The purpose of this article is to review recent findings regarding the mechanisms by which GM1 may mimic or potentiate certain actions of neurotrophic factors, including promotion of neuronal survival. It is proposed that the neuroprotective activity of GM1 is due, at least in part, to its ability to favor the dimerization of neurotrophic factor tyrosine kinases and thereby mimicking the action of their corresponding ligands. This may manifest both in the absence of ligand (thereby triggering a subset of neurotrophic-factor responses such as prevention of apoptosis) and in the presence of ligand (thereby potentiating responses to neurotrophic factors).
No takes yet. Share an insight, caveat, or question.
Ferrari et al. (1998) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: