ArticleProceedings of the National Academy of Sciences of the United States of America2002
Inclusion body myositis-like phenotype induced by transgenic overexpression of beta APP in skeletal muscle.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 105 citations in OpenAlex.
- Mutual reinforcement of lymphotoxin-driven myositis and impaired autophagy in murine muscle.Brain : a journal of neurology · 2025Article
- Recent advances in immunological mechanisms and murine disease models of idiopathic inflammatory myopathies.Inflammation and regeneration · 2025Review
- Human induced pluripotent stem cell-derived myotubes to model inclusion body myositis.Acta neuropathologica communications · 2025Article
- APP in the Neuromuscular Junction for the Development of Sarcopenia and Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Unravelling inclusion body myositis using a patient-derived fibroblast model.Journal of cachexia, sarcopenia and muscle · 2023Article
- Loss of TDP-43 function and rimmed vacuoles persist after T cell depletion in a xenograft model of sporadic inclusion body myositis.Science translational medicine · 2022Article
- Desmin forms toxic, seeding-competent amyloid aggregates that persist in muscle fibers.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Endoplasmic Reticulum Stress Induces Myostatin High Molecular Weight Aggregates and Impairs Mature Myostatin Secretion.Molecular neurobiology · 2018Article
- High Fat With High Sucrose Diet Leads to Obesity and Induces Myodegeneration.Frontiers in physiology · 2018Review
- Modeling Alzheimer's and Other Age Related Human Diseases in Embryonic Systems.Journal of developmental biology · 2017Article
- Article
- Mitochondrial oxygen consumption deficits in skeletal muscle isolated from an Alzheimer's disease-relevant murine model.BMC neuroscience · 2014Article
- Primary over-expression of AβPP in muscle does not lead to the development of inclusion body myositis in a new lineage of the MCK-AβPP transgenic mouse.International journal of experimental pathology · 2013Article
- Unfolded protein response and activated degradative pathways regulation in GNE myopathy.PloS one · 2013Article
- Mitochondrial dysfunction in skeletal muscle of amyloid precursor protein-overexpressing mice.The Journal of biological chemistry · 2012Article
- Animal models of inflammatory myopathy.Current rheumatology reports · 2012Review
- APP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD).Neuroscience and biobehavioral reviews · 2012Review
- Foxo/atrogin induction in human and experimental myositis.Neurobiology of disease · 2012Article
- Neurologic and motor dysfunctions in APP transgenic mice.Reviews in the neurosciences · 2012Review
- Expression of human amyloid precursor protein in the skeletal muscles of Drosophila results in age- and activity-dependent muscle weakness.BMC physiology · 2011Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Inclusion body myositis (IBM), the most common age-related muscle disease in the elderly population, is an incurable disorder leading to severe disability. Sporadic IBM has an unknown etiology, although affected muscle fibers are characterized by many of the pathobiochemical alterations traditionally associated with neurodegenerative brain disorders such as Alzheimer's disease. Accumulation of the amyloid-beta peptide, which is derived from proteolysis of the larger amyloid-beta precursor protein (betaAPP), seems to be an early pathological event in Alzheimer's disease and also in IBM, where in the latter, it predominantly occurs intracellularly within affected myofibers. To elucidate the possible role of betaAPP mismetabolism in the pathogenesis of IBM, transgenic mice were derived in which we selectively targeted betaAPP overexpression to skeletal muscle by using the muscle creatine kinase promoter. Here we report that older (>10 months) transgenic mice exhibit intracellular immunoreactivity to betaAPP and its proteolytic derivatives in skeletal muscle. In this transgenic model, selective overexpression of betaAPP leads to the development of a subset of other histopathological and clinical features characteristic of IBM, including centric nuclei, inflammation, and deficiencies in motor performance. These results are consistent with a pathogenic role for betaAPP mismetabolism in human IBM.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.