My NCBI | Sign In
RSS Settings
  • Search:

Display Settings:

Format

Send to:

Choose Destination

    J Clin Invest. 2007 Jun;117(6):1595-604.

    Sustained hippocampal IL-1 beta overexpression mediates chronic neuroinflammation and ameliorates Alzheimer plaque pathology.

    Shaftel SS, Kyrkanides S, Olschowka JA, Miller JN, Johnson RE, O'Banion MK.

    Department of Neurobiology and Anatomy, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA.

    Comment in:

    Neuroinflammation is a conspicuous feature of Alzheimer disease (AD) pathology and is thought to contribute to the ultimate neurodegeneration that ensues. IL-1 beta has emerged as a prime candidate underlying this response. Here we describe a transgenic mouse model of sustained IL-1 beta overexpression that was capable of driving robust neuroinflammation lasting months after transgene activation. This response was characterized by astrocytic and microglial activation in addition to induction of proinflammatory cytokines. Surprisingly, when triggered in the hippocampus of the APPswe/PS1dE9 mouse model of AD, 4 weeks of IL-1 beta overexpression led to a reduction in amyloid pathology. Congophilic plaque area fraction and frequency as well as insoluble amyloid beta 40 (A beta 40) and A beta 42 decreased significantly. These results demonstrate a possible adaptive role for IL-1 beta-driven neuroinflammation in AD and may help explain recent failures of antiinflammatory therapeutics for this disease.

    PMID: 17549256 [PubMed - indexed for MEDLINE]

    PMCID: 1878531

    Publication Types, MeSH Terms, Substances, Grant Support

    Publication Types:

    MeSH Terms:

    Substances:

    Grant Support:

    LinkOut - more resources

    Full Text Sources:

    Medical:

    Molecular Biology Databases:

    Miscellaneous:

    Libraries:

    Supplemental Content

    Click here to read Click here to read

    Related articles

    Cited by 6 PubMed Central articles

    All links from this record

    • Related Articles

      Calculated set of PubMed citations closely related to the selected article(s) retrieved using a word weight algorithm. Related articles are displayed in ranked order from most to least relevant, with the “linked from” citation displayed first.

    • Gene

      Gene records that cite the current articles. Citations in Gene are added manually by NCBI or imported from outside public resources.

    • HomoloGene

      HomoloGene clusters of homologous genes and sequences that cite the current articles. These are references on the Gene and sequence records in the HomoloGene entry.

    • Nucleotide (RefSeq)

      NCBI nucleotide Reference Sequences (RefSeqs) that are cited in the current articles, included in the corresponding Gene Reference into Function, or that include the PubMed articles as references.

    • Nucleotide (Weighted)

      Nucleotide records associated with the current articles through the Gene database. These are the related sequences on the Gene record that are added manually by NCBI.

    • Protein (RefSeq)

      NCBI protein Reference Sequences (RefSeqs) that are cited in the current articles, included in the corresponding Gene Reference into Function, or that include the PubMed articles as references.

    • Protein (Weighted)

      Protein records associated with the current articles through related Gene database records. These are the related sequences on the Gene record that are added manually by NCBI.

    • References for this PMC Article

      Citation referenced in PubMed article. Only valid for PubMed citations that are also in PMC.

    • Substance (MeSH Keyword)

      PubChem chemical substance (submitted) records that are classified under the same Medical Subject Headings (MeSH) controlled vocabulary as the current articles.

    • Taxonomy via GenBank

      Taxonomy records associated with the current articles through taxonomic information on related molecular database records (Nucleotide, Protein, Gene, SNP, Structure).

    • UniGene

      UniGene clusters of expressed sequences that are associated with the current articles through references on the clustered sequence records and related Gene records.

    • GEO Profiles

      Gene Expression Omnibus (GEO) Profiles of molecular abundance data. The current articles are references on the Gene record associated with the GEO profile.

    • Free in PMC

      Free full text articles in PMC

    • Cited in PMC

      Full-text articles in the PubMed Central Database that cite the current articles.

    Recent activity