Ibuprofen Suppresses Plaque Pathology and Inflammation in a Mouse Model for Alzheimer's Disease

• DOI: 10.1523/jneurosci.20-15-05709.2000
• Publication Date: 2018-04-06T20:45:39Z
• Authors: G. P. Lim; F. Yang; T. Chu; P. Chen; W. Beech; B. Teter; T. Tran; O. Ubeda; K. Hsiao Ashe; S. A. Frautschy; G. M. Cole
• Keywords: Ibuprofen; Amyloid (mycology)

The brain in Alzheimer's disease (AD) shows a chronic inflammatory response characterized by activated glial cells and increased expression of cytokines complement factors surrounding amyloid deposits. Several epidemiological studies have demonstrated reduced risk for AD patients using nonsteroidal anti-inflammatory drugs (NSAIDs), prompting further inquiries about how NSAIDs might influence the development pathology inflammation CNS. We tested impact orally administered ibuprofen, most commonly used NSAID, transgenic model displaying widespread microglial activation, age-related deposits, dystrophic neurites. These mice were created overexpressing variant precursor protein found familial AD. Transgene-positive (Tg+) negative (Tg−) began receiving chow containing 375 ppm ibuprofen at 10 months age, when plaques first appear, fed continuously 6 months. This treatment produced significant reductions final interleukin-1β fibrillary acidic levels, as well diminution ultimate number total area β-amyloid Reductions deposition supported ELISA measurements showing significantly decreased SDS-insoluble Aβ. Ibuprofen also numbers ubiquitin-labeled neurites percentage per plaque anti-phosphotyrosine-labeled microglia. Thus, drug which has been associated with human studies, can delay some forms pathology, including deposition, early course mouse