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HERO ID
3199635
Reference Type
Journal Article
Title
Reactive oxygen species mediate cognitive deficits in experimental temporal lobe epilepsy
Author(s)
Pearson, JN; Rowley, S; Liang, LP; White, AM; Day, BJ; Patel, M
Year
2015
Is Peer Reviewed?
1
Journal
Neurobiology of Disease
ISSN:
0969-9961
EISSN:
1095-953X
Volume
82
Page Numbers
289-297
Language
English
PMID
26184893
DOI
10.1016/j.nbd.2015.07.005
Abstract
Cognitive dysfunction is an important comorbidity of temporal lobe epilepsy (TLE). However, no targeted therapies are available and the mechanisms underlying cognitive impairment, specifically deficits in learning and memory associated with TLE remain unknown. Oxidative stress is known to occur in the pathogenesis of TLE but its functional role remains to be determined. Here, we demonstrate that oxidative stress and resultant processes contribute to cognitive decline associated with epileptogenesis. Using a synthetic catalytic antioxidant, we show that pharmacological removal of reactive oxygen species (ROS) prevents 1) oxidative stress, 2) deficits in mitochondrial oxygen consumption rates, 3) hippocampal neuronal loss and 4) cognitive dysfunction without altering the intensity of the initial status epilepticus (SE) or epilepsy development in a rat model of SE-induced TLE. Moreover, the effects of the catalytic antioxidant on cognition persisted beyond the treatment period suggestive of disease-modification. The data implicate oxidative stress as a novel mechanism by which cognitive dysfunction can arise during epileptogenesis and suggest a potential disease-modifying therapeutic approach to target it.
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