The Potential for Circuit Reconstruction by Expanded Neural Precursor Cells Explored through Porcine Xenografts in a Rat Model of Parkinson's Disease

2002 ◽  
Vol 175 (1) ◽  
pp. 98-111 ◽  
Author(s):  
Richard J.E. Armstrong ◽  
Carrie B. Hurelbrink ◽  
Pam Tyers ◽  
Emma L. Ratcliffe ◽  
Andrew Richards ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor

Transplantation of expanded neural precursor cells from the developing pig ventral mesencephalon in a rat model of Parkinson's disease

2003 ◽  
Vol 151 (2) ◽  
pp. 204-217 ◽  
Author(s):  
Richard J. E. Armstrong ◽  
Pamela Tyers ◽  
Meena Jain ◽  
Andrew Richards ◽  
Stephen B. Dunnett ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Ventral Mesencephalon

scholarly journals Bioluminescence‐driven optogenetic activation of transplanted neural precursor cells improves motor deficits in a Parkinson's disease mouse model

2018 ◽  
Vol 98 (3) ◽  
pp. 458-468 ◽  
Author(s):  
Jessica R. Zenchak ◽  
Brandon Palmateer ◽  
Nicolai Dorka ◽  
Tariq M. Brown ◽  
Lina‐Marie Wagner ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Motor Deficits ◽  
Neural Precursor

scholarly journals Dual Effects of Human Placenta-Derived Neural Cells on Neuroprotection and the Inhibition of Neuroinflammation in a Rodent Model of Parkinson’s Disease

2018 ◽  
Vol 27 (5) ◽  
pp. 814-830 ◽  
Author(s):  
Han Wool Kim ◽  
Hyun-Seob Lee ◽  
Jun Mo Kang ◽  
Sang-Hun Bae ◽  
Chul Kim ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Human Placenta ◽  
Precursor Cells ◽  
Rodent Model ◽  
Neural Precursor Cells ◽  
Substantia Nigra Pars Compacta ◽  
Neural Precursor ◽  
Age Related ◽  
Therapeutic Mechanisms

Parkinson’s disease (PD) is the second most common age-related neurodegenerative disease in the elderly and the patients suffer from uncontrolled movement disorders due to loss of dopaminergic (DA) neurons on substantia nigra pars compacta (SNpc). We previously reported that transplantation of human fetal midbrain-derived neural precursor cells restored the functional deficits of a 6-hydroxy dopamine (6-OHDA)-treated rodent model of PD but its low viability and ethical issues still remain to be solved. Albeit immune privilege and neural differentiation potentials suggest mesenchymal stem cells (MSCs) from various tissues including human placenta MSCs (hpMSCs) for an alternative source, our understanding of their therapeutic mechanisms is still limited. To expand our knowledge on the MSC-mediated PD treatment, we here investigated the therapeutic mechanism of hpMSCs and hpMSC-derived neural phenotype cells (hpNPCs) using a PD rat model. Whereas both hpMSCs and hpNPCs protected DA neurons in the SNpc at comparable levels, the hpNPC transplantation into 6-OHDA treated rats exhibited longer lasting recovery in motor deficits than either the saline or the hpMSC treated rats. The injected hpNPCs induced delta-like ligand (DLL)1 and neurotrophic factors, and influenced environments prone to neuroprotection. Compared with hpMSCs, co-cultured hpNPCs more efficiently protected primary neural precursor cells from midbrain against 6-OHDA as well as induced their differentiation into DA neurons. Further experiments with conditioned media from hpNPCs revealed that the secreted factors from hpNPCs modulated immune responses and neural protection. Taken together, both DLL1-mediated contact signals and paracrine factors play critical roles in hpNPC-mediated improvement. First showing here that hpMSCs and their neural derivative hpNPCs were able to restore the PD-associated deficits via dual mechanisms, neuroprotection and immunosuppression, this study expanded our knowledge of therapeutic mechanisms in PD and other age-related diseases.

Comparison of the therapeutic potential of adult and embryonic neural precursor cells in a rat model of Parkinson disease

2008 ◽  
Vol 108 (1) ◽  
pp. 149-159 ◽  
Author(s):  
Kenichiro Muraoka ◽  
Tetsuro Shingo ◽  
Takao Yasuhara ◽  
Masahiro Kameda ◽  
Wen Ji Yuen ◽  
...  
Keyword(s):  
Parkinson Disease ◽  
Rat Model ◽  
Fluorescent Protein ◽  
Therapeutic Potential ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Therapeutic Effects ◽  
Adenoviral Infection

Object The therapeutic effects of adult and embryonic neural precursor cells (NPCs) were evaluated and their therapeutic potential compared in a rat model of Parkinson disease. Methods Adult NPCs were obtained from the subventricular zone and embryonic NPCs were taken from the ganglionic eminence of 14-day-old embryos. Each NPC type was cultured with epidermal growth factor. The in vitro neuronal differentiation rate of adult NPCs was approximately equivalent to that of embryonic NPCs after two passages. Next, the NPCs were transfected with either green fluorescent protein or glial cell line–derived neurotrophic factor (GDNF) by adenoviral infection and transplanted into the striata in a rat model of Parkinson disease (PD) induced by unilateral intrastriatal injection of 6-hydroxydopamine. An amphetamine-induced rotation test was used to evaluate rat behavioral improvement, and immunohistochemical analysis was performed to compare grafted cell survival, differentiation, and host tissue changes. Results The rats with GDNF-transfected NPCs had significantly fewer amphetamine-induced rotations and less histological damage. Except for the proportion of surviving grafted cells, there were no significant differences between adult and embryonic NPCs. Conclusions Adult and embryonic NPCs have a comparable therapeutic potential in a rat model of PD.

scholarly journals Neural precursor cells are decreased in the hippocampus of the delayed carbon monoxide encephalopathy rat model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shinichiro Ochi ◽  
Keisuke Sekiya ◽  
Naoki Abe ◽  
Yu Funahashi ◽  
Hiroshi Kumon ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Cognitive Impairment ◽  
Rat Model ◽  
Cell Number ◽  
Lipid Binding ◽  
Precursor Cells ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Neural Precursor Cells ◽  
Neural Precursor

AbstractThe pathophysiology of delayed carbon monoxide (CO) encephalopathy remains unclear. In this study, the effects of CO exposure on the dentate gyrus (DG) were investigated in a Wistar rat model by histochemical and molecular methods. Model rats showed significant cognitive impairment in the passive-avoidance test beginning 7 days after CO exposure. Immunohistochemistry showed that compared to the control, the cell number of SRY (sex-determining region Y)-box 2 (SOX2)+/brain lipid binding protein (BLBP)+/glial fibrillary acidic protein (GFAP)+ cells in the DG was significantly less, but the number of SOX2+/GFAP− cells was not, reflecting a decreased number of type 1 and type 2a neural precursor cells. Compared to the control, the numbers of CD11b+ cells and neuron glial antigen 2+ cells were significantly less, but the number of SOX2−/GFAP+ cells was not. Flow cytometry showed that the percent of live microglial cells isolated from the hippocampus in this CO rat model was significantly lower than in controls. Furthermore, mRNA expression of fibroblast growth factor 2 and glial cell-derived neurotrophic factor, which are neurogenic factors, was significantly decreased in that area. We conclude that, in this rat model, there is an association between delayed cognitive impairment with dysregulated adult hippocampal neurogenesis and glial changes in delayed CO encephalopathy.

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