• Corpus ID: 147486009

Purine Nucleoside Mediated Neuroprotection in the 6-Hydroxydopamine Rodent Model of Parkinson's Disease

  title={Purine Nucleoside Mediated Neuroprotection in the 6-Hydroxydopamine Rodent Model of Parkinson's Disease},
  author={B. Terpstra},
Purine Nucleoside Mediated Neuroprotection in the 6-Hydroxydopamine Rodent Model of Parkinson’s Disease Brian T. Terpstra, Doctor of Philosophy, 2010 Dissertation directed by: Timothy J. Collier, Ph.D. Professor of Translational Science and Molecular Medicine ______________________________ Signature Parkinson’s Disease (PD) is a progressive, neurodegenerative disorder characterized by bradykinesia, akinesia, and resting tremor. While dopamine replacement therapy effectively eliminates symptoms… 
Disrupted and transgenic urate oxidase alter urate and dopaminergic neurodegeneration
A neuroprotective role of endogenous urate in dopaminergic neurons is supported and the rationale for developing urate-elevating strategies as potential disease-modifying therapy for Parkinson’s disease is strengthened.


Etiology and Pathogenesis of Parkinson’s Disease
Genetic factors clearly contribute to the pathogenesis of Parkinson’s disease, and many studies have shed light on their implication in, not only monogenic, but also sporadic forms of PD.
3,4-Methylenedioxy-N-methamphetamine (ecstasy) promotes the survival of fetal dopamine neurons in culture
During development, animals prenatally exposed to MDMA showed an increase in tyrosine hydroxylase-positive neurons in the substantia nigra but not in the ventral tegmental area, suggesting that during development, MDMA can increase the survival of DA neurons through its action at its transporter.
Stimulation of the rat subthalamic nucleus is neuroprotective following significant nigral dopamine neuron loss
STN-DBS between 2 and 4 weeks after intrastriatal 6-hydroxydopamine (6-OHDA) provided significant sparing of DA neurons in the SN of rats, which was not due to inadvertent lesioning of the STN and was dependent upon proper electrode placement.
Reassessment of Caspase Inhibition to Augment Grafted Dopamine Neuron Survival
Examining the efficacy of two different caspase inhibitors to augment mesencephalic tyrosine hydroxylase-immunoreactive (TH-ir) neuron survival in culture and following implantation into the denervated striatum of rats concluded that treatment with Ac-YVAD-CMK provided partial but nonsignificant protection for TH-ir neurons against serum withdrawal.
Dopamine cell replacement: Parkinson's disease.
Basic scientific knowledge of neural transplants is incomplete and warrants a prudent approach toward application of neural transplantation techniques in clinical research.
Transplantation of embryonic dopamine neurons for severe Parkinson's disease.
After improvement in the first year, dystonia and dyskinesias recurred in 15 percent of the patients who received transplants, even after reduction or discontinuation of the dose of levodopa.
Glial cell line-derived neurotrophic factor increases survival, growth and function of intrastriatal fetal nigral dopaminergic grafts.
Findings show that supply of exogenous glial cell line-derived neurotrophic factor to the transplantation site improves survival, growth and function of transplanted fetal nigral dopaminergic neurons in the rat Parkinson model.
Interference with anoikis‐induced cell death of dopamine neurons: Implications for augmenting embryonic graft survival in a rat model of Parkinson's disease
Pretreatment with tenascin may prove beneficial to prevent anoikis‐induced cell death in dilute cell suspension grafts, while long‐term in vivo delivery methods need to be explored to determine if L1 can prevent anOikis in grafts of mesencephalic dopamine neurons after transplantation.
BDNF Enhances the Functional Reinnervation of the Striatum by Grafted Fetal Dopamine Neurons
It is suggested that application of this factor might similarly improve the clinical efficacy of neural transplantation employed in the treatment for Parkinson's disease by exerting a significant effect on the functional reinnervation of the striatum by transplanted fetal dopamine neurons in the rat.
Changes in somatodendritic but not terminal dopamine
regulation in aged rhesus monkeys
In comparison to the massive loss of DA neurons responsible for the movement dysfunctions seen in Parkinson's disease, pronounced functional changes in DA release in the SN and putamen may significantly contribute to the motoric Dysfunctions characterizing normal aging in rhesus monkeys.