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Updated: Jun 12, 2026

Neurodegeneration in an Animal Model of Chronic Amyloid-beta Oligomer Infusion Is Counteracted by Antibody Treatment Infused with Osmotic Pumps
Published on: August 14, 2016
Effects of nonsteroidal anti-inflammatory drugs on amyloid-beta pathology in mouse skeletal muscle
Tina L Beckett1, Dana M Niedowicz, Christa M Studzinski
1Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40536-0230, USA.
Abstract:
Sporadic inclusion body myositis (sIBM) is a common age-related inflammatory myopathy characterized by the presence of intracellular inclusions that contain the amyloid-beta (Abeta) peptide, a derivative of the amyloid precursor protein (APP). Abeta 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 Abeta 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 Abeta in brain and cultured cells. Only ibuprofen lowered Abeta 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 Abeta alone cannot account for skeletal muscle dysfunction in these mice.
Insights
This study investigated if Alzheimer's disease (AD) treatments could help sporadic inclusion body myositis (sIBM). Researchers found that while ibuprofen reduced amyloid-beta (Abeta) in muscle, it did not improve sIBM symptoms in mice.
Area of Science:
- Neurology
- Molecular Biology
- Biochemistry
Background:
- Sporadic inclusion body myositis (sIBM) is an age-related inflammatory myopathy.
- sIBM muscle tissue contains amyloid-beta (Abeta) peptides, similar to Alzheimer's disease (AD).
- This suggests a potential link between sIBM and AD, and the possibility of shared therapeutic targets.
Purpose of the Study:
- To investigate if treatments effective for AD, specifically those reducing Abeta, could benefit sIBM.
- To test the hypothesis that lowering Abeta in skeletal muscle might alleviate sIBM pathology.
Main Methods:
- Transgenic mice overexpressing amyloid precursor protein (APP) in skeletal muscle were used.
- Mice were treated for six months with various nonsteroidal anti-inflammatory drugs (NSAIDs): naproxen, ibuprofen, carprofen, and R-flurbiprofen.
- Abeta levels in muscle tissue and phenotypic improvements were assessed.
Main Results:
- Only ibuprofen demonstrated a reduction in Abeta levels within the skeletal muscle of treated mice.
- This reduction in Abeta did not correlate with any observable improvements in the mice's muscle phenotype.
- The study found that NSAIDs might have different effects in the brain compared to other tissues.
Conclusions:
- Amyloid-beta alone may not be the sole driver of skeletal muscle dysfunction in sIBM.
- Therapeutic strategies targeting Abeta in the brain may not directly translate to treating sIBM effectively.
- Further research is needed to understand the complex mechanisms underlying sIBM and identify appropriate treatments.
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