ArticleThe American journal of pathology1998
Transgenic mice over-expressing the C-99 fragment of betaPP with an alpha-secretase site mutation develop a myopathy similar to human inclusion body myositis.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 66 citations in OpenAlex.
- Animal Models of Idiopathic Inflammatory Myopathies: Bridging Mechanistic Insights and Clinical Translation.International journal of molecular sciences · 2026Review
- Prevention of ribosome collision-induced neuromuscular degeneration by SARS CoV-2-encoded Nsp1.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Inefficient quality control of ribosome stalling during APP synthesis generates CAT-tailed species that precipitate hallmarks of Alzheimer's disease.Acta neuropathologica communications · 2021Article
- High Fat With High Sucrose Diet Leads to Obesity and Induces Myodegeneration.Frontiers in physiology · 2018Review
- The multifaceted nature of amyloid precursor protein and its proteolytic fragments: friends and foes.Acta neuropathologica · 2015Review
- A ketogenic diet improves motor performance but does not affect β-amyloid levels in a mouse model of Alzheimer's disease.Brain research · 2013Article
- Increased expression and local accumulation of the prion protein, Alzheimer Aβ peptides, superoxide dismutase 1, and nitric oxide synthases 1 & 2 in muscle in a rabbit model of diabetes.BMC physiology · 2010Article
- Effects of nonsteroidal anti-inflammatory drugs on amyloid-beta pathology in mouse skeletal muscle.Neurobiology of disease · 2010Article
- Theories of the pathogenesis of inclusion body myositis.Current rheumatology reports · 2010Review
- In AbetaPP-overexpressing cultured human muscle fibers proteasome inhibition enhances phosphorylation of AbetaPP751 and GSK3beta activation: effects mitigated by lithium and apparently relevant to sporadic inclusion-body myositis.Journal of neurochemistry · 2010Article
- How citation distortions create unfounded authority: analysis of a citation network.BMJ (Clinical research ed.) · 2009Article
- Immunization with amyloid-beta attenuates inclusion body myositis-like myopathology and motor impairment in a transgenic mouse model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Inclusion body myositis: review of recent literature.Current neurology and neuroscience reports · 2009Review
- Inclusion body myositis: a view from the Caenorhabditis elegans muscle.Molecular neurobiology · 2008Review
- Interrelation of inflammation and APP in sIBM: IL-1 beta induces accumulation of beta-amyloid in skeletal muscle.Brain : a journal of neurology · 2008Article
- AbetaPP-overexpression and proteasome inhibition increase alphaB-crystallin in cultured human muscle: relevance to inclusion-body myositis.Neuromuscular disorders : NMD · 2006Article
- Intracellular accumulation of amyloidogenic fragments of amyloid-beta precursor protein in neurons with Niemann-Pick type C defects is associated with endosomal abnormalities.The American journal of pathology · 2004Article
- Newest pathogenetic considerations in inclusion-body myositis: possible role of amyloid-beta, cholesterol, relation to aging and to Alzheimer's disease.Current rheumatology reports · 2002Review
- Inclusion body myositis-like phenotype induced by transgenic overexpression of beta APP in skeletal muscle.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Accumulation of amyloid-beta protein in exocrine glands of transgenic mice overexpressing a carboxyl terminal portion of amyloid protein precursor.International journal of experimental pathology · 2000Article
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Abstract
Inclusion body myositis (IBM) is the most common muscle disease in the elderly. Amyloid-beta protein (A beta) has been shown to accumulate abnormally in the vacuolated fibers and to localize to amyloid-like fibrils in muscles from IBM patients. We studied the skeletal muscles from a line of transgenic mice over-expressing the carboxyl-terminal 99 amino acids (C99) of the beta-amyloid precursor protein (betaPP) with a substitution of lysine-612 to valine (K612V), intended to abolish alpha-secretase recognition and to preserve the A beta domain of C99. The majority (87%) of the 24-month-old transgenic mice showed myopathic changes, and approximately one-third of them had degenerating fibers with sarcoplasmic vacuoles and thioflavin-S-positive deposits. Ultrastructurally, the inclusions were aggregates of short thin amyloid-like fibrils, 6 to 8 nm in diameter. These features are similar to those of human IBM. Immunocytochemistry using an antibody against A beta showed membranous staining in most muscle fibers of transgenic mice, as well as granular or vacuolar cytoplasmic staining in the atrophic fibers. Western blots showed a high level of accumulation of carboxyl-terminal fragments of betaPP in the muscles of the transgenic mice with the most severe IBM-like lesions. The expression of IBM-like lesions was age dependent. These transgenic mice provide a model for the study of IBM and for the peripheral expression of a key element in the pathogenesis of Alzheimer disease.
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