as a treatment for Parkinson's disease." Life Sciences 65, no. 23 (October 1999): 2427–37. http://dx.doi.org/10.1016/s0024-3205(99)00254-4.

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18

Barbaro, N. "Factors affecting the clinical outcome after neural transplantation in Parkinson's disease." Yearbook of Neurology and Neurosurgery 2007 (January 2007): 320–22. http://dx.doi.org/10.1016/s0513-5117(08)70221-7.

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19

Piccini, Paola, Nicola Pavese, Peter Hagell, Jan Reimer, Anders Björklund, Wolfgang H. Oertel, Niall P. Quinn, David J. Brooks, and Olle Lindvall. "Factors affecting the clinical outcome after neural transplantation in Parkinson's disease." Brain 128, no. 12 (October 24, 2005): 2977–86. http://dx.doi.org/10.1093/brain/awh649.

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20

Soderstrom, Katherine, Jennifer O'malley, Kathy Steece-Collier, and Jeffrey H. Kordower. "Neural Repair Strategies for Parkinson's Disease: Insights from Primate Models." Cell Transplantation 15, no. 3 (March 2006): 251–65. http://dx.doi.org/10.3727/000000006783982025.

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Nonhuman primate models of Parkinson's disease (PD) have been invaluable to our understanding of the human disease and in the advancement of novel therapies for its treatment. In this review, we attempt to give a brief overview of the animal models of PD currently used, with a more comprehensive focus on the advantages and disadvantages presented by their use in the nonhuman primate. In particular, discussion addresses the 6-hydroxydopamine (6-OHDA), 1-methyl-1,2,3,6-tetrahydopyridine (MPTP), rotenone, paraquat, and maneb parkinsonian models. Additionally, the role of primate PD models in the development of novel therapies, such as trophic factor delivery, grafting, and deep brain stimulation, are described. Finally, the contribution of primate PD models to our understanding of the etiology and pathology of human PD is discussed.

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21

Constantine Bell, Nikki Melina. "Regulating Transfer and Use of Fetal Tissue in Transplantation Procedures: The Ethical Dimensions." American Journal of Law & Medicine 20, no. 3 (1994): 277–94. http://dx.doi.org/10.1017/s0098858800007188.

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For twenty years scientists have worked to find an effective treatment to ease the quivering, the stiffness, and the difficulty in controlling bodily movements which are the primary symptoms of Parkinson's disease. The disease can be treated with L-dopa, a drug that mimics the dopamine that coordinates neural transmission in the human brain, which Parkinson's sufferers have ceased to produce in sufficient quantities. The L-dopa, however, produces damaging side-effects and sometimes proves ineffectual. Researchers discovered in animal experiments that the effects of a laboratory-developed disease simulating Parkinson's disease could be mitigated using fetal brain tissue transplants, which produced the natural dopamine the animals’ cells failed to produce adequately.These experiments were replicated with human subjects, and fetal tissue transplants have shown great potential as a treatment for Parkinson's disease. Fetal tissue is ideal for transplantation because it is in a stage of primitive development in which it adjusts easily to a new environment.

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Chen, Weibai. "Neural Stem Cells Therapy to Treat Neurodegenerative Diseases." E3S Web of Conferences 271 (2021): 03076. http://dx.doi.org/10.1051/e3sconf/202127103076.

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Neural stem cells have the ability to proliferation, differentiate and renew, which plays an important role in the growth, maturation and senescence of the human brain. But according to researches, neural stem cells in the brain do not remain active throughout an organism's lifetime. Many neural stem cells become dormant when the brain matures, and may be activated when the body is sick to selectively heal the disease. In recent years, there are many studies on neural stem cells. Joshua[1] and Ting Zhang[2] show that neurodegenerative diseases such as ischemic stroke, Alzheimer's disease and Parkinson's disease can be improved by the transplantation of neural stem cells, however the specific mechanism is not clear. This paper investigates three main questions: Why neural stem cell transplantation is chosen as a treatment? Where does NSCs derive from in clinical transplantation? How does neural stem cell transplantation treat brain diseases? And we also figure out the answers to these three questions. Firstly, transplantation of hypothalamic NSCs can delay the process of aging in the host, and Chemokines and EVs which secreted by neural stem cells can delay aging and defend neurodegenerative diseases. Secondly, the sources of NSCs can be divided into three types. The first is to isolate NSCs from primary tissue and cultivate them in vitro. The second is to produce the required cells by inducing pluripotent stem cells and embryonic stem cells. The third way to get NCS is through transdifferentiation of somatic cells. Thirdly, in brain diseases, transplanted NSCs can migrate from the aggregation site to the site of the disease, reducing damage to the blood-brain barrier, repairing learning and memory abilities that depend on the hippocampus and secreting neurotrophic factors.

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23

Hjelmgren, J., J. Reimer, U. Persson, O. Ghatnekar, M. Gabrowski, O. Lindvall, and P. Hagell. "PNM12 EARLY DECISION MAKING MODELLING IN PARKINSON'S DISEASE—THE CASE OF NEURAL TRANSPLANTATION IN PATIENTS WITH ADVANCED PARKINSON'S DISEASE." Value in Health 6, no. 6 (November 2003): 765–66. http://dx.doi.org/10.1016/s1098-3015(10)61951-1.

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Barker, Roger A., Jessica Barrett, Sarah L. Mason, and Anders Björklund. "Fetal dopaminergic transplantation trials and the future of neural grafting in Parkinson's disease." Lancet Neurology 12, no. 1 (January 2013): 84–91. http://dx.doi.org/10.1016/s1474-4422(12)70295-8.

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Linazasoro, G. "Rate of progression determines the clinical outcome after neural transplantation in Parkinson's disease." Brain 129, no. 7 (July 1, 2006): E48. http://dx.doi.org/10.1093/brain/awl112.

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Ballagi, Andrea E., Per Odin, Agneta Othberg-Cederström, Anja Smits, Wei-Ming Duandr, Olle Lindvall, and Keiko Funa. "Platelet-Derived Growth Factor Receptor Expression after Neural Grafting in a Rat Model of Parkinson's Disease." Cell Transplantation 3, no. 6 (November 1994): 453–60. http://dx.doi.org/10.1177/096368979400300602.

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Platelet-derived growth factor (PDGF) has trophic effect on dopaminergic neurons in vitro. We have previously shown dynamic changes in the expression of PDGF in embryonic mesencephalic grafts and surrounding host striatal tissue following intracerebral transplantation in a rat model of Parkinson's disease. In this study the expression of the PDGF receptors was examined in the same model using immunohistochemistry. Most ventral mesencephalic (VM) cells from E13–E15 rat embryos possessed both PDGF α-and β-receptors before implantation. Double immunofluorescence staining revealed that about 10% of the cells also expressed tyrosine hydroxylase (TH). The PDGF α-receptor was detectable in the graft up to 1 wk after transplantation but had disappeared at 3 wk. In the host tissue, scattered glial cells were positive for the α-receptor but the expression was unchanged following transplantation. The β-receptor expression almost completely disappeared from the grafted tissue by 4 h following transplantation, and only a few cells of the host striatum showed immunoreactivity. However, after 3 wk β-receptor positive cells were again detectable in the graft. These cells appeared to be endothelial cells as identified by an antibody against von Willebrand's factor. Our data suggest that PDGF might act locally on embryonic dopaminergic cells in an autocrine or juxtacrine manner before and shortly after transplantation, and on surrounding glial cells in a paracrine manner after transplantation. Furthermore, PDGF-BB might influence neovascularization in the graft.

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Breeze, Robert E., and Marjorie C. Wang. "An overview of central nervous system transplantation in human disease." Neurosurgical Focus 7, no. 3 (September 1999): E3. http://dx.doi.org/10.3171/foc.1999.7.3.4.

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Although its roots date back over a century, the field of neurotransplantation has been shaped mostly by advances over the past 30 years. Animal models of nigrostriatal disconnection in the 1970s allowed investigators to explore the feasibility of neural grafting. By the end of that decade, functional and behavioral effects had been demonstrated using fetal tissue grafts. In the 1980s, animal experimentation continued, as did clinical trials involving patients with idiopathic Parkinson's disease. Both autologous adrenal medullary tissue and fetal allografts were tested in the clinical setting, with the latter proving to yield superior results. Animal models of striatal cell loss provided the impetus for limited clinical trials in patients with Huntington's disease by the early 1990s, and work with both diseases continues today. Although much has been learned, neural grafting remains experimental. Broader applications are being explored even now, though, as transplant techniques are applied to animal models of dementia, spinal cord injury, cortical injury, and pain. Some very limited human trials have already begun in some of these areas. In this review some of the advances in the field are highlighted.

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Goldman, Steven A., and Martha S. Windrem. "Cell replacement therapy in neurological disease." Philosophical Transactions of the Royal Society B: Biological Sciences 361, no. 1473 (July 31, 2006): 1463–75. http://dx.doi.org/10.1098/rstb.2006.1886.

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Diseases of the brain and spinal cord represent especially daunting challenges for cell-based strategies of repair, given the multiplicity of cell types within the adult central nervous system, and the precision with which they must interact in both space and time. Nonetheless, a number of diseases are especially appropriate for cell-based therapy, in particular those in which single phenotypes are lost, and in which the re-establishment of vectorially specific connections is not entirely requisite for therapeutic benefit. We review here a set of potential therapeutic indications that meet these criteria as potentially benefiting from the transplantation of neural stem and progenitor cells. These include: (i) transplantation of phenotypically restricted neuronal progenitor cells into diseases of a single neuronal phenotype, such as Parkinson's disease; (ii) implantation of mixed progenitor pools into diseases characterized by the loss of a limited number of discrete phenotypes, such as spinal cord injury and the motor neuronopathies; (iii) transplantation of glial and nominally oligodendrocytic progenitor cells as a means of treating disorders of myelin; and (iv) transplantation of neural stem cells as a means of treating lysosomal storage disorders and other diseases of enzymatic deficiency. Among the diseases potentially approachable by these strategies, the myelin disorders, including the paediatric leucodystrophies as well as adult traumatic and inflammatory demyelinations, may present the most compelling targets for cell-based neurological therapy.

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Piccini, P. "Reply: Rate of progression determines the clinical outcome after neural transplantation in Parkinson's disease." Brain 129, no. 7 (July 1, 2006): E49. http://dx.doi.org/10.1093/brain/awl113.

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Wianny, Florence, and Julien Vezoli. "Transplantation in the nonhuman primate MPTP model of Parkinson's disease: update and perspectives." Primate Biology 4, no. 2 (October 11, 2017): 185–213. http://dx.doi.org/10.5194/pb-4-185-2017.

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Abstract. In order to calibrate stem cell exploitation for cellular therapy in neurodegenerative diseases, fundamental and preclinical research in NHP (nonhuman primate) models is crucial. Indeed, it is consensually recognized that it is not possible to directly extrapolate results obtained in rodent models to human patients. A large diversity of neurological pathologies should benefit from cellular therapy based on neural differentiation of stem cells. In the context of this special issue of Primate Biology on NHP stem cells, we describe past and recent advances on cell replacement in the NHP model of Parkinson's disease (PD). From the different grafting procedures to the various cell types transplanted, we review here diverse approaches for cell-replacement therapy and their related therapeutic potential on behavior and function in the NHP model of PD.

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Barker, Roger A., A. Lisa Kendall, Håkan Widner, H. Widner, L. Larsson, K. A. Czech, P. Anderson, et al. "Neural Tissue Xenotransplantation: What is Needed Prior to Clinical Trials in Parkinson's Disease?" Cell Transplantation 9, no. 2 (March 2000): 235–46. http://dx.doi.org/10.1177/096368970000900209.

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Embryonic allografted human tissue in patients with Parkinson's disease has been shown to survive and ameliorate many of the symptoms of this disease. Despite this success, the practical problems of using this tissue coupled to the ethical restrictions of using aborted human fetal tissue have lead to an exploration for alternative sources of suitable material for grafting, including xenogeneic embryonic dopaminergic-rich neural tissue. Nevertheless, xenografted neural tissue itself generates a number of practical, ethical, safety, and immunological issues that have to be addressed prior to any clinical xenotransplant program. In this article we review these critical issues and set out the criteria that we consider need to be met in the development of our clinical xenotransplantation research programs. We advocate that these, or similar, criteria should be adopted and made explicit by other centers contemplating similar clinical trials.

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Bartlett, L. E., and I. Mendez. "Dopaminergic Reinnervation of the Globus Pallidus by Fetal Nigral Grafts in the Rodent Model of Parkinson's Disease." Cell Transplantation 14, no. 2-3 (February 2005): 119–27. http://dx.doi.org/10.3727/000000005783983241.

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The current neural transplantation strategy for Parkinson's disease (PD) involves the dopaminergic reinnervation of the striatum (STR). Although up to 85% reinnervation of the STR has been attained by neural transplantation, functional recovery in animal models and transplanted patients is incomplete. This limitation may be due to an incomplete restoration of the dopaminergic input to other basal ganglia structures such as the external segment of the globus pallidus (GPe, homologue of the rodent GP), which normally receives dopaminergic input from the substantia nigra (SN). As part of our investigation into a multiple grafting strategy for PD, we have explored the effects of dopaminergic grafts in the GP of rodents with unilateral 6-hydroxydopamine (6-OHDA) lesions. In this experiment, lesioned rats received either 300,000 fetal ventral mesencephalic (FVM) cells or a sham injection into the GP. Functional assessment consisted of rotational behavior at 3 and 6 weeks posttransplantation. A fluorogold tracer study was conducted to rule out any behavioral improvement due to striatal outgrowth of the GP graft. Sections were stained for glial fibrillary acidic protein (GFAP) to assess the degree of trauma in the GP by the graft in comparison to the sham injection. Immunohistochemistry for tyrosine hydroxylase (TH) was performed after transplantation to assess graft survival. Animals with GP grafts demonstrated a significant improvement in rotational behavior at 3 and 6 weeks posttransplantation (p < 0.05) while sham control animals did not improve. All animals receiving FVM cells showed TH-immunoreactive grafts in the GP posttransplantation. TH-positive neurons in the GP showed no double labeling with an intrastriatal injection of fluorogold, indicating that behavioral improvement was not due to striatal innervation by the GP graft. These observations suggest that functional recovery was the result of dopaminergic reinnervation of the GP and that this nucleus may be a potential target for neural transplantation in clinical PD.

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Nikkhah, Guido. "Neural transplantation therapy for Parkinson’s disease: potential and pitfalls." Brain Research Bulletin 56, no. 6 (December 2001): 509. http://dx.doi.org/10.1016/s0361-9230(01)00662-1.

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Rohrer, Daniel C., Gajanan Nilaver, Valerie Nipper, and Curtis A. Machida. "Genetically Modified Pc 12 Brain Grafts: Survivability and Inducible Nerve Growth Factor Expression." Cell Transplantation 5, no. 1 (January 1996): 57–68. http://dx.doi.org/10.1177/096368979600500111.

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Neural transplantation of genetically modified cells has been successfully employed to reverse functional deficits in animal models of neurodegenerative disorders, including Parkinson's disease. While implanted PC12 cells secrete dopamine in vivo and can ameliorate dopamine deficiency in parkinsonian rat model systems, these cells either degenerate within 2-3 wk postimplantation (presumably due to the lack of neural trophic factor support at the site of implantation), or in some cases, form a tumor mass leading to the death of the host animal. To address these limitations, we have developed a genetically modified PC12 cell line that can synthesize nerve growth factor (NGF) under the control of a zinc-inducible metallothionein promoter. When implanted in the rat striatum and under in vivo zinc stimulation, these cells will neurodifferentiate, express tyrosine hydroxylase, and will undergo survival through potential autocrine trophic support. This regulatable cell line and general approach may provide additional insight on the potential utilization of cell transplants for treatment of Parkinson's disease and other neurodegenerative disorders.

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Abe, Koji, Toru Yamashita, Shunya Takizawa, Satoshi Kuroda, Hiroyuki Kinouchi, and Nobutaka Kawahara. "Stem Cell Therapy for Cerebral Ischemia: From Basic Science to Clinical Applications." Journal of Cerebral Blood Flow & Metabolism 32, no. 7 (January 18, 2012): 1317–31. http://dx.doi.org/10.1038/jcbfm.2011.187.

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Recent stem cell technology provides a strong therapeutic potential not only for acute ischemic stroke but also for chronic progressive neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis with neuroregenerative neural cell replenishment and replacement. In addition to resident neural stem cell activation in the brain by neurotrophic factors, bone marrow stem cells (BMSCs) can be mobilized by granulocyte-colony stimulating factor for homing into the brain for both neurorepair and neuroregeneration in acute stroke and neurodegenerative diseases in both basic science and clinical settings. Exogenous stem cell transplantation is also emerging into a clinical scene from bench side experiments. Early clinical trials of intravenous transplantation of autologous BMSCs are showing safe and effective results in stroke patients. Further basic sciences of stem cell therapy on a neurovascular unit and neuroregeneration, and further clinical advancements on scaffold technology for supporting stem cells and stem cell tracking technology such as magnetic resonance imaging, single photon emission tomography or optical imaging with near-infrared could allow stem cell therapy to be applied in daily clinical applications in the near future.

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Emerich, Dwaine F., Shelley R. Winn, Lisa Christenson, Meg A. Palmatier, Frank T. Gentile, and Paul R. Sanberg. "A novel approach to neural transplantation in Parkinson's disease: Use of polymer-encapsulated cell therapy." Neuroscience & Biobehavioral Reviews 16, no. 4 (January 1992): 437–47. http://dx.doi.org/10.1016/s0149-7634(05)80185-x.

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Yasuhara, T., N. Matsukawa, K. Hara, G. Yu, L. Xu, M. Maki, S. U. Kim, and C. V. Borlongan. "Transplantation of Human Neural Stem Cells Exerts Neuroprotection in a Rat Model of Parkinson's Disease." Journal of Neuroscience 26, no. 48 (November 29, 2006): 12497–511. http://dx.doi.org/10.1523/jneurosci.3719-06.2006.

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Döbrössy, Máté, Monica Busse, Tobias Piroth, Anne Rosser, Stephen Dunnett, and Guido Nikkhah. "Review: Neurorehabilitation With Neural Transplantation." Neurorehabilitation and Neural Repair 24, no. 8 (July 20, 2010): 692–701. http://dx.doi.org/10.1177/1545968310363586.

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Cell replacement therapy has been tested clinically in Parkinson’s disease (PD) and Huntington’s disease (HD), epilepsy, spinal cord injury, and stroke. The clinical outcomes have been variable, perhaps partly because of the differing levels of preclinical, basic experimental evidence that was available prior to the trials. The most promising results have been seen in PD trials, with encouraging ones in HD. A common feature of most trials is that they have concentrated on the biological and technical aspects of transplantation without presupposing that the outcomes might be influenced by events after the surgery. The growing evidence of plasticity demonstrated by the brain and grafts in response to environmental and training stimuli such as rehabilitation interventions has been mostly neglected throughout the clinical application of cell therapy. This review suggests that a different approach may be required to maximize recovery: postoperative experiences, including rehabilitation with explicit behavioral retraining, could have marked direct as well as positive secondary effects on the integration and function of grafted cells in the host neural system. The knowledge gained about brain plasticity following brain damage needs to be linked with what we know about promoting intrinsic recovery processes and how this can boost neurobiological and surgical strategies for repair at the clinical level. With proof of principle now established, a rich area for innovative research with profound therapeutic application is open for investigation.

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Mendez, Ivar, Murray Hong, Stephen Smith, Alain Dagher, and Jacques Desrosiers. "Neural transplantation cannula and microinjector system: experimental and clinical experience." Journal of Neurosurgery 92, no. 3 (March 2000): 493–99. http://dx.doi.org/10.3171/jns.2000.92.3.0493.

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✓ The authors present a simple, reliable, and safe system for performing neural transplantation in the human brain. The device consists of a transplantation cannula and microinjector system that has been specifically designed to reduce implantation-related trauma and to maximize the number of graft deposits per injection. The system was evaluated first in an experimental rat model of Parkinson's disease (PD). Animals in which transplantation with this system had been performed showed excellent graft survival with minimal trauma to the brain. Following this experimental stage, the cannula and microinjector system were used in eight patients with PD enrolled in the Halifax Neural Transplantation Program who received bilateral putaminal transplants of fetal ventral mesencephalic tissue. A total of 16 transplantation operations and 64 trajectories were performed in the eight patients, and there were no intraoperative or perioperative complications. Magnetic resonance imaging studies obtained 24 hours after surgery revealed no evidence of tissue damage or hemorrhage. Transplant survival was confirmed by fluorodopa positron emission tomography scans obtained 6 and 12 months after surgery.As neural transplantation procedures for the treatment of neurological conditions evolve, the ability to deliver viable grafts safely will become critically important. The device presented here has proved to be of value in maximizing the number of graft deposits while minimizing implantation-related trauma to the host brain.

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Martínez-Serrano, Alberto, Marta P. Pereira, Natalia Avaliani, Anna Nelke, Merab Kokaia, and Tania Ramos-Moreno. "Short-Term Grafting of Human Neural Stem Cells: Electrophysiological Properties and Motor Behavioral Amelioration in Experimental Parkinson's Disease." Cell Transplantation 25, no. 12 (December 2016): 2083–97. http://dx.doi.org/10.3727/096368916x692069.

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Cell replacement therapy in Parkinson's disease (PD) still lacks a study addressing the acquisition of electrophysiological properties of human grafted neural stem cells and their relation with the emergence of behavioral recovery after transplantation in the short term. Here we study the electrophysiological and biochemical profiles of two ventral mesencephalic human neural stem cell (NSC) clonal lines (C30-Bcl-XL and C32-Bcl-XL) that express high levels of Bcl-XL to enhance their neurogenic capacity, after grafting in an in vitro parkinsonian model. Electrophysiological recordings show that the majority of the cells derived from the transplants are not mature at 6 weeks after grafting, but 6.7% of the studied cells showed mature electrophysiological profiles. Nevertheless, parallel in vivo behavioral studies showed a significant motor improvement at 7 weeks postgrafting in the animals receiving C30-Bcl-XL, the cell line producing the highest amount of TH+ cells. Present results show that, at this postgrafting time point, behavioral amelioration highly correlates with the spatial dispersion of the TH+ grafted cells in the caudate putamen. The spatial dispersion, along with a high number of dopaminergic-derived cells, is crucial for behavioral improvements. Our findings have implications for long-term standardization of stem cell-based approaches in Parkinson's disease.

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Ryu, M. Y., M. A. Lee, Y. H. Ahn, K. S. Kim, S. H. Yoon, E. Y. Snyder, K. G. Cho, and S. U. Kim. "Brain Transplantation of Neural Stem Cells Cotransduced with Tyrosine Hydroxylase and GTP Cyclohydrolase 1 in Parkinsonian Rats." Cell Transplantation 14, no. 4 (April 2005): 193–202. http://dx.doi.org/10.3727/000000005783983133.

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Neural stem cells (NSCs) of the central nervous system (CNS) recently have attracted a great deal of interest not only because of their importance in basic research on neural development, but also in terms of their therapeutic potential in neurological diseases, such as Parkinson's disease (PD). To examine if genetically modified NSCs are a suitable source for the cell and gene therapy of PD, an immortalized mouse NSC line, C17.2, was transduced with tyrosine hydroxylase (TH) gene and with GTP cyclohydrolase 1 (GTPCH1) gene, which are important enzymes in dopamine biosynthesis. The expression of TH in transduced C17.2-THGC cells was confirmed by RT-PCR, Western blot analysis, and immunocytochemistry, and expression of GTPCH1 by RT-PCR. The level of L-DOPA released by C17.2-THGC cells, as determined by HPLC assay, was 3793 pmol/106 cells, which is 760-fold higher than that produced by C17.2-TH cells, indicating that GTPCH1 expression is important for L-DOPA production by transduced C17.2 cells. Following the implantation of C17.2-THGcC NSCs into the striata of parkinsonian rats, a marked improvement in amphetamine-induced turning behavior was observed in parkinsonian rats grafted with C17.2-THGC cells but not in the control rats grafted with C17.2 cells. These results indicate that genetically modified NSCs grafted into the brain of the parkinsonian rats are capable of survival, migration, and neuronal differentiation. Collectively, these results suggest that NSCs have great potential as a source of cells for cell therapy and an effective vehicle for therapeutic gene transfer in Parkinson's disease.

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Mendez, Ivar, Murray Hong, Stephen Smith, Alain Dagher, and Jacques Desrosiers. "A neural transplantation cannula and microinjector system: experimental and clinical experience." Neurosurgical Focus 7, no. 3 (September 1999): E4. http://dx.doi.org/10.3171/foc.1999.7.3.5.

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The authors present a simple, reliable, and safe system for performing neural transplantation in the human brain. The device consists of a transplantation cannula and microinjector system that has been specifically designed to reduce implantation-related trauma and to maximize the number of graft deposits for each injection. The system was evaluated first in an experimental rat model of Parkinson's disease (PD). Animal transplantation with this system showed excellent graft survival with minimal trauma to the brain. Following this experimental stage, the cannula and microinjector system was used in eight patients with PD enrolled in the Halifax Neural Transplantation Program who received bilateral putaminal transplants of fetal ventral mesencephalic tissue. A total of 16 transplantation operations and 64 trajectories were performed in the eight patients, and there were no intra- or perioperative complications. Magnetic resonance imaging studies obtained 24 hours after surgery revealed no evidence of tissue damage or hemorrhage. Transplant survival was confirmed on fluorodopa positron emission tomography scans 6 and 12 months after surgery. As neural transplantation procedures for the treatment of neurological conditions evolve, the ability to deliver viable grafts safely will become of critical importance. The device presented here has been proven to be of value in maximizing the number of graft deposits while minimizing implantation-related trauma to the host brain.

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Deacon, Terrence, James Schumacher, Jonathan Dinsmore, Christine Thomas, Prather Palmer, Stephen Kott, Albert Edge, et al. "Histological evidence of fetal pig neural cell survival after transplantation into a patient with Parkinson's disease." Nature Medicine 3, no. 3 (March 1997): 350–53. http://dx.doi.org/10.1038/nm0397-350.

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Pogarell, O., and W. H. Oertel. "Neural Transplantation in Parkinson's Disease and Its Effects on Rest Tremor: A Review of the Literature." Movement Disorders 13, S3 (October 20, 2008): 101–2. http://dx.doi.org/10.1002/mds.870131317.

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Kefalopoulou, Zinovia, Iciar Aviles-Olmos, and Thomas Foltynie. "Critical Aspects of Clinical Trial Design for Novel Cell and Gene Therapies." Parkinson's Disease 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/804041.

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Neural cell transplantation and gene therapy have attracted considerable interest as promising therapeutic alternatives for patients with Parkinson's disease (PD). Preclinical and open-label studies have suggested that grafted fetal neural tissue or viral vector gene transfer can achieve considerable biochemical and clinical improvements, whereas subsequent double-blind, placebo-controlled protocols have produced rather more modest and variable results. Detailed evaluation of these discordant findings has highlighted several crucial issues such as patient selection criteria, details surrounding transplantation or gene therapy methodologies, as well as the study designs themselves that ought to be carefully considered in the planning phases of future clinical trials. Beyond the provision of symptomatic efficacy and safety data, it also remains to be identified whether the possibilities offered by stem cell and gene therapy technological advances might translate to meaningful neuroprotection and/or disease-modifying effects or alleviate the nonmotor aspects of PD and thus offer additional benefits beyond those achieved through conventional pharmacotherapy or deep brain stimulation (DBS).

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Duan, Wei-Ming, Cecilia M. P. Rodrigures, Li-Ru Zhao, Clifford J. Steer, and Walter C. Low. "Tauroursodeoxycholic Acid Improves the Survival and Function of Nigral Transplants in a Rat Model of Parkinson's Disease." Cell Transplantation 11, no. 3 (April 2002): 195–205. http://dx.doi.org/10.3727/096020198389960.

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There is accumulating evidence showing that the majority of cell death in neural grafts results from apoptosis when cells are implanted into the brain. Tauroursodeoxycholic acid (TUDCA), a taurine-conjugated hydrophilic bile acid, has been found to possess antiapoptotic properties. In the present study we have examined whether the supplementation of TUDCA to cell suspensions prior to transplantation can lead to enhanced survival of nigral grafts. We first conducted an in vitro study to examine the effects of TUDCA on the survival of dopamine neurons in serum-free conditions. The number of tyrosine hydroxylase (TH)-positive neurons in the TUDCA-treated cultures was significantly greater than that of control cultures 7 days in vitro. In addition, a terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) assay showed that the number of apoptotic cells in the TUDCA-treated cultures was dramatically smaller than that in the control cultures. In the transplantation study, a 50 μM concentration of TUDCA was added to the media when nigral tissue from Sprague-Dawley (SD) rats was trypsinized and dissociated. Two microliters of cell suspension containing TUDCA was then stereotaxically injected into the striatum of adult SD rats subjected to an extensive unilateral 6-hydroxydopamine lesion of the nigrastriatal dopamine pathway. At 2 weeks after transplantation, the rats that received a cell suspension with TUDCA exhibited a significant reduction in amphetamine-induced rotation scores when compared with pretransplantation value. There was a significant increase (approximately threefold) in the number of TH-positive cells in the neural grafts for the TUDCA-treated group when compared with the controls 6 weeks postgrafting. The number of apoptotic cells was much smaller in the graft areas in the TUDCA-treated groups than in the control group 4 days after transplantation. These data demonstrate that pretreatment of the cell suspension with TUDCA can reduce apoptosis and increase the survival of grafted cells, resulting in an improvement of behavioral recovery.

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Chou, Chung-Hsing, Hueng-Chuen Fan, and Dueng-Yuan Hueng. "Potential of Neural Stem Cell-Based Therapy for Parkinson’s Disease." Parkinson's Disease 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/571475.

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Neural stem cell (NSC) transplantation is an emerging strategy for restoring neuronal function in neurological disorders, such as Parkinson’s disease (PD), which is characterized by a profound and selective loss of nigrostriatal dopaminergic (DA) neurons. Adult neurogenesis generates newborn neurons that can be observed at specialized niches where endothelial cells (ECs) play a significant role in regulating the behavior of NSCs, including self-renewal and differentiating into all neural lineage cells. In this minireview, we highlight the importance of establishing an appropriate microenvironment at the target site of NSC transplantation, where grafted cells integrate into the surroundings in order to enhance DA neurotransmission. Using a novel model of NSC-EC coculture, it is possible to combine ECs with NSCs, to generate such a neurovascular microenvironment. With appropriate NSCs selected, the composition of the transplant can be investigated through paracrine and juxtacrine signaling within the neurovascular unit (NVU). With target site cellular and acellular compartments of the microenvironment recognized, guided DA differentiation of NSCs can be achieved. As differentiated DA neurons integrate into the existing nigrostriatal DA pathway, the symptoms of PD can potentially be alleviated by reversing characteristic neurodegeneration.

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Xiao, Jia-Jia, Ming Yin, Ze-Jian Wang, and Xiao-Ping Wang. "Transplanted Neural Stem Cells: Playing a Neuroprotective Role by Ceruloplasmin in the Substantia Nigra of PD Model Rats?" Oxidative Medicine and Cellular Longevity 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/618631.

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Although mounting evidence suggests that ceruloplasmin (CP) deficiency and iron deposition are pivotal factors responsible for exacerbating demise of dopaminergic neurons in the substantia nigra (SN) of the Parkinsonism and neural stem cells (NSCs) are believed to be excellent candidates for compensating the lost dopaminergic neurons, there are few researches to explore the change of CP expression and of iron deposition in the pathological microenvironment of SN after NSCs transplantation and the ability of grafted NSCs to differentiate directionally into dopaminergic neurons under the changed homeostasis. With substantia nigral stereotaxic technique and NSCs transplantation, we found that tyrosine hydroxylase and CP expression decreased and iron deposition increased in the lesioned SN after 6-OHDA administration compared with control, while tyrosine hydroxylase and CP expression increased and iron deposition decreased after NSCs transplantation compared to 6-OHDA administration alone. Only a small number of embedding NSCs are able to differentiate into dopaminergic neurons. These results suggest that grafted NSCs have an influence on improving the content of CP expression, which may play a neuroprotective role by decreasing iron deposition and ameliorating damage of dopaminergic neurons and possibly underline the iron-related common mechanism of Parkinson’s disease and Wilson’s disease.

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Staudt, Michael D., Andrea R. Di Sebastiano, Hu Xu, Mandar Jog, Susanne Schmid, Paula Foster, and Matthew O. Hebb. "Advances in Neurotrophic Factor and Cell-Based Therapies for Parkinson's Disease: A Mini-Review." Gerontology 62, no. 3 (September 1, 2015): 371–80. http://dx.doi.org/10.1159/000438701.

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Parkinson's disease (PD) affects an estimated 7-10 million people worldwide and remains without definitive or disease-modifying treatment. There have been many recent developments in cell-based therapy (CBT) to replace lost circuitry and provide chronic biological sources of therapeutic agents to the PD-affected brain. Early neural transplantation studies underscored the challenges of immune compatibility, graft integration and the need for renewable, autologous graft sources. Neurotrophic factors (NTFs) offer a potential class of cytoprotective pharmacotherapeutics that may complement dopamine (DA) replacement and CBT strategies in PD. Chronic NTF delivery may be an integral goal of CBT, with grafts consisting of autologous drug-producing (e.g., DA, NTF) cells that are capable of integration and function in the host brain. In this mini-review, we outline the past experience and recent advances in NTF technology and CBT as promising and integrated approaches for the treatment of PD.

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Wang, F., M. Kameda, T. Yasuhara, N. Tajiri, Y. Kikuchi, H. B. Liang, J. T. Tayra, et al. "GDNF-pretreatment enhances the survival of neural stem cells following transplantation in a rat model of Parkinson's disease." Neuroscience Research 71, no. 1 (September 2011): 92–98. http://dx.doi.org/10.1016/j.neures.2011.05.019.

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Journal articles on the topic 'Neural transplantation; Parkinson's disease'

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