Effects of nonsteroidal anti-inflammatory drugs on amyloid-β pathology in mouse skeletal muscle

被引：22

作者：

Beckett, Tina L. ^{[1
]}

Niedowicz, Dana M. ^{[1
,2
]}

Studzinski, Christa M. ^{[1
]}

Weidner, Adam M. ^{[1
,2
]}

Webb, Robin L. ^{[2
]}

Holler, Christopher J. ^{[2
]}

Ahmed, Rachel R. ^{[1
,2
]}

LeVine, Harry, III ^{[1
,2
]}

Murphy, M. Paul ^{[1
,2
,3
]}

机构：

[1] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40536 USA

[2] Univ Kentucky, Dept Mol & Cellular Biochem, Lexington, KY 40536 USA

[3] Univ Kentucky, UK Ctr Muscle Biol, Lexington, KY 40536 USA

来源：

NEUROBIOLOGY OF DISEASE | 2010年 / 39卷 / 03期

关键词：

Amyloid; Sporadic inclusion body myositis; Alzheimer's disease; Amyloid-beta precursor protein; Inflammation; INCLUSION-BODY MYOSITIS; GAMMA-SECRETASE; ALZHEIMERS-DISEASE; MITOCHONDRIAL ABNORMALITIES; TRANSGENIC MICE; A-BETA-42; DEPOSITION; OVEREXPRESSION; FLURBIPROFEN; IMMUNIZATION;

D O I：

10.1016/j.nbd.2010.05.018

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Sporadic inclusion body myositis (sIBM) is a common age-related inflammatory myopathy characterized by the presence of intracellular inclusions that contain the amyloid-beta (A beta) peptide, a derivative of the amyloid precursor protein (APP). A beta is believed to cause Alzheimer's disease (AD), suggesting that a link may exist between the two diseases. If AD and sIBM are linked, then treatments that lower A beta in brain may prove useful for sIBM. To test this hypothesis, transgenic mice that overexpress APP in skeletal muscle were treated for 6 months with a variety of nonsteroidal anti-inflammatory drugs (NSAIDs: naproxen, ibuprofen, carprofen or R-flurbiprofen), a subset of which reduce A beta in brain and cultured cells. Only ibuprofen lowered A beta in muscle, and this was not accompanied by corresponding improvements in phenotype. These results indicate that the effects of NSAIDs in the brain may be different from other tissues and that A beta alone cannot account for skeletal muscle dysfunction in these mice. (C) 2010 Elsevier Inc. All rights reserved.

引用

页码：449 / 456

页数：8

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