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January 23, 2006Neurology

Mitochondrial abnormalities in inclusion-body myositis

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Population

Patients with sporadic inclusion-body myositis (s-IBM) and age-matched controls

Design

Review

Authors

AOAnders OldforsAMA.‐R. MoslemiLJLena Jonasson

Discussion

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Overview

Mitochondrial dysfunction may contribute to s-IBM weakness; hypothesis-generating for targeted therapies.

Structured PICO

P
Population
Patients with sporadic inclusion-body myositis (s-IBM) and age-matched controls
O
Outcome
Mitochondrial changes including cytochrome c oxidase (COX)-deficient muscle fibers and large-scale mitochondrial DNA (mtDNA) deletionssurrogate

Impaired mitochondrial function from COX-deficient fibers likely contributes to muscle weakness in s-IBM, suggesting potential for treatments used in mitochondrial myopathies.

Cite This Study

Oldfors et al. (2006) studied this question.

synapsesocial.com/papers/6a825668f2e4e6540e2a5644https://doi.org/10.1212/01.wnl.0000192127.63013.8d
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Thymidine Phosphorylase Gene Mutations in MNGIE, a Human Mitochondrial Disorder1999 · 902 citations
  2. 2Inclusion body myositis1978 · 310 citations
  3. 331 P NMR spectroscopy and ergometer exercise test as evidence for muscle oxidative performance improvement with coenzyme Q in mitochondrial myopathies1992 · 104 citations
  4. 4Distribution of wild-type and common deletion forms of mtDNA in normal and respiration-deficient muscle fibers from patients with mitochondrial myopathy1994 · 306 citations
  5. 5Mitochondrial myopathies2001 · 64 citations