Chapter title |
Phenotypic Screening of Small-Molecule Inhibitors: Implications for Therapeutic Discovery and Drug Target Development in Traumatic Brain Injury.
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Chapter number | 37 |
Book title |
Injury Models of the Central Nervous System
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Published in |
Methods in molecular biology, January 2016
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DOI | 10.1007/978-1-4939-3816-2_37 |
Pubmed ID | |
Book ISBNs |
978-1-4939-3814-8, 978-1-4939-3816-2
|
Authors |
Hassan Al-Ali, Vance P. Lemmon, John L. Bixby Ph.D., John L. Bixby |
Editors |
Firas H. Kobeissy, C. Edward Dixon, Ronald L. Hayes, Stefania Mondello |
Abstract |
The inability of central nervous system (CNS) neurons to regenerate damaged axons and dendrites following traumatic brain injury (TBI) creates a substantial obstacle for functional recovery. Apoptotic cell death, deposition of scar tissue, and growth-repressive molecules produced by glia further complicate the problem and make it challenging for re-growing axons to extend across injury sites. To date, there are no approved drugs for the treatment of TBI, accentuating the need for relevant leads. Cell-based and organotypic bioassays can better mimic outcomes within the native CNS microenvironment than target-based screening methods and thus should speed the discovery of therapeutic agents that induce axon or dendrite regeneration. Additionally, when used to screen focused chemical libraries such as small-molecule protein kinase inhibitors, these assays can help elucidate molecular mechanisms involved in neurite outgrowth and regeneration as well as identify novel drug targets. Here, we describe a phenotypic cellular (high content) screening assay that utilizes brain-derived primary neurons for screening small-molecule chemical libraries. |
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