Inclusion-body myositis

@article{Askanas2006InclusionbodyM,
  title={Inclusion-body myositis},
  author={Valerie Askanas and W. King Engel},
  journal={Neurology},
  year={2006},
  volume={66},
  pages={S39 - S48}
}
Sporadic inclusion-body myositis (s-IBM), the most common muscle disease of older persons, is of unknown cause and there is no successful treatment. We summarize our most recent findings, which provide a better understanding of the steps in the pathogenetic cascade. We suggest that s-IBM is primarily a myodegenerative disease. Intriguing are the phenotypic similarities between s-IBM muscle fibers and the brains of Alzheimer disease, the most common neurodegenerative disease of older persons. In… 
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Pathogenic Considerations in Sporadic Inclusion-Body Myositis, a Degenerative Muscle Disease Associated With Aging and Abnormalities of Myoproteostasis
TLDR
This work reviews the presumably most important known molecular abnormalities that occur in s-IBM myofibers and that likely contribute to s- IBM pathogenesis and suggests interventions in the complex, interwoven pathogenic cascade of s-ibM are suggested.
Sporadic inclusion-body myositis: A degenerative muscle disease associated with aging, impaired muscle protein homeostasis and abnormal mitophagy.
Inclusion-body myositis: muscle-fiber molecular pathology and possible pathogenic significance of its similarity to Alzheimer’s and Parkinson’s disease brains
TLDR
Diagnostic criteria is summarized, and it is suggested 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.
Synaptic defects associated with s-inclusion body myositis are prevented by copper
TLDR
The results suggest that Aβ-oligomers are the toxic Aβ species that trigger neuromuscular junction dysfunction.
Sporadic inclusion-body myositis: conformational multifactorial ageing-related degenerative muscle disease associated with proteasomal and lysosomal inhibition, endoplasmic reticulum stress, and accumulation of amyloid-β42 oligomers and phosphorylated tau.
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
Overall, the degenerative phenomena in s-IBM muscle fibers seem to be the major cause of the progressive, unstoppable weakness, rather than the lymphocytic inflammation.
Proteomic study of sporadic inclusion body myositis
TLDR
This study reveals a unique pattern of protein expression in s-IBM, which should be further investigated in a wider cohort of IBM patients to fully realize the potential diagnostic or therapeutic benefits.
Sporadic inclusion body myositis: Pathogenic considerations
TLDR
A brief overview of the validity of the various controversial observations is examined and the justification for the two major hypotheses for the primary role of inflammation versus degeneration are critically reviewed.
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.
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