The role of oxidative stress in nervous system aging.

While oxidative stress is implicated in aging, the impact of oxidative stress on aging in the peripheral nervous system is not well understood. To determine a potential mechanism for age-related deficits in the peripheral nervous system, we examined both functional and morphological changes and util...

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Main Authors: Catrina Sims-Robinson, Junguk Hur, John M Hayes, Jacqueline R Dauch, Peter J Keller, Susan V Brooks, Eva L Feldman
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2013-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3699525?pdf=render
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spelling doaj-8acd5e6c307a40c99f6352279bd72a262020-11-24T20:50:00ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0187e6801110.1371/journal.pone.0068011The role of oxidative stress in nervous system aging.Catrina Sims-RobinsonJunguk HurJohn M HayesJacqueline R DauchPeter J KellerSusan V BrooksEva L FeldmanWhile oxidative stress is implicated in aging, the impact of oxidative stress on aging in the peripheral nervous system is not well understood. To determine a potential mechanism for age-related deficits in the peripheral nervous system, we examined both functional and morphological changes and utilized microarray technology to compare normal aging in wild-type mice to effects in copper/zinc superoxide dismutase-deficient (Sod1(-/-)) mice, a mouse model of increased oxidative stress. Sod1(-/-) mice exhibit a peripheral neuropathy phenotype with normal sensory nerve function and deficits in motor nerve function. Our data indicate that a decrease in the synthesis of cholesterol, which is vital to myelin formation, correlates with the structural deficits in axons, myelin, and the cell body of motor neurons in the Sod1(+/+) mice at 30 months and the Sod1(-/-) mice at 20 months compared with mice at 2 months. Collectively, we have demonstrated that the functional and morphological changes within the peripheral nervous system in our model of increased oxidative stress are manifested earlier and resemble the deficits observed during normal aging.http://europepmc.org/articles/PMC3699525?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Catrina Sims-Robinson
Junguk Hur
John M Hayes
Jacqueline R Dauch
Peter J Keller
Susan V Brooks
Eva L Feldman
spellingShingle Catrina Sims-Robinson
Junguk Hur
John M Hayes
Jacqueline R Dauch
Peter J Keller
Susan V Brooks
Eva L Feldman
The role of oxidative stress in nervous system aging.
PLoS ONE
author_facet Catrina Sims-Robinson
Junguk Hur
John M Hayes
Jacqueline R Dauch
Peter J Keller
Susan V Brooks
Eva L Feldman
author_sort Catrina Sims-Robinson
title The role of oxidative stress in nervous system aging.
title_short The role of oxidative stress in nervous system aging.
title_full The role of oxidative stress in nervous system aging.
title_fullStr The role of oxidative stress in nervous system aging.
title_full_unstemmed The role of oxidative stress in nervous system aging.
title_sort role of oxidative stress in nervous system aging.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2013-01-01
description While oxidative stress is implicated in aging, the impact of oxidative stress on aging in the peripheral nervous system is not well understood. To determine a potential mechanism for age-related deficits in the peripheral nervous system, we examined both functional and morphological changes and utilized microarray technology to compare normal aging in wild-type mice to effects in copper/zinc superoxide dismutase-deficient (Sod1(-/-)) mice, a mouse model of increased oxidative stress. Sod1(-/-) mice exhibit a peripheral neuropathy phenotype with normal sensory nerve function and deficits in motor nerve function. Our data indicate that a decrease in the synthesis of cholesterol, which is vital to myelin formation, correlates with the structural deficits in axons, myelin, and the cell body of motor neurons in the Sod1(+/+) mice at 30 months and the Sod1(-/-) mice at 20 months compared with mice at 2 months. Collectively, we have demonstrated that the functional and morphological changes within the peripheral nervous system in our model of increased oxidative stress are manifested earlier and resemble the deficits observed during normal aging.
url http://europepmc.org/articles/PMC3699525?pdf=render
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