ArticleThe American journal of pathology1998
Amyloid-beta deposition in skeletal muscle of transgenic mice: possible model of inclusion body myopathy.
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 29 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
29 citing papers in PubMed, 89 citations in OpenAlex.
- Animal Models of Idiopathic Inflammatory Myopathies: Bridging Mechanistic Insights and Clinical Translation.International journal of molecular sciences · 2026Review
- Research progress on resistance exercise therapy for improving cognitive function in patients with AD and muscle atrophy.Frontiers in aging neuroscience · 2025Review
- Age Related Changes in Muscle Mass and Force Generation in the Triple Transgenic (3xTgAD) Mouse Model of Alzheimer's Disease.Frontiers in aging neuroscience · 2022Article
- High Fat With High Sucrose Diet Leads to Obesity and Induces Myodegeneration.Frontiers in physiology · 2018Review
- Article
- A ketogenic diet improves motor performance but does not affect β-amyloid levels in a mouse model of Alzheimer's disease.Brain research · 2013Article
- Foxo/atrogin induction in human and experimental myositis.Neurobiology of disease · 2012Article
- 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
- APP(DeltaNL695) expression in murine tissue downregulates CNBP expression.Neuroscience letters · 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
- Anesthetic sevoflurane causes neurotoxicity differently in neonatal naïve and Alzheimer disease transgenic mice.Anesthesiology · 2010Article
- 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
- Nasal inoculation of an adenovirus vector encoding 11 tandem repeats of Abeta1-6 upregulates IL-10 expression and reduces amyloid load in a Mo/Hu APPswe PS1dE9 mouse model of Alzheimer's disease.The journal of gene medicine · 2007Article
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5 authors at 1 institution in 1 country.
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Abstract
Inclusion body myopathy is a progressive muscle disorder characterized by nuclear and cytoplasmic inclusions and vacuolation of muscle fibers. Affected muscle fibers contain deposits of congophilic amyloid, amyloid-beta immunoreactive filaments, and paired helical filaments, all of which are pathological hallmarks of Alzheimer's disease in brain. Accumulations of amyloid-beta and its precursor are thought to play important roles in the pathogenesis of both inclusion body myopathy and Alzheimer's disease. Overexpression of mutant forms of beta protein precursor in transgenic mice by neuron-specific promoters has been reported to cause amyloid deposits in the brain. Here we report that overexpression in transgenic mice of the signal plus 99-amino acid carboxyl-terminal sequences of beta protein precursor, under the control of a cytomegalovirus enhancer/beta-actin promoter, resulted in vacuolation and increasing accumulation of the 4-kd amyloid-beta and the carboxyl-terminus in skeletal muscle fibers during aging. These deposits in transgenic muscle only rarely showed Congo red birefringence. Thus, overexpression of part of beta protein precursor in transgenic mice led to development of some of the characteristic features of inclusion body myopathy. These mice may be a useful model of inclusion body myopathy, which shares a number of pathological markers with Alzheimer's disease.
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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.