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Ganglioside GM1 for ischemic stroke: An update (2005-2015)

Li Li

Department of Anesthesiology, Xuanwu Hospital, Capital Medical University, Beijing, China

E-mail : lili2009kaoyan@163.com

Tianlong Wang

Department of Anesthesiology, Xuanwu Hospital, Capital Medical University, Beijing, China

E-mail : w_tl5595@hotmail.com

DOI: 10.15761/PCCM.1000105

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Abstract

Aim of review

 Ganglioside GM1is a major ganglioside component, which has been shown to potentiate the action of neurotrophins and display a wide variety of CNS functions amongst many neurologic conditions including cerebral ischemic injury. This mini-review aims to summarize the latest knowledge of the possible neuro-reparative properties of GM1 in ischemic stroke in the past ten years.

Method

 The literature was searched using Medline between 2005 and the present using search terms including “Ganglioside GM1”, “ischemic stroke ”, “ ischemic brain injury ” and “stroke ” . The search terms were cross-referenced and the search was limited to English language articles. All of the articles, found including those associated with the initial search results, were evaluated

for methodology and results, and were included if deemed applicable to this review.

Recent findings

 GM1 treatment has been shown robust and reproducible neuroprotective effects both in the neonatal and adult ischemic brain insult, however, the clinical efficacy of GM1 in stroke patients remains uncertain. The issues exist in the present clinical trials may account for some of the failure.

Summary

More well-designed clinical trials are necessary to re-assess the potential efficacy of GM1 in stroke patients.

Introduction

There is considerable research interest in Ganglioside GM1, a major ganglioside component. This pattern began in reports published in the early 1970s covering its role as a receptor for the bacterial toxin responsible for the cholera pathogenesis [1]. At that time, gangliosides were a relatively hot topic and the subject of many international meetings. Soon afterwards it was also found to be able to potentiate the action of neurotrophins and display a wide variety of central nervous system (CNS) functions including promoting survival, differentiation [2], neurodegeneration [3-5], axon stability, and regeneration [6]. Although the development of the acute inflammatory polyneuropathy Guillain-Barre´ syndrome (GBS) after intravenous ganglioside treatment resulted in the withdrawal of GM1 from the European market [7], this adverse effect was shown to be rare [8].These drugs are still available and have been extensively prescribed in other markets, including in China, where a multitude of neurological maladies are treated with gangliosides in the absence of resultant GBS or other severe adverse events [9-12]. Recently, a plethora of studies have suggested that GM1 may be involved in the stroke process, specifically orchestration of cell death and subsequent neurological dysfunctions [13].

GM1 in neonatal ischemic brain injury

White matter injury is the predominant form of brain damage in neonatal hypoxic-ischemic (HI). The concentration of GM1 has been found to undergo a significant decrease in this process [14]. Exogenous GM1 injection has been shown to reduce the damage of myelin sheaths, the primary characteristic of white matter injury, and eventually prevent brain injury. The neuroprotective effect of GM1 might involve promoting the association of neurofascin 155 (or other important proteins) with lipid rafts, increasing the expression of myelin basic protein, and subsequent stabilizing the structure of paranodes [13,14]. In a recent study by Whitehead et al. [15], middle cerebral artery occlusion (MCAO) resulted in a transient induction of GM1 at the border of the infarcted tissue in adult mice. Consistent with this finding, another adult rat experimental study performed by Kwak et al. [16] emonstrated an increase in the mRNA for GM1 synthase and an obvious increase of GM1 expression to protect the cerebral cortex from ischemic damage. One possible e