Journal of Neurodegeneration and RegenerationAbstracts
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Journal of Neurodegeneration and Regeneration
Fall 2011, Volume 3
, Number 1

Complete Fall 2011 Issue of JNDR
Fall 2011; pages 1-78

Editorial: Bromodeoxyuridine labeling: Beware of the limitations and pitfalls
Philippe Taupin, PhD
Fall 2011; pages 7-8


Exposure to Cry protoxins induces oxidative stress, dopamine neuron death, and intraneuronal a-synuclein-positive inclusions in the substantia nigra of rats
Emilio FernŠndez-Espejo, PhD, MD
Fall 2011; pages 9-18

Cry protoxins are endotoxin molecules produced by Bacillus thuringiensis. Oxidative effects of these protoxins on hepatic cells are well known; however, the potential oxidative effects of these toxins over neural cells such as substantia nigra dopamine neurons have not yet been studied. In this study, 6-month-old rats were intraperitoneally injected with Dipel daily for 20 successive days. Dipel is an insecticide that contains several Cry protoxins. The findings revealed that Cry protoxin exposure induced spontaneous hyperkinesia from the 10th month. Some rats showed rotations after amphetamine. Six months after Cry exposure, enzymelinked immunosorbent assay revealed that an oxidation process took place in the substantia nigra as revealed through the reduction of glutathione and superoxide dismutase. At 22 months, the neuropathological study revealed signs of neurodegeneration in the substantia nigra such as regional and unilateral degeneration of dopamine neurons and intraneuronal presence of diffusely distributed a-synuclein or a-synuclein-positive inclusions. Other brain centers such as dorsal striatum, red nucleus, and dorsal raphe were also affected, suggesting a widespread degeneration. Nigral oxidative stress was detected bilaterally, but nigral degeneration was partial, indicating that other phenomena apart from oxidation caused neurodegeneration. In summary, exposure to Cry protoxins in rats induce i) sustained hyperkinesia, ii) an oxidant process in the nigrostriatal circuit, and iii) a neurodegenerative disorder affecting the nigrostriatal system and other brain nuclei, which is characterized by dopamine cell death and some Parkinson-like features. Keywords: Cry protoxin, Substantia nigra, Dopamine, Degeneration, Lewy DOI:10.5055/jndr.2011.0002

Spermatogonial stem cells isolated from adult primate testes produce nerve trunks with dopaminergic characteristics
Chad Maki, BS; Kyle Howerton, BS, MS; Jason Pacchiarotti, BS; Thomas Ramos, BS, MS, MBA; Jadelind Wong,BS; Joel Marh, BS; Jane Pham, BS; Jessie Kinjo, BS; Constance Yuen, BS; Yung-Chiong Chow, MD, PhD; Jianyu Rao, MD, FCAP; Fariborz Izadyar, DVM, PhD
Fall 2011; pages 19-31

Objective: The aim of this study was to investigate the ability of the adult spermatogonial stem cells (SSCs) to differentiate into the dopaminergic lineage. Design: First, a mixture of testicular cells were aggregated to form embryoid bodies and then cultured on the PA6 cells (stromal cell line) in the presence of growth factors. Second, enriched populations of SSCs were sorted by Stage-specific embryonic antigen-4 and cultured on the mouse embryonic fibroblasts in the presence of growth factors. Results: In both conditions, structures with the morphology of neural trunks were formed. These trunks were extended and branched in time, which eventually made a network. Immunohistochemical localization and reverse transcription polymerase chain reaction analyses revealed that the trunks were positive for dopamine-specific markers. Conclusions: These results clearly show that SSCs from adult primate testes have the ability to differentiate into neural trunks with dopaminergic characteristics, suggesting that SSCs can be considered as an alternative cell source for cell replacement therapy of Parkinsonís disease. Keywords: Germ line, Stem cells, Neurogenesis, Regeneration, Parkinson DOI:10.5055/jndr.2011.0003

Human olfactory-derived neural progenitors diminish locomotory deficits following spinal cord contusion injury
Chengliang Lu, MD; Jodi J. Hallgren, LAT; Yu Lin, MD; Deborah S. Black, MS; Linda C. Ekstrom, AAS; Ian H. Fentie, PhD; Guy Brock, PhD; Ying Song, BA; Welby I. Winstead, MD; Fred J. Roisen, PhD
Fall 2011; pages 33-50

Objective: To investigate the therapeutic utility of human adult olfactory epithelial-derived neural progenitors (hONPs) as an autologous cell-based treatment for spinal cord injuries (SCIs). Design: To characterize and compare populations of hONPs obtained from cyrostorage. Enzyme-linked immunosorbent assay (ELISA) was used to evaluate in vitro synthesis and release of neurotrophins (brain-derived neurotrophic factor, nerve growth factor, cilliary neurotrophic factor (CTNF), neurotrophin 3, and glial-derived neurotrophic factor) as well as fibroblast growth factor and vascular endothelial growth factor. To determine the efficacy of hONP engraftment on rats with computer-controlled moderately severe T9 contusions, the improvement compared to fibroblast engrafted and nonengrafted controls was evaluated. Studies employing behavioral, biochemical, electrophysiological, and morphological techniques were applied to SCI animals and isolated cords. Setting: Endoscopic biopsies of the olfactory epithelium were obtained from volunteer patients undergoing elective nasal sinus surgery. After long-term culture, as previously described, more than 150 patient-specific hONP lines were cryopreserved. In this study, the hONP lines were obtained from cryostorage and expanded as needed. Main outcome measures: Immunofluorescent characterization of hONP lines was done using cell type-specific antibodies. Open field locomotion was used to determine the degree of deficit. ELISA of isolated cord segments was used to analyze neurotrophic microenvironments. Microscopic analysis was used to examine the effect of hONP on the morphological response to SCI. Results: hONP engraftment into the contusion epicenter facilitated locomotion over nonengrafted and fibroblast engrafted controls 6 weeks following engraftment in more than 40 percent of the animals. The epicenter of hONP-engrafted animals had higher absolute axonal numbers and enriched neurotrophic microenvironments when compared with the nonengrafted controls. Conclusions: The noninvasive ability to harvest and isolate hONPs coupled with their unique regenerative capacity suggests that they are ideal candidates for an autologous cell-based strategy for treatment of human SCIs. Keywords: Olfactory-derived progenitors, Adult stem cells, Neurotrophic molecules, Spinal cord injury, Transplantation, Brain-derived neurotrophic factor, Nerve growth factor, Ciliary neurotrophic factor, Fibroblast growth factor, Vascular endothelial growth factor, Choline acetyl transferase, Neurotrophin 3, Glial cell line-derived neurotrophic factor, Locomotory behavior, Regeneration DOI:10.5055/jndr.2011.0004

Neurogenic drugs for treating neurological diseases and disorders
Philippe Taupin, PhD
Fall 2011; pages 51-53


Are we approaching research into the repair of spinal cord trauma from the best perspective?
Damien P. Kuffler, PhD
Fall 2011; pages 55-77

Spinal cord trauma immediately kills neurons and their processes and sequelae triggered by trauma typically cause the death of large additional numbers of neurons. The smaller the number of neurons killed and connections lost, the smaller the neurological losses and the number of neural circuits that must be re-established to restore normal neurological function. The inability to induce neurological recovery is not only due to spinal cord complexity in terms of number and types of neurons, other cells, and their connections, but also the cellular environment of the spinal cord contains factors that inhibit axon regeneration, it lacks factors necessary to promote axon regeneration, to induce target recognition and to induce the formation of appropriate functional synaptic connections. The literature is full of promising approaches, some providing neuroprotection in the immediate aftermath of trauma, others for neutralizing axon regeneration-inhibiting factors, whereas others induce and direct axon regeneration. Although each technique separately is generally inadequate for the required task, when viewed in a unifying light, combining various techniques should lead to clinically applicable tools for promoting axon regeneration leading to neurological recovery. This article examines spinal cord trauma and its sequelae, neurotoxicity following trauma, factors involved in the inhibition of axon regeneration, techniques providing neuroprotection and for promoting axon regeneration with the aim of inducing neurological recovery and their applicability for clinical use. Keywords: Spinal cord lesion, Neurological recovery, Axon regeneration, Platelet-rich fibrin DOI:10.5055/jndr.2011.0006