Inclusion body myositis: Review of recent literature

@article{Greenberg2009InclusionBM,
  title={Inclusion body myositis: Review of recent literature},
  author={Steven A. Greenberg},
  journal={Current Neurology and Neuroscience Reports},
  year={2009},
  volume={9},
  pages={83-89}
}
  • S. Greenberg
  • Published 2009
  • Biology
  • Current Neurology and Neuroscience Reports
Inclusion body myositis (IBM) is a progressive inflammatory skeletal muscle disease of unknown cause and without effective treatment. This article discusses existing literature, emphasizing disease mechanisms and models. In particular, it addresses limitations in the β-amyloid-mediated theory of IBM myofiber injury, flawed rationales of animal models of this disease, and recent reports regarding treatment. 
Theories of the Pathogenesis of Inclusion Body Myositis
  • S. Greenberg
  • Biology, Medicine
    Current rheumatology reports
  • 2010
TLDR
Specific theories of its pathogenesis are reviewed and general considerations pertaining to modeling of this disease discussed, and the critical role of biomarkers and methodologic issues in their discovery are considered.
Inclusion body myositis: old and new concepts
Inclusion body myositis (IBM) is the most common idiopathic inflammatory myopathy occurring in patients over the age of 50 years and probably accounts for about 30% of all inflammatory myopathies.
Inclusion body myositis: therapeutic approaches.
TLDR
Various treatments that have been employed in IBM will be discussed even though none of the interventions has sufficient evidence to support its routine use, because IBM is a slowly progressive disease so assessment of treatment efficacy is problematic.
Evaluation and treatment of inflammatory myopathies
TLDR
Greater understanding of the pathogenic bases of these disorders should hopefully lead to better treatment and well designed, prospective, double blind, placebo controlled trials are needed to determine the best therapeutic options for these different disorders.
Mitochondrial Biology in Sporadic Inclusion Body Myositis
TLDR
The role of the mitochondria in the development of sIBM and the role of amyloid beta on mitochondrial function in skeletal muscle are evaluated to help to identify novel prevention and/ or treatment strategies.
Amyloid deposits and inflammatory infiltrates in sporadic inclusion body myositis: the inflammatory egg comes before the degenerative chicken
TLDR
It is imperative that neurologists and rheumatologists recognize this disorder which may, through clinical and pathological similarities, mimic other myopathies, especially polymyositis, which responds to immunosuppressant drug therapy poorly.
Vacuolar myopathy in a dog resembling human sporadic inclusion body myositis
TLDR
Observations constitute the first evidence that both the inflammatory and degenerative features of human sIBM can occur in a non-human species.
Sporadic inclusion body myositis: possible pathogenesis inferred from biomarkers.
TLDR
Therapies aimed at improving protein homeostasis, instead of targeting a specific protein that may or may not accumulate in all sIBM patients, could be useful future strategies for this devastating and enigmatic disorder.
Long-term observational study of sporadic inclusion body myositis.
TLDR
It is confirmed that sporadic inclusion body myositis is slowly progressive but not lethal and that immunosuppressive treatments do not ameliorate its natural course, thus confirming findings from smaller studies.
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References

SHOWING 1-10 OF 94 REFERENCES
Inclusion-body myositis, a multifactorial muscle disease associated with aging: current concepts of pathogenesis
TLDR
It is suggested that an intramuscle fiber degenerative component is primary, leading to muscle-fiber destruction, while the lymphocytic inflammatory component may only slightly contribute to sporadic inclusion-body myositis muscle- fiber damage.
Inclusion-body myositis
TLDR
It is proposed that the identified abnormal accumulation, misfolding, and aggregation of proteins, perhaps provoked by the aging milieu and aggravated by the oxidative stress, lead to the s-IBM-specific vacuolar degeneration and atrophy of muscle fibers.
Expression of transglutaminase 2 does not differentiate focal myositis from generalized inflammatory myopathies
TLDR
This study investigates TG2 expression in FM in comparison with other IIM and finds an increased transglutaminase 2 (TG2) expression has been found in DM, PM and s‐IBM.
β‐Amyloid is a substrate of autophagy in sporadic inclusion body myositis
Sporadic Inclusion Body Myositis (sIBM) is the most common acquired muscle disease in patients above 50 years of age. Apart from inflammation in the skeletal muscle, overexpression of amyloid
Treatment of inclusion body myositis with cyclosporin-A or tacrolimus: successful long-term management in patients with earlier active disease and concomitant autoimmune features.
TLDR
Calcineurin inhibitors may represent a useful option for the long-term management of s-IBM, possibly in a subset characterized by a short duration with high disease activity or associated autoimmune manifestations.
Inflammation induces tau pathology in inclusion body myositis model via glycogen synthase kinase‐3β
TLDR
The mechanisms by which inflammation modulates Aβ and tau, two hallmark features of inclusion body myositis, are addressed.
Epidemiology of inclusion body myositis in the Netherlands: A nationwide study
Article abstract Epidemiologic data on inclusion body myositis (IBM) are scarce, and possibly biased, because they are derived from larger neuromuscular centers. The present nationwide collaborative
Inclusion body myositis: Clinical and pathological boundaries
TLDR
This study retrospectively reviewed the pattern of weakness and other clinical features of 46 patients newly diagnosed with either inclusion body myositis, polymyposis, or dermatomyosities and supports the recently proposed criteria for defintie and possible inclusion bodyMyositis.
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