Neuroprotective levels of IGF-1 exacerbate epileptogenesis after brain injury

DSpace/Manakin Repository

Neuroprotective levels of IGF-1 exacerbate epileptogenesis after brain injury

Citable link to this page

 

 
Title: Neuroprotective levels of IGF-1 exacerbate epileptogenesis after brain injury
Author: Song, Yu; Pimentel, Corrin; Walters, Katherine; Boller, Lauren; Ghiasvand, Shabnam; Liu, Jing; Staley, Kevin J.; Berdichevsky, Yevgeny

Note: Order does not necessarily reflect citation order of authors.

Citation: Song, Yu, Corrin Pimentel, Katherine Walters, Lauren Boller, Shabnam Ghiasvand, Jing Liu, Kevin J. Staley, and Yevgeny Berdichevsky. 2016. “Neuroprotective levels of IGF-1 exacerbate epileptogenesis after brain injury.” Scientific Reports 6 (1): 32095. doi:10.1038/srep32095. http://dx.doi.org/10.1038/srep32095.
Full Text & Related Files:
Abstract: Exogenous Insulin-Like Growth Factor-1 (IGF-1) is neuroprotective in animal models of brain injury, and has been considered as a potential therapeutic. Akt-mTOR and MAPK are downstream targets of IGF-1 signaling that are activated after brain injury. However, both brain injury and mTOR are linked to epilepsy, raising the possibility that IGF-1 may be epileptogenic. Here, we considered the role of IGF-1 in development of epilepsy after brain injury, using the organotypic hippocampal culture model of post-traumatic epileptogenesis. We found that IGF-1 was neuroprotective within a few days of injury but that long-term IGF-1 treatment was pro-epileptic. Pro-epileptic effects of IGF-1 were mediated by Akt-mTOR signaling. We also found that IGF-1 – mediated increase in epileptic activity led to neurotoxicity. The dualistic nature of effects of IGF-1 treatment demonstrates that anabolic enhancement through IGF-1 activation of mTOR cascade can be beneficial or harmful depending on the stage of the disease. Our findings suggest that epilepsy risk may need to be considered in the design of neuroprotective treatments for brain injury.
Published Version: doi:10.1038/srep32095
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4999804/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:29407676
Downloads of this work:

Show full Dublin Core record

This item appears in the following Collection(s)

 
 

Search DASH


Advanced Search
 
 

Submitters