Cited by 73Neuroinflammation and Neurodegeneration MechanismsTryptophan and brain disordersAlzheimer's disease research and treatments

Increased IL-1β in cortex of aged rats is accompanied by downregulation of ERK and PI-3 kinase

Maher, F.O, Martin, D.S.D, Lynch, M.A·2004·Neurobiology of Aging

Abstract

Ageing is accompanied by a myriad of changes, which lead to deficits in synaptic function and recent studies have identified an increase in concentration of the proinflammatory cytokine, interleukin-1beta (IL-1beta), as a factor which significantly contributes to deterioration of cell function. Here, we consider that increased IL-1beta concentration and upregulation of IL-1beta-induced cell signalling cascades may be accompanied by downregulation of survival signals, perhaps as a consequence of decreased neurotrophins-associated signalling. The data indicate that increased IL-1beta concentration was coupled with downregulation of ERK and phosphoinositide-3 kinase (PI-3 kinase) in cortical tissue prepared from aged rats. These changes could not be attributed to decreased concentration of NGF or BDNF but the evidence suggested that they may be a consequence of an age-related change in the anti-inflammatory cytokine, IL-4. Significantly, treatment of aged rats with eicosapentaenoic acid reversed the age-related increases in IL-1beta and IL-1beta-induced signalling and also the age-related changes in IL-4, ERK and PI-3 kinase.

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Crossref · 10.1016/j.neurobiolaging.2003.08.007

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  • Associated with these morphological alterations are biochemical changes, such as elevated expression of antigen presentation molecules (MHCII), Toll-like receptors, pro-inflammatory cytokines (IL-1β), reduced expression of regulatory molecules (CX3CR1 and CD200R), DNA methylation changes and telomere shortening.

    “Associated with these morphological alterations are biochemical changes, such as elevated expression of antigen presentation molecules (MHCII), Toll-like receptors, pro-inflammatory cytokines (IL-1β), reduced expression of regulatory molecules (CX3CR1 and CD200R) (Frank et al, 2006;Maher et al, 2004), DNA methylation changes and telomere shortening (Flanary and Streit, 2003;Zannas et al, 2015).”

    From Microglia Priming with Aging and Stress (2017) · cites this paper as Maher et al, 2004

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Authors
Maher, F. O., Martin, D. S. D., & Lynch, M. A.
Affiliations
Trinity College Dublin (IE)
Corresponding author
Lynch, M.A
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2004-07
Volume
25
Issue
6
Pages
795-806
ISSN
0197-4580 (ISSN-L)
OpenAlex
W2086192199
Cited by
73
References
73
Citations by year
2026: 2 · 2025: 1 · 2024: 1 · 2022: 1 · 2021: 4 · 2020: 3 · 2019: 5 · 2018: 5 · 2017: 4 · 2016: 3 · 2015: 5 · 2014: 6 · 2012: 6
FWCI
1.79
Type
journal article
Language
en
Open access
closed
Locations
  • Neurobiology of Aging (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Keywords
IL-1β, aging, cerebral cortex, ERK signaling, PI3-kinase, neurotrophin signaling, IL-4, eicosapentaenoic acid, neuroinflammation, synaptic dysfunction, nerve growth factor, brain-derived neurotrophic factor
MeSH terms
Aging, Animals, Bacterial Proteins, Butadienes, Carrier Proteins, Cells, Cultured, Cerebral Cortex, Chromones, Drug Interactions, Enzyme Inhibitors, Gene Expression Regulation, Interleukin-1, Male, Membrane Proteins, Morpholines, Nitriles, Blotting, Western, Down-Regulation, Rats, Wistar, Receptors, Interleukin-1, Brain-Derived Neurotrophic Factor, Phosphatidylinositol 3-Kinases, Caspases, Receptor, trkA, Mitogen-Activated Protein Kinases, Nerve Growth Factor, Rats, Caspase 3

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