Neuronal hyperexcitability following mTBI: Cellular molecular mechanisms and therapeutical implications

Nicola Maggio; Vardit Rubovitch; Barry J. Hoffer; Bruce A. Citron; Nigel H. Greig; Chaim G. Pick

doi:10.1016/B978-0-12-812344-7.00006-6

Neuronal hyperexcitability following mTBI: Cellular molecular mechanisms and therapeutical implications

Nicola Maggio, Vardit Rubovitch, Barry J. Hoffer, Bruce A. Citron, Nigel H. Greig, Chaim G. Pick

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

Abstract

Traumatic brain injury (TBI) remains the major cause of brain damage for children and young adults. While preventative measures may act to reduce the incidence of initial blunt trauma, well-tolerated drugs are needed to target the neurologically damaging internal cascade of molecular mechanisms that follow. Such processes, known collectively as the secondary injury phase, include inflammation, excitotoxicity, and apoptosis among other changes still subject to research. In this chapter, we aim to review the current trends in the molecular and cellular mechanisms in charge of neurological damage following mild TBI (mTBI) with a particular focus on neural hyperexcitability as well as discussing positive treatment findings that aim to mitigate the neuronal damage following mTBI.

Original language	English
Title of host publication	Neurosensory Disorders in Mild Traumatic Brain Injury
Publisher	Elsevier
Pages	67-81
Number of pages	15
ISBN (Electronic)	9780128123447
ISBN (Print)	9780128125489
DOIs	https://doi.org/10.1016/B978-0-12-812344-7.00006-6
State	Published - 1 Jan 2019

Keywords

Chronic traumatic encephalopathy
Injury
Molecular mechanisms
Neuronal hyperexcitability
Novel therapeutical implications
mTBI

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10.1016/B978-0-12-812344-7.00006-6

Cite this

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Neuronal hyperexcitability following mTBI: Cellular molecular mechanisms and therapeutical implications

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Keywords

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