File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Mechanisms of late-onset cognitive decline after early-life stress

TitleMechanisms of late-onset cognitive decline after early-life stress
Authors
KeywordsReferences (75) View In Table Layout
Issue Date2005
PublisherSociety for Neuroscience. The Journal's web site is located at http://www.jneurosci.org
Citation
Journal of Neuroscience, 2005, v. 25 n. 41, p. 9328-9338 How to Cite?
AbstractProgressive cognitive deficits that emerge with aging are a result of complex interactions of genetic and environmental factors. Whereas much has been learned about the genetic underpinnings of these disorders, the nature of "acquired" contributing factors, and the mechanisms by which they promote progressive learning and memory dysfunction, remain largely unknown. Here, we demonstrate that a period of early-life "psychological" stress causes late-onset, selective deterioration of both complex behavior and synaptic plasticity: two forms of memory involving the hippocampus, were severely but selectively impaired in middle-aged, but not young adult, rats exposed to fragmented maternal care during the early postnatal period. At the cellular level, disturbances to hippocampal long-term potentiation paralleled the behavioral changes and were accompanied by dendritic atrophy and mossy fiber expansion. These findings constitute the first evidence that a short period of stress early in life can lead to delayed, progressive impairments of synaptic and behavioral measures of hippocampal function, with potential implications to the basis of age-related cognitive disorders in humans. Copyright © 2005 Society for Neuroscience.
Persistent Identifierhttp://hdl.handle.net/10722/90951
ISSN
2015 Impact Factor: 5.924
2015 SCImago Journal Rankings: 5.105
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBrunson, KLen_HK
dc.contributor.authorKramár, Een_HK
dc.contributor.authorLin, Ben_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorColgin, LLen_HK
dc.contributor.authorYanagihara, TKen_HK
dc.contributor.authorLynch, Gen_HK
dc.contributor.authorBaram, TZen_HK
dc.date.accessioned2010-09-17T10:10:49Z-
dc.date.available2010-09-17T10:10:49Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal of Neuroscience, 2005, v. 25 n. 41, p. 9328-9338en_HK
dc.identifier.issn0270-6474en_HK
dc.identifier.urihttp://hdl.handle.net/10722/90951-
dc.description.abstractProgressive cognitive deficits that emerge with aging are a result of complex interactions of genetic and environmental factors. Whereas much has been learned about the genetic underpinnings of these disorders, the nature of "acquired" contributing factors, and the mechanisms by which they promote progressive learning and memory dysfunction, remain largely unknown. Here, we demonstrate that a period of early-life "psychological" stress causes late-onset, selective deterioration of both complex behavior and synaptic plasticity: two forms of memory involving the hippocampus, were severely but selectively impaired in middle-aged, but not young adult, rats exposed to fragmented maternal care during the early postnatal period. At the cellular level, disturbances to hippocampal long-term potentiation paralleled the behavioral changes and were accompanied by dendritic atrophy and mossy fiber expansion. These findings constitute the first evidence that a short period of stress early in life can lead to delayed, progressive impairments of synaptic and behavioral measures of hippocampal function, with potential implications to the basis of age-related cognitive disorders in humans. Copyright © 2005 Society for Neuroscience.en_HK
dc.languageengen_HK
dc.publisherSociety for Neuroscience. The Journal's web site is located at http://www.jneurosci.orgen_HK
dc.relation.ispartofJournal of Neuroscienceen_HK
dc.subjectReferences (75) View In Table Layouten_HK
dc.titleMechanisms of late-onset cognitive decline after early-life stressen_HK
dc.typeArticleen_HK
dc.identifier.emailLin, B:blin@hku.hken_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1523/JNEUROSCI.2281-05.2005en_HK
dc.identifier.pmid16221841-
dc.identifier.pmcidPMC3100717-
dc.identifier.scopuseid_2-s2.0-26844446451en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-26844446451&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue41en_HK
dc.identifier.spage9328en_HK
dc.identifier.epage9338en_HK
dc.identifier.isiWOS:000232546300002-
dc.identifier.f10001120-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats