Monosialoganglioside effects following cerebral ischemia: relationship with anti-neuronotoxic and pro-neuronotrophic effects

Increasing evidence is available indicating that systemically administered GM1 is able to provide for functional recovery in different experimental models of CNS injury, including cerebral ischemia. Current evidence indicates that the GM1 effects are associated, in the acute phase, with attenuation...

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Veröffentlicht in:Acta neurobiologiae experimentalis 1990, Vol.50 (4-5), p.489
Hauptverfasser: Lipartiti, M, Seren, M S, Lazzaro, A, Koga, T, Mazzari, S, Facci, L, Fusco, M, Toffano, G, Leon, A
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container_issue 4-5
container_start_page 489
container_title Acta neurobiologiae experimentalis
container_volume 50
creator Lipartiti, M
Seren, M S
Lazzaro, A
Koga, T
Mazzari, S
Facci, L
Fusco, M
Toffano, G
Leon, A
description Increasing evidence is available indicating that systemically administered GM1 is able to provide for functional recovery in different experimental models of CNS injury, including cerebral ischemia. Current evidence indicates that the GM1 effects are associated, in the acute phase, with attenuation of secondary neuronal damage due to its capability to antagonize excitatory amino acid-related neurotoxicity in vivo as in vitro. Furthermore, the ganglioside is able to facilitate occurrence of long-term reparative processes, an effect most likely reflecting the potentiation of the action of neuronotrophic factors. This bifaceted action of GM1 makes the ganglioside ideally suited for clinical treatment of patients afflicted by cerebrovascular insufficiencies.
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source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
subjects Animals
Brain Ischemia - drug therapy
Brain Ischemia - physiopathology
G(M1) Ganglioside - pharmacology
G(M1) Ganglioside - therapeutic use
Humans
Ischemic Attack, Transient - drug therapy
Ischemic Attack, Transient - physiopathology
Neurons - drug effects
Neurons - pathology
Neurons - physiology
title Monosialoganglioside effects following cerebral ischemia: relationship with anti-neuronotoxic and pro-neuronotrophic effects
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