ReviewActa neuropathologica2008
Inclusion-body myositis: muscle-fiber molecular pathology and possible pathogenic significance of its similarity to Alzheimer's and Parkinson's disease brains.
Review in Acta neuropathologica, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
44 citing papers in PubMed.
- The immune system in sporadic inclusion body myositis patients is not compromised by blood-flow restricted exercise training.Arthritis research & therapy · 2019Trial
- Pilot trial of simvastatin in the treatment of sporadic inclusion-body myositis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2011Trial
- The NORAD-Pumilio regulatory axis in the evolution of inclusion body myositis.Journal of neuropathology and experimental neurology · 2026Article
- N-formyl methionine peptide-driven neutrophil activation in idiopathic inflammatory myopathies.Rheumatology (Oxford, England) · 2026Article
- Resistance Exercise Training as a New Trend in Alzheimer's Disease Research: From Molecular Mechanisms to Prevention.International journal of molecular sciences · 2024Review
- Effects of sporadic inclusion body myositis on skeletal muscle fibre type specific morphology and markers of regeneration and inflammation.Rheumatology international · 2024Article
- Mitochondrial defects in sporadic inclusion body myositis-causes and consequences.Frontiers in cell and developmental biology · 2024Review
- Article
- Review
- Emerging Evidences for an Implication of the Neurodegeneration-Associated Protein TAU in Cancer.Brain sciences · 2020Review
- The Expanding Clinical Universe of Polyglutamine Disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2019Review
- Dropped Head Syndrome and the Presence of Rimmed Vacuoles in a Muscle Biopsy in Scleroderma-polymyositis Overlap Syndrome Associated with Anti-Ku Antibody.Internal medicine (Tokyo, Japan) · 2018Article
- High Fat With High Sucrose Diet Leads to Obesity and Induces Myodegeneration.Frontiers in physiology · 2018Review
- Co-expression Network Approach Reveals Functional Similarities among Diseases Affecting Human Skeletal Muscle.Frontiers in physiology · 2017Article
- BACE-1, PS-1 and sAPPβ Levels Are Increased in Plasma from Sporadic Inclusion Body Myositis Patients: Surrogate Biomarkers among Inflammatory Myopathies.Molecular medicine (Cambridge, Mass.) · 2016Article
- Molecular events linking cholesterol to Alzheimer's disease and inclusion body myositis in a rabbit model.American journal of neurodegenerative disease · 2016Article
- The Presence of Select Tau Species in Human Peripheral Tissues and Their Relation to Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2016Article
- ER stress: Autophagy induction, inhibition and selection.Autophagy · 2015Article
- The protein oxidation repair enzyme methionine sulfoxide reductase a modulates Aβ aggregation and toxicity in vivo.Antioxidants & redox signaling · 2015Article
- Compartment-dependent mitochondrial alterations in experimental ALS, the effects of mitophagy and mitochondriogenesis.Frontiers in cellular neuroscience · 2015Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Sporadic inclusion-body myositis (s-IBM), the most common muscle disease of older persons, is of unknown cause and lacks successful treatment. Here we summarize diagnostic criteria and discuss our current understanding of the steps in the pathogenic cascade. While it is agreed that both degeneration and mononuclear-cell inflammation are components of the s-IBM pathology, how each relates to the pathogenesis remains unsettled. We suggest that the intra-muscle-fiber degenerative component plays the primary role, leading to muscle-fiber destruction and clinical weakness, since anti-inflammatory treatments are not of sustained benefit. We discuss possible treatment strategies aimed toward ameliorating a degenerative component, for example, lithium and resveratrol. Also discussed are the intriguing phenotypic similarities between s-IBM muscle fibers and the brains of Alzheimer and Parkinson's diseases, the most common neurodegenerative diseases associated with aging. Similarities include, in the respective tissues, cellular aging, mitochondrial abnormalities, oxidative and endoplasmic-reticulum stresses, proteasome inhibition and multiprotein aggregates.
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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.