ArticleThe American journal of pathology2006
Genetically augmenting Abeta42 levels in skeletal muscle exacerbates inclusion body myositis-like pathology and motor deficits in transgenic mice.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 73 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
- Effects and mechanisms of APP and its cleavage product Aβ in the comorbidity of sarcopenia and Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Sporadic inclusion body myositis-derived myotube culture revealed muscle cell-autonomous expression profiles.PloS one · 2024Article
- Revisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis.Cells · 2021Review
- Neurochemical Aspects of Alzheimer's Disease and Movement Disturbances: A Theory of β-Amyloid and τ-Protein.American journal of Alzheimer's disease and other dementias · 2018Article
- Inhibition of cyclin-dependent kinase 5 affects early neuroinflammatory signalling in murine model of amyloid beta toxicity.Journal of neuroinflammation · 2018Article
- High Fat With High Sucrose Diet Leads to Obesity and Induces Myodegeneration.Frontiers in physiology · 2018Review
- Clinical, imaging, pathological, and biochemical characterization of a novel presenilin 1 mutation (N135Y) causing Alzheimer's disease.Neurobiology of aging · 2017Article
- Amyloid deposits and inflammatory infiltrates in sporadic inclusion body myositis: the inflammatory egg comes before the degenerative chicken.Acta neuropathologica · 2015Review
- De novo prion aggregates trigger autophagy in skeletal muscle.Journal of virology · 2014Article
- Oleuropein aglycone protects transgenic C. elegans strains expressing Aβ42 by reducing plaque load and motor deficit.PloS one · 2013Article
- APP transgenic mice for modelling behavioural and psychological symptoms of dementia (BPSD).Neuroscience and biobehavioral reviews · 2012Review
- Neurologic and motor dysfunctions in APP transgenic mice.Reviews in the neurosciences · 2012Review
- 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
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The pathogenic basis of inclusion body myositis (IBM), the leading muscle degenerative disease afflicting the elderly, is unknown, although the histopathological features are remarkably similar to those observed in Alzheimer's disease. One leading hypothesis is that the buildup of amyloid-beta (Abeta) peptide within selective skeletal muscle fibers contributes to the degenerative phenotype. Abeta is a small peptide derived via endoproteolysis of the amyloid precursor protein (APP). To determine the pathogenic effect of augmenting Abeta42 levels in skeletal muscle, we used a genetic approach to replace the endogenous wild-type presenilin-1 (PS1) allele with the PS1(M146V) allele in MCK-APP mice. Although APP transgene expression was unaltered, Abeta levels, particularly Abeta42, were elevated in skeletal muscle of the double transgenic (MCK-APP/PS1) mice compared to the parental MCK-APP line. Elevated phospho-tau accumulation was found in the MCK-APP/PS1 mice, and the greater activation of GSK-3beta and cdk5 were observed. Other IBM-like pathological features, such as inclusion bodies and inflammatory infiltrates, were more severe and prominent in the MCK-APP/PS1 mice. Motor coordination and balance were more adversely affected and manifested at an earlier age in the MCK-APP/PS1 mice. The data presented here provide experimental evidence that Abeta42 plays a proximal and critical role in the muscle degenerative process.
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Registered trials
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.