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Selective CDK Inhibitors: Promising Candidates for Future Clinical Traumatic Brain Injury Trials

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Date 2014 Nov 5
PMID 25368642
Citations 8
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Abstract

Traumatic brain injury induces secondary injury that contributes to neuroinflammation, neuronal loss, and neurological dysfunction. One important injury mechanism is cell cycle activation which causes neuronal apoptosis and glial activation. The neuroprotective effects of both non-selective (Flavopiridol) and selective (Roscovitine and CR-8) cyclin-dependent kinase inhibitors have been shown across multiple experimental traumatic brain injury models and species. Cyclin-dependent kinaseinhibitors, administered as a single systemic dose up to 24 hours after traumatic brain injury, provide strong neuroprotection-reducing neuronal cell death, neuroinflammation and neurological dysfunction. Given their effectiveness and long therapeutic window, cyclin-dependent kinase inhibitors appear to be promising candidates for clinical traumatic brain injury trials.

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References
1.
Urrea C, Castellanos D, Sagen J, Tsoulfas P, Bramlett H, Dietrich W . Widespread cellular proliferation and focal neurogenesis after traumatic brain injury in the rat. Restor Neurol Neurosci. 2007; 25(1):65-76. View

2.
Byrnes K, Loane D, Stoica B, Zhang J, Faden A . Delayed mGluR5 activation limits neuroinflammation and neurodegeneration after traumatic brain injury. J Neuroinflammation. 2012; 9:43. PMC: 3308916. DOI: 10.1186/1742-2094-9-43. View

3.
Kabadi S, Stoica B, Byrnes K, Hanscom M, Loane D, Faden A . Selective CDK inhibitor limits neuroinflammation and progressive neurodegeneration after brain trauma. J Cereb Blood Flow Metab. 2011; 32(1):137-49. PMC: 3323296. DOI: 10.1038/jcbfm.2011.117. View

4.
Di Giovanni S, Movsesyan V, Ahmed F, Cernak I, Schinelli S, Stoica B . Cell cycle inhibition provides neuroprotection and reduces glial proliferation and scar formation after traumatic brain injury. Proc Natl Acad Sci U S A. 2005; 102(23):8333-8. PMC: 1149422. DOI: 10.1073/pnas.0500989102. View

5.
Taupin P . BrdU immunohistochemistry for studying adult neurogenesis: paradigms, pitfalls, limitations, and validation. Brain Res Rev. 2006; 53(1):198-214. DOI: 10.1016/j.brainresrev.2006.08.002. View