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MELAS and L-arginine therapy: pathophysiology of stroke-like episodes

Yasutoshi Koga1, Nataliya Povalko, Junko Nishioka

  • 1Department of Pediatrics and Child Health, Kurume University School of Medicine, Kurume, Fukuoka, Japan. yasukoga@med.kurume-u.ac.jp

Annals of the New York Academy of Sciences
|July 24, 2010
PubMed

Insights

Stroke-like episodes in MELAS patients may stem from mitochondrial angiopathy. L-arginine therapy shows promise for treating these episodes in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes.

Area of Science:

  • Neurology
  • Mitochondrial Diseases
  • Vascular Biology

Background:

  • Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is a multisystem mitochondrial disorder with unclear stroke-like episode mechanisms.
  • Mitochondrial angiopathy and endothelial dysfunction are hypothesized contributors to stroke-like episodes in MELAS.

Purpose of the Study:

  • To review the current understanding of pathogenic mechanisms behind stroke-like episodes in MELAS.
  • To explore the potential therapeutic role of L-arginine in managing MELAS-related stroke-like episodes.

Main Methods:

  • Review of clinical symptoms, muscle/brain pathology, molecular functions, and neuroimaging (MRI, MRS, SPECT) in MELAS.
  • Analysis of the proposed mechanism of action for L-arginine therapy in MELAS patients.

Main Results:

  • The exact pathogenic mechanism of stroke-like episodes in MELAS remains under investigation.
  • L-arginine therapy is proposed as a potentially beneficial treatment for stroke-like episodes in MELAS.

Conclusions:

  • Mitochondrial angiopathy is a leading hypothesis for MELAS stroke-like episodes.
  • L-arginine therapy presents a promising avenue for treating stroke-like episodes in MELAS patients.

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