Age-related neuroinflammatory changes negatively impact on neuronal function

Neuroinflammatory changes, characterized by an increase in microglial activation and often accompanied by upregulation of inflammatory cytokines like interleukin-1β (IL-1β), are common to many, if not all, neurodegenerative diseases. Similar, though less dramatic neuroinflammatory...

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Main Author: Marina A Lynch
Format: Article
Language:English
Published: Frontiers Media S.A. 2010-01-01
Series:Frontiers in Aging Neuroscience
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/neuro.24.006.2009/full
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spelling doaj-11c014b237314b83a78907afa19d28d72020-11-24T23:43:38ZengFrontiers Media S.A.Frontiers in Aging Neuroscience1663-43652010-01-01110.3389/neuro.24.006.20091206Age-related neuroinflammatory changes negatively impact on neuronal functionMarina A Lynch0Trinity College DublinNeuroinflammatory changes, characterized by an increase in microglial activation and often accompanied by upregulation of inflammatory cytokines like interleukin-1&beta; (IL-1&beta;), are common to many, if not all, neurodegenerative diseases. Similar, though less dramatic neuroinflammatory changes are also known to occur with age. Among the consequences of these changes is an impairment in synaptic function and the evidence suggests that inflammatory cytokines may be the primary contributory factor responsible for the deficits in synaptic plasticity which have been identified in aged rodents. Specifically a decrease in the ability of aged rats to sustain long-term potentiation (LTP) in perforant path-granule cells of the hippocampus is associated with increased microglial activation. This review considers the evidence which suggests a causal relationship between these changes and the factors which contribute to the age-related microglial activation, and reflects on data which demonstrate that agents which inhibit microglial activation also improve ability of rats to sustain LTP. <input id="gwProxy" type="hidden" /> <!--Session data--> <input id="jsProxy" onclick="jsCall();" type="hidden" />http://journal.frontiersin.org/Journal/10.3389/neuro.24.006.2009/fullcell-cell interactionNeuroinflammationinflammatory cytokinesinterleukin-1β (IL-1β)long-term potentiation (LTP)microglial activation
collection DOAJ
language English
format Article
sources DOAJ
author Marina A Lynch
spellingShingle Marina A Lynch
Age-related neuroinflammatory changes negatively impact on neuronal function
Frontiers in Aging Neuroscience
cell-cell interaction
Neuroinflammation
inflammatory cytokines
interleukin-1β (IL-1β)
long-term potentiation (LTP)
microglial activation
author_facet Marina A Lynch
author_sort Marina A Lynch
title Age-related neuroinflammatory changes negatively impact on neuronal function
title_short Age-related neuroinflammatory changes negatively impact on neuronal function
title_full Age-related neuroinflammatory changes negatively impact on neuronal function
title_fullStr Age-related neuroinflammatory changes negatively impact on neuronal function
title_full_unstemmed Age-related neuroinflammatory changes negatively impact on neuronal function
title_sort age-related neuroinflammatory changes negatively impact on neuronal function
publisher Frontiers Media S.A.
series Frontiers in Aging Neuroscience
issn 1663-4365
publishDate 2010-01-01
description Neuroinflammatory changes, characterized by an increase in microglial activation and often accompanied by upregulation of inflammatory cytokines like interleukin-1&beta; (IL-1&beta;), are common to many, if not all, neurodegenerative diseases. Similar, though less dramatic neuroinflammatory changes are also known to occur with age. Among the consequences of these changes is an impairment in synaptic function and the evidence suggests that inflammatory cytokines may be the primary contributory factor responsible for the deficits in synaptic plasticity which have been identified in aged rodents. Specifically a decrease in the ability of aged rats to sustain long-term potentiation (LTP) in perforant path-granule cells of the hippocampus is associated with increased microglial activation. This review considers the evidence which suggests a causal relationship between these changes and the factors which contribute to the age-related microglial activation, and reflects on data which demonstrate that agents which inhibit microglial activation also improve ability of rats to sustain LTP. <input id="gwProxy" type="hidden" /> <!--Session data--> <input id="jsProxy" onclick="jsCall();" type="hidden" />
topic cell-cell interaction
Neuroinflammation
inflammatory cytokines
interleukin-1β (IL-1β)
long-term potentiation (LTP)
microglial activation
url http://journal.frontiersin.org/Journal/10.3389/neuro.24.006.2009/full
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