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Systemic Inflammation Mediates Age-Related Cognitive Deficits
The association between systemic inflammation and cognitive deficits is well-documented. Further, previous studies have shown that systemic inflammation levels increase with age. The present study took a novel approach by examining the extent to which systemic inflammation levels mediated age-relate...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6088306/ https://www.ncbi.nlm.nih.gov/pubmed/30127734 http://dx.doi.org/10.3389/fnagi.2018.00236 |
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author | Lin, Tian Liu, Gene A. Perez, Eliany Rainer, Robert D. Febo, Marcelo Cruz-Almeida, Yenisel Ebner, Natalie C. |
author_facet | Lin, Tian Liu, Gene A. Perez, Eliany Rainer, Robert D. Febo, Marcelo Cruz-Almeida, Yenisel Ebner, Natalie C. |
author_sort | Lin, Tian |
collection | PubMed |
description | The association between systemic inflammation and cognitive deficits is well-documented. Further, previous studies have shown that systemic inflammation levels increase with age. The present study took a novel approach by examining the extent to which systemic inflammation levels mediated age-related cognitive decline. Forty-seven young and 46 older generally healthy adults completed two cognitive tasks measuring processing speed and short-term memory, respectively. Serum concentrations of three inflammatory biomarkers (including interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), C-reactive protein (CRP)) were measured in each participant. Both cognitive measures showed age-related deficits. In addition, levels of IL-6 and TNF-α were elevated with age. IL-6 partially mediated the difference in processing speed between the young and the older participant age group; there was no mediation effect for TNF-α and CRP. Considering chronological age, IL-6 partially accounted for age-related impairment in processing speed within older but not young participants. No effects were found for short-term memory. Evidence from this research supports the role of inflammatory processes in age-related cognitive decline. Processes involved in this mediation and differences in inflammatory influence on specific cognitive functions are discussed. |
format | Online Article Text |
id | pubmed-6088306 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-60883062018-08-20 Systemic Inflammation Mediates Age-Related Cognitive Deficits Lin, Tian Liu, Gene A. Perez, Eliany Rainer, Robert D. Febo, Marcelo Cruz-Almeida, Yenisel Ebner, Natalie C. Front Aging Neurosci Neuroscience The association between systemic inflammation and cognitive deficits is well-documented. Further, previous studies have shown that systemic inflammation levels increase with age. The present study took a novel approach by examining the extent to which systemic inflammation levels mediated age-related cognitive decline. Forty-seven young and 46 older generally healthy adults completed two cognitive tasks measuring processing speed and short-term memory, respectively. Serum concentrations of three inflammatory biomarkers (including interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), C-reactive protein (CRP)) were measured in each participant. Both cognitive measures showed age-related deficits. In addition, levels of IL-6 and TNF-α were elevated with age. IL-6 partially mediated the difference in processing speed between the young and the older participant age group; there was no mediation effect for TNF-α and CRP. Considering chronological age, IL-6 partially accounted for age-related impairment in processing speed within older but not young participants. No effects were found for short-term memory. Evidence from this research supports the role of inflammatory processes in age-related cognitive decline. Processes involved in this mediation and differences in inflammatory influence on specific cognitive functions are discussed. Frontiers Media S.A. 2018-08-06 /pmc/articles/PMC6088306/ /pubmed/30127734 http://dx.doi.org/10.3389/fnagi.2018.00236 Text en Copyright © 2018 Lin, Liu, Perez, Rainer, Febo, Cruz-Almeida and Ebner. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Lin, Tian Liu, Gene A. Perez, Eliany Rainer, Robert D. Febo, Marcelo Cruz-Almeida, Yenisel Ebner, Natalie C. Systemic Inflammation Mediates Age-Related Cognitive Deficits |
title | Systemic Inflammation Mediates Age-Related Cognitive Deficits |
title_full | Systemic Inflammation Mediates Age-Related Cognitive Deficits |
title_fullStr | Systemic Inflammation Mediates Age-Related Cognitive Deficits |
title_full_unstemmed | Systemic Inflammation Mediates Age-Related Cognitive Deficits |
title_short | Systemic Inflammation Mediates Age-Related Cognitive Deficits |
title_sort | systemic inflammation mediates age-related cognitive deficits |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6088306/ https://www.ncbi.nlm.nih.gov/pubmed/30127734 http://dx.doi.org/10.3389/fnagi.2018.00236 |
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