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The Role of Polyamine Metabolism in Neuronal Injury Following Cerebral Ischemia

Published online by Cambridge University Press:  02 December 2014

Grace H. Kim ,
Ricardo J. Komotar ,
Margy E. McCullough-Hicks ,
Marc L. Otten ,
Robert M. Starke ,
Christopher P. Kellner ,
Matthew C. Garrett ,
Maxwell B. Merkow ,
Michal Rynkowski  and
Kelly A. Dash
...Show all authors
Grace H. Kim
Affiliation:
Department of Neurological Surgery, Columbia University, New York, New York, USA
Ricardo J. Komotar*
Affiliation:
Department of Neurological Surgery, Columbia University, New York, New York, USA
Margy E. McCullough-Hicks
Affiliation:
Department of Neurological Surgery, Columbia University, New York, New York, USA
Marc L. Otten
Affiliation:
Department of Neurological Surgery, Columbia University, New York, New York, USA
Robert M. Starke
Affiliation:
Department of Neurological Surgery, Columbia University, New York, New York, USA
Christopher P. Kellner
Affiliation:
Department of Neurological Surgery, Columbia University, New York, New York, USA
Matthew C. Garrett
Affiliation:
Department of Neurological Surgery, Columbia University, New York, New York, USA
Maxwell B. Merkow
Affiliation:
Department of Neurological Surgery, Columbia University, New York, New York, USA
Michal Rynkowski
Affiliation:
Department of Neurological Surgery, Columbia University, New York, New York, USA
Kelly A. Dash
Affiliation:
Department of Neurological Surgery, Columbia University, New York, New York, USA
E. Sander Connolly
Affiliation:
Department of Neurological Surgery, Columbia University, New York, New York, USA
*
Department of Neurosurgery, Columbia University, 710 West 168th Street, Room 431, New York, New York, 10032, USA.
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Abstract

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Stroke is a leading cause of morbidity and mortality in the US, with secondary damage following the initial insult contributing significantly to overall poor outcome. Prior investigations have shown that the metabolism of certain polyamines such as spermine, spermidine, and putrescine are elevated in ischemic parenchyma, resulting in an increase in their metabolite concentration. Polyamine metabolites tend to be cytotoxic, leading to neuronal injury in the penumbra following stroke and expansion of the area of infarcted tissue. Although the precise mechanism is unclear, the presence of reactive aldehydes produced through polyamine metabolism, such as 3-aminopropanal and acrolein, have been shown to correlate with the incidence of cerebral vasospasm, disruption of oxidative metabolism and mitochondrial functioning, and disturbance of cellular calcium ion channels. Regulation of the polyamine metabolic pathway, therefore, may have the potential to limit injury following cerebral ischemia. To this end, we review this pathway in detail with an emphasis on clinical applicability.

Type
Review Article
Information
Canadian Journal of Neurological Sciences , Volume 36 , Issue 1 , January 2009 , pp. 14 - 19
Copyright
Copyright © The Canadian Journal of Neurological 2009

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