ArticleThe American journal of pathology1998
Light and electron microscopic immunolocalization of presenilin 1 in abnormal muscle fibers of patients with sporadic inclusion-body myositis and autosomal-recessive 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 16 papers.
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Who cites it
16 citing papers in PubMed, 55 citations in OpenAlex.
- The NORAD-Pumilio regulatory axis in the evolution of inclusion body myositis.Journal of neuropathology and experimental neurology · 2026Article
- Mitochondrial dysfunction underlying sporadic inclusion body myositis is ameliorated by the mitochondrial homing drug MA-5.PloS one · 2020Article
- Sporadic inclusion body myositis: the genetic contributions to the pathogenesis.Orphanet journal of rare diseases · 2014Review
- Foxo/atrogin induction in human and experimental myositis.Neurobiology of disease · 2012Article
- How citation distortions create unfounded authority: analysis of a citation network.BMJ (Clinical research ed.) · 2009Article
- Inclusion body myositis: a degenerative muscle disease associated with intra-muscle fiber multi-protein aggregates, proteasome inhibition, endoplasmic reticulum stress and decreased lysosomal degradation.Brain pathology (Zurich, Switzerland) · 2009Review
- Inclusion-body myositis: muscle-fiber molecular pathology and possible pathogenic significance of its similarity to Alzheimer's and Parkinson's disease brains.Acta neuropathologica · 2008Review
- Inclusion body myositis: a view from the Caenorhabditis elegans muscle.Molecular neurobiology · 2008Review
- Genetically augmenting Abeta42 levels in skeletal muscle exacerbates inclusion body myositis-like pathology and motor deficits in transgenic mice.The American journal of pathology · 2006Article
- Macroautophagy--a novel Beta-amyloid peptide-generating pathway activated in Alzheimer's disease.The Journal of cell biology · 2005Article
- Regulation of the rapsyn promoter by kaiso and delta-catenin.Molecular and cellular biology · 2004Article
- 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
- Association of active extracellular signal-regulated protein kinase with paired helical filaments of inclusion-body myositis muscle suggests its role in inclusion-body myositis tau phosphorylation.The American journal of pathology · 2000Article
- Paired helical filaments of inclusion-body myositis muscle contain RNA and survival motor neuron protein.The American journal of pathology · 2000Article
- 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.The American journal of pathology · 1998Article
- Amyloid-beta deposition in skeletal muscle of transgenic mice: possible model of inclusion body myopathy.The American journal of pathology · 1998Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sporadic inclusion-body myositis (s-IBM) is the most common progressive muscle disease of older persons. The muscle biopsy demonstrates mononuclear cell inflammation and vacuolated muscle fibers containing paired helical filaments and 6- to 10-nm fibrils, both resembling those of Alzheimer disease brain and Congo red positivity. The term hereditary inclusion-body myopathies (h-IBMs) designates autosomal-recessive or autosomal-dominant disorders with muscle biopsies cytopathologically similar to s-IBM but without inflammation. Vacuolated muscle fibers of both s-IBM and the h-IBMs contain accumulations of several "Alzheimer-characteristic proteins" including beta-amyloid protein and beta-amyloid precursor protein, and their paired helical filaments are composed of phosphorylated tau. We used six well characterized antibodies against several residues of presenilin 1 (PS1) to immunostain muscle biopsies of 12 patients with s-IBM, 5 patients with autosomal-recessive inclusion-body myopathy, and 16 normal and disease controls. Seventy to eighty percent of the vacuolated muscle fibers of both s-IBM and autosomal-recessive inclusion-body myopathy had inclusions that were strongly PS1-immunoreactive, which by immunoelectron microscopy localized mainly to paired helical filaments and 6- to 10-nm filaments. None of the control biopsies had PS1-positive inclusions characteristic of the s- and h-IBM abnormal muscle fibers. Mutations of the newly discovered PS1 gene are responsible for early-onset familial Alzheimer disease (AD), and PS1 is abnormally accumulated in sporadic and familial AD brain. Our study provides the first demonstration of PS1 abnormality in non-neural tissue and in diseases other than AD and suggests that the cytopathogenesis in AD brain and IBM muscle may share similarities.
Indexed as
Identifiers
9546349PMC1858253W2143938364What OpenQuestion holds
Registered trials
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