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The Journal of Neuroscience, August 1, 2000, 20(15):5709-5714
Ibuprofen Suppresses Plaque Pathology and Inflammation in a Mouse
Model for Alzheimer's Disease
G. P.
Lim1, 3,
F.
Yang1, 3,
T.
Chu1, 3,
P.
Chen1, 3,
W.
Beech1, 3,
B.
Teter1, 3,
T.
Tran1, 3,
O.
Ubeda1, 3,
K. Hsiao
Ashe5,
S. A.
Frautschy1, 2, 3, 4, and
G. M.
Cole1, 2, 3, 4
University of California Los Angeles, Departments of
1 Medicine and 2 Neurology, Los Angeles,
California 90095, 3 The Greater Los Angeles Veterans
Affairs Healthcare System, and 4 Veterans Administration
Medical Center Geriatric Research, Education, and Clinic Center,
Sepulveda, California 91343, and 5 Center for Clinical and
Molecular Neurobiology, Departments of Neurology and Neuroscience,
University of Minnesota, Minneapolis, Minnesota 55455
The brain in Alzheimer's disease (AD) shows a chronic inflammatory
response characterized by activated glial cells and increased expression of cytokines and complement factors surrounding amyloid deposits. Several epidemiological studies have demonstrated a reduced
risk for AD in patients using nonsteroidal anti-inflammatory drugs
(NSAIDs), prompting further inquiries about how NSAIDs might influence
the development of AD pathology and inflammation in the CNS. We tested
the impact of chronic orally administered ibuprofen, the most commonly
used NSAID, in a transgenic model of AD displaying widespread
microglial activation, age-related amyloid deposits, and dystrophic
neurites. These mice were created by overexpressing a variant of the
amyloid precursor protein found in familial AD. Transgene-positive (Tg+) and negative (Tg ) mice began receiving chow
containing 375 ppm ibuprofen at 10 months of age, when amyloid plaques first appear, and were fed continuously for 6 months. This
treatment produced significant reductions in final interleukin-1 and
glial fibrillary acidic protein levels, as well as a significant diminution in the ultimate number and total area of -amyloid deposits. Reductions in amyloid deposition were supported by ELISA measurements showing significantly decreased SDS-insoluble A. Ibuprofen also decreased the numbers of ubiquitin-labeled dystrophic neurites and the percentage area per plaque of
anti-phosphotyrosine-labeled microglia. Thus, the anti-inflammatory
drug ibuprofen, which has been associated with reduced AD risk in human
epidemiological studies, can significantly delay some forms of AD
pathology, including amyloid deposition, when administered early in the
disease course of a transgenic mouse model of AD.
Key words:
inflammation; cytokines; microglia; amyloid; Alzheimer; NSAID
Copyright © 2000 Society for Neuroscience 0270-6474/00/20155709-06$05.00/0
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