Institution
ReNeuron
About: ReNeuron is a based out in . It is known for research contribution in the topics: Neural stem cell & Stem cell. The organization has 87 authors who have published 113 publications receiving 5975 citations.
Topics: Neural stem cell, Stem cell, Transplantation, Cellular differentiation, Neuroepithelial cell
Papers published on a yearly basis
Papers
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TL;DR: It is reported that PINK1 plays a neuroprotective role in the mitochondria of mammalian neurons, especially against stress such as staurosporine, and evidence that cellular compensatory mechanisms such as mitochondrial biogenesis and upregulation of lysosomal degradation pathways occur in Pink1 deficiency.
Abstract: Parkinson's disease (PD) is a common age-related neurodegenerative disease and it is critical to develop models which recapitulate the pathogenic process including the effect of the ageing process. Although the pathogenesis of sporadic PD is unknown, the identification of the mendelian genetic factor PINK1 has provided new mechanistic insights. In order to investigate the role of PINK1 in Parkinson's disease, we studied PINK1 loss of function in human and primary mouse neurons. Using RNAi, we created stable PINK1 knockdown in human dopaminergic neurons differentiated from foetal ventral mesencephalon stem cells, as well as in an immortalised human neuroblastoma cell line. We sought to validate our findings in primary neurons derived from a transgenic PINK1 knockout mouse. For the first time we demonstrate an age dependent neurodegenerative phenotype in human and mouse neurons. PINK1 deficiency leads to reduced long-term viability in human neurons, which die via the mitochondrial apoptosis pathway. Human neurons lacking PINK1 demonstrate features of marked oxidative stress with widespread mitochondrial dysfunction and abnormal mitochondrial morphology. We report that PINK1 plays a neuroprotective role in the mitochondria of mammalian neurons, especially against stress such as staurosporine. In addition we provide evidence that cellular compensatory mechanisms such as mitochondrial biogenesis and upregulation of lysosomal degradation pathways occur in PINK1 deficiency. The phenotypic effects of PINK1 loss-of-function described here in mammalian neurons provides mechanistic insight into the age-related degeneration of nigral dopaminergic neurons seen in PD.
325 citations
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TL;DR: Single intracerebral doses of CTX-DP up to 20 million cells induced no adverse events and were associated with improved neurological function and support further investigation of CTx-DP in stroke patients.
295 citations
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TL;DR: Transplantation of human neural stem cell line CTX0E03 in a rat model of stroke (MCAo) caused statistically significant improvements in both sensorimotor function and gross motor asymmetry at 6-12 weeks post-grafting, and indicates that the cell line has the appropriate biological and manufacturing characteristics necessary for development as a therapeutic cell line.
295 citations
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TL;DR: It is demonstrated that GRID-enhanced MRI can reliably identify transplanted stem cells and their migration in the brain.
281 citations
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TL;DR: It is hypothesize that transitioning to defined manufacturing platforms will increase consistency of the exosome product and improve their clinical advancement as a new therapeutic tool.
268 citations
Authors
Showing all 87 results
Name | H-index | Papers | Citations |
---|---|---|---|
Jeffrey A. Gray | 90 | 305 | 40643 |
David Parkinson | 62 | 283 | 16221 |
Helen Hodges | 38 | 69 | 4304 |
Michel Modo | 37 | 119 | 5135 |
John Sinden | 31 | 89 | 3232 |
Caroline A Hicks | 28 | 44 | 2312 |
David Virley | 27 | 49 | 2330 |
Lara Stevanato | 19 | 34 | 1423 |
Sara Patel | 18 | 24 | 1813 |
Erik Miljan | 15 | 20 | 1439 |
Fiza Rashid-Doubell | 13 | 32 | 853 |
Randolph Corteling | 12 | 22 | 661 |
Paul Stroemer | 11 | 13 | 723 |
G. A. Grigor'yan | 10 | 25 | 866 |
Z. Dong | 9 | 11 | 1212 |