Journal
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES
Volume 74, Issue 22-24, Pages 1460-1468Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15287394.2011.618973
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Funding
- NIH/NIA [P50 AG16573]
- Louisiana State University
- Alzheimer Association [IIRG-09-131729]
- NIH [NIA AG18031, NIA AG038834]
- NATIONAL INSTITUTE ON AGING [R01AG018031, R01AG038834, P50AG016573] Funding Source: NIH RePORTER
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A mouse-and human-brain-abundant, nuclear factor (NF)-kappa B-regulated, micro RNA-146a (miRNA-146a) is an important modulator of the innate immune response and inflammatory signaling in specific immunological and brain cell types. Levels of miRNA-146a are induced in human brain cells challenged with at least five different species of single-or double-stranded DNA or RNA neurotrophic viruses, suggesting a broad role for miRNA-146a in the brain's innate immune response and antiviral immunity. Upregulated miRNA-146a is also observed in pro-inflammatory cytokine-, A beta 42 peptide-and neurotoxic metal-induced, oxidatively stressed human neuronal-glial primary cell cocultures, in murine scrapie and in Alzheimer's disease (AD) brain. In AD, miRNA-146a levels are found to progressively increase with disease severity and co-localize to brain regions enriched in inflammatory neuropathology. This study provides evidence of upregulation of miRNA-146a in extremely rare (incidence 1-10 per 100 million) human prion-based neurodegenerative disorders, including sporadic Creutzfeldt-Jakob disease (sCJD) and Gerstmann-Straussler-Scheinker syndrome (GSS). The findings suggest that an upregulated miRNA-146a may be integral to innate immune or inflammatory brain cell responses in prion-mediated infections and to progressive and irreversible neurodegeneration of both the murine and human brain.
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