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Neurological diseases

Making steps in stroke therapy

Nature Reviews Neuroscience volume 7, page 173 (2006)Cite this article

Rupture or blockage of a blood vessel in the brain causes rapid cell death in the core of the injured region, and triggers mechanisms in the surrounding area — the penumbra — that lead, for example, to increases in the concentrations of intracellular Ca2+ and reactive oxygen species (ROS), which initiate cell death. Targeting these mechanisms is a promising route for the development of therapies for the treatment of stroke.

One such strategy, reported by Jiang and colleagues, involved using the metal chelator PAN-811 (also known as Triapine) to 'mop up' intracellular Ca2+. PAN-811 was also shown to scavenge ROS, and so protects neurons from the degenerative effects of both chemical species. In a rat model of ischaemic stroke, intracerebroventricular administration of PAN-811 one hour after occlusion of the middle cerebral artery (MCA) led to a 59% reduction in infarction volume. In addition, PAN-811 has been shown to have a favourable safety and pharmacodynamic profile in the range required for neuroprotection.

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ORIGINAL RESEARCH PAPERS

  1. Jiang, Z.-G. et al. A multifunctional cytoprotective agent that reduces neurodegeneration after ischemia. Proc. Natl Acad. Sci. USA 103, 1581–1586 (2006)

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  2. Kawano, T. et al. Prostaglandin E2 EP1 receptors: downstream effectors of COX-2 neurotoxicity. Nature Med. 12, 1–5 (2006)

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  3. Nishimura, N. et al. Targeted insult to subsurface cortical blood vessels using ultrashort laser pulses: three models of stroke. Nature Methods 3, 99–108 (2006)

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Authors
  1. Samantha Barton
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Barton, S. Making steps in stroke therapy. Nat Rev Neurosci 7, 173 (2006). https://doi.org/10.1038/nrn1880

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