Cited by 327Neuroinflammation and Neurodegeneration MechanismsGenetics, Aging, and Longevity in Model OrganismsPhagocytosis and Immune Regulation

mRNA up-regulation of MHC II and pivotal pro-inflammatory genes in normal brain aging

Frank, Matthew G., Barrientos, Ruth M., Biedenkapp, Joseph C., Rudy, Jerry W., Watkins, Linda R., Maier, Steven F.·2006·Neurobiology of Aging

Abstract

In normal brain aging, CNS resident macrophages exhibit increased expression of major histocompatibility complex (MHC) II expression. However, the transcriptional basis for this observation has not been clarified nor have age-related alterations in pivotal pro-inflammatory genes been characterized. Age-related mRNA alterations in MHC II, MHC II accessory molecules and several pro-inflammatory mediators were measured in older (24 months) and younger (3 months) male F344xBN F1 rats. Real time RT-PCR was utilized to measure steady state mRNA levels in hippocampus. Older as compared to younger animals exhibited increased mRNA levels of MHC II, CD86, CIITA and IFN-gamma. Furthermore, IL-10 and CD200 mRNA, molecules that down-regulate macrophage activation, was decreased in older animals. The present results indicate that normal brain aging is characterized by a shift towards a pro-inflammatory microenvironment in the CNS.

Integrity signals

Registry

Crossref · 10.1016/j.neurobiolaging.2005.03.013

Cites

51 of 51 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • 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 Frank et al, 2006

  • Microglia under normal aging showed upregulation of genes associated with antigen presentation, such as MHCII, CD86, and CIITA, and suppression of anti-inflammatory genes, such as IL-10 and CD200.

    “Microglia under normal aging (ie, aging in absence of neurodegeneration) showed upregulation of genes associated with antigen presentation, such as MHCII, CD86, and CIITA (Frank et al, 2006;Godbout et al, 2005;VanGuilder et al, 2011), and suppression of anti-inflammatory genes, such as IL-10 and CD200 (Frank et al, 2006).”

    From Microglia Priming with Aging and Stress (2017) · cites this paper as Frank et al, 2006

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Frank, M. G., Barrientos, R. M., Biedenkapp, J. C., Rudy, J. W., Watkins, L. R., & Maier, S. F.
Affiliations
University of Colorado Boulder (US)
Corresponding author
Frank, Matthew G.
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2006-05
Volume
27
Issue
5
Pages
717-722
ISSN
0197-4580 (ISSN-L)
OpenAlex
W2078514181
Cited by
327
References
51
Citations by year
2026: 7 · 2025: 7 · 2024: 12 · 2023: 15 · 2022: 20 · 2021: 24 · 2020: 21 · 2019: 17 · 2018: 19 · 2017: 13 · 2016: 24 · 2015: 18 · 2014: 17 · 2013: 13 · 2012: 18
FWCI
6.24
Type
journal article
Language
en
Open access
closed
Locations
  • Neurobiology of Aging (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5f32mh064339-03)
  • National Institute of Mental Health (5 F32 MH064339-03)
  • National Institute on Drug Abuse (F32DA015591)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
Keywords
brain aging, MHC class II, microglia, pro-inflammatory genes, hippocampus, CD86, CIITA, interferon-gamma, IL-10, CD200, macrophage activation, neuroinflammation, gene expression
MeSH terms
Aging, Animals, Brain, Genes, MHC Class II, Inflammation, Male, Neurons, Rats, Inbred F344, Receptors, Immunologic, RNA, Messenger, Antigens, CD, Up-Regulation, DNA Primers, DNA, Complementary, Gene Expression Regulation, Developmental, Reverse Transcriptase Polymerase Chain Reaction, Rats

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review