scholarly journals VCE-003.2, a novel cannabigerol derivative, enhances neuronal progenitor cell survival and alleviates symptomatology in murine models of Huntington’s disease

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Javier Díaz-Alonso ◽  
Juan Paraíso-Luna ◽  
Carmen Navarrete ◽  
Carmen del Río ◽  
Irene Cantarero ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Cell Survival ◽  
Huntington’S Disease ◽  
Progenitor Cell ◽  
Murine Models ◽  
Neuronal Progenitor ◽  
Neuronal Progenitor Cell

scholarly journals Creatine supplementation improves neural progenitor cell survival in Huntington's disease

2016 ◽  
Vol 2 (3) ◽  
pp. 133 ◽  
Author(s):  
HansR Widmer ◽  
RobertH Andres ◽  
Theo Wallimann
Keyword(s):  
Huntington's Disease ◽  
Cell Survival ◽  
Huntington’S Disease ◽  
Progenitor Cell ◽  
Creatine Supplementation ◽  
Neural Progenitor Cell ◽  
Neural Progenitor

Murine Models of Huntington’s Disease for Evaluating Therapeutics

2018 ◽  
pp. 179-207 ◽  
Author(s):  
Natalia Kosior ◽  
Blair R. Leavitt
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Murine Models

Increased Serotonin Transporter Expression in Huntington’s Disease Patients Is Not Consistently Replicated in Murine Models

2019 ◽  
Vol 8 (4) ◽  
pp. 449-457
Author(s):  
Yanqing He ◽  
Yalikun Suofu ◽  
Svitlana Yablonska ◽  
Xiaoming Wang ◽  
Timothy M. Larkin ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Serotonin Transporter ◽  
Murine Models ◽  
Transporter Expression

Regulated expression of neurogenic basic helix-loop-helix transcription factors during differentiation of the immortalized neuronal progenitor cell line HC2S2 into neurons

1998 ◽  
Vol 293 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Toshiyuki Ohtsuka ◽  
Minoru Asahi ◽  
Nobuki Matsuura ◽  
Haruhiko Kikuchi ◽  
Masato Hojo ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Cell Line ◽  
Progenitor Cell ◽  
Basic Helix Loop Helix ◽  
Helix Loop Helix ◽  
Neuronal Progenitor ◽  
Neuronal Progenitor Cell ◽  
Regulated Expression ◽  
Progenitor Cell Line

Expression of apoptosis-related proteins during differentiation in the human neuronal progenitor cell line VM197

2007 ◽  
Vol 2007 (Fall) ◽  
Author(s):  
Alexandra Jaeger ◽  
Susanne Klum ◽  
Dieter G. Weiss ◽  
Ralf Kriehuber
Keyword(s):  
Cell Line ◽  
Progenitor Cell ◽  
Neuronal Progenitor ◽  
Neuronal Progenitor Cell ◽  
Related Proteins ◽  
Progenitor Cell Line

Investigation of neuronal progenitor cell origin after transient focal cerebral ischemia in mice

2010 ◽  
Vol 68 (3) ◽  
pp. 256-259
Author(s):  
Jan-Kolja Strecker ◽  
Jens Minnerup ◽  
Sevgi Sevimli ◽  
E. Bernd Ringelstein ◽  
Wolf-Rüdiger Schäbitz ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Progenitor Cell ◽  
Focal Cerebral Ischemia ◽  
Neuronal Progenitor ◽  
Transient Focal Cerebral Ischemia ◽  
Neuronal Progenitor Cell

Neuregulin 1 growth factors regulate proliferation but not apoptosis of a CNS neuronal progenitor cell line

2006 ◽  
Vol 1108 (1) ◽  
pp. 63-75 ◽  
Author(s):  
J. Michelle Edwards ◽  
Jane E. Bottenstein
Keyword(s):  
Growth Factors ◽  
Cell Line ◽  
Progenitor Cell ◽  
Neuregulin 1 ◽  
Neuronal Progenitor ◽  
Neuronal Progenitor Cell ◽  
Progenitor Cell Line

scholarly journals Neuroprotective strategies for NMDAR-mediated excitotoxicity in Huntington’s Disease

2016 ◽  
Author(s):  
KD Girling ◽  
YT Wang
Keyword(s):  
Cell Death ◽  
Huntington's Disease ◽  
Cell Survival ◽  
Huntington’S Disease ◽  
Glutamate Release ◽  
Clinical Approach ◽  
Wide Range ◽  
Pubmed Search ◽  
Nmdar Activation ◽  
Cell Death Signaling

AbstractBACKGROUNDHuntington’s Disease (HD) is an autosomal dominant neurodegenerative disease causing severe neurodegeneration of the striatum as well as marked cognitive and motor disabilities. Excitotoxicity, caused by overstimulation of NMDA receptors (NMDARs) has been shown to have a key role in the neuropathogenesis of HD, suggesting that targeting NMDAR-dependent signaling may be an effective clinical approach for HD. However, broad NMDAR antagonists are generally poor therapeutics in clinical practice. It has been suggested that GluN2A-containing, synaptically located NMDARs activate cell survival signaling pathways, while GluN2B-containing, primarily extrasynaptic NMDARs trigger cell death signaling. A better approach to development of effective therapeutics for HD may be to target, specifically, the cell-death specific pathways associated with extrasynaptic GluN2B NMDAR activation, while maintaining or potentiating the cell-survival activity of GluN2A-NMDARs.OBJECTIVEThis review outlines the role of NMDAR-mediated excitotoxicity in HD and overviews current efforts to develop better therapeutics for HD where NMDAR excitotoxicity is the target.METHODSA systematic review process was conducted using the PubMed search engine focusing on research conducted in the past 5-10 years. 250 articles were consulted for the review, with key search terms including “Huntington’s Disease”, “excitotoxicity”, “NMDAR” and “therapeutics”.RESULTSA wide range of NMDAR excitotoxicity-based targets for HD were identified and reviewed, including targeting NMDARs directly by blocking GluN2B, extrasynaptic NMDARs and/or potentiating GluN2A, synaptic NMDARs, targeting glutamate release or uptake, or targeting specific downstream cell-death signaling of NMDARs.CONCLUSIONThe current review identifies NMDAR-mediated excitotoxicity as a key player in HD pathogenesis and points to various excitotoxicity-focused targets as potential future preventative therapeutics for HD.

scholarly journals Impact of a cytomegalovirus kinase inhibitor on infection and neuronal progenitor cell differentiation

2016 ◽  
Vol 129 ◽  
pp. 67-73 ◽  
Author(s):  
Tarin M. Bigley ◽  
Jered V. McGivern ◽  
Allison D. Ebert ◽  
Scott S. Terhune
Keyword(s):  
Cell Differentiation ◽  
Progenitor Cell ◽  
Kinase Inhibitor ◽  
Neuronal Progenitor ◽  
Neuronal Progenitor Cell
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