Relevance of motoneuron specification and programmed cell death in embryos to therapy of ALS
Birth Defects Research Part C - Embryo Today: Reviews, ISSN: 1542-975X, Vol: 75, Issue: 4, Page: 294-304
2005
- 3Citations
- 15Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations3
- Citation Indexes3
- CrossRef1
- Captures15
- Readers15
- 15
Review Description
The molecular cues that generate spinal motoneurons in early embryonic development are well defined. Motoneurons are generated in excess and consequently undergo a natural period of programmed cell death. Although it is not known exactly how motoneurons compete for survival in embryonic development, it is hypothesized that they rely on the ability to access limited amounts of trophic factors from peripheral tissues, a process that is tightly regulated by skeletal muscle activity. Attempts to elucidate the molecular mechanisms that underlie motoneuron generation and programmed cell death in embryos have led to various effective strategies for treating injury and disease in animal models. Such studies provide great hope for the amelioration of human amyotrophic lateral sclerosis (ALS), a devastating progressive motoneuron degenerative disease. Here we review the clinical relevance of studying motoneuron specification and death during embryonic development. © 2006 Wiley-Liss, Inc.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=32644443605&origin=inward; http://dx.doi.org/10.1002/bdrc.20051; http://www.ncbi.nlm.nih.gov/pubmed/16425251; https://onlinelibrary.wiley.com/doi/10.1002/bdrc.20051; http://doi.wiley.com/10.1002/bdrc.20051; https://onlinelibrary.wiley.com/doi/abs/10.1002/bdrc.20051
Wiley
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