AI Article Synopsis

  • Research indicates that GM1 ganglioside can slow neuronal death in Parkinson's disease but has limited clinical use due to its inability to cross the blood-brain barrier.
  • A recent study identified the GM1 oligosaccharide head group (GM1-OS) as the active component that activates cellular pathways beneficial for neuron survival and repair.
  • GM1-OS was found to significantly enhance neuronal survival and reduce harmful mitochondrial effects in models exposed to MPTP, a toxin related to Parkinson's disease, by improving mitochondrial function and lowering oxidative stress.

Article Abstract

Past evidence has shown that the exogenous administration of GM1 ganglioside slowed neuronal death in preclinical models of Parkinson's disease, a neurodegenerative disorder characterized by the progressive loss of dopamine-producing neurons: however, the physical and chemical properties of GM1 (i.e., amphiphilicity) limited its clinical application, as the crossing of the blood-brain barrier is denied. Recently, we demonstrated that the GM1 oligosaccharide head group (GM1-OS) is the GM1 bioactive portion that, interacting with the TrkA-NGF complex at the membrane surface, promotes the activation of a multivariate network of intracellular events regulating neuronal differentiation, protection, and reparation. Here, we evaluated the GM1-OS neuroprotective potential against the Parkinson's disease-linked neurotoxin MPTP, which destroys dopaminergic neurons by affecting mitochondrial bioenergetics and causing ROS overproduction. In dopaminergic and glutamatergic primary cultures, GM1-OS administration significantly increased neuronal survival, preserved neurite network, and reduced mitochondrial ROS production enhancing the mTOR/Akt/GSK3β pathway. These data highlight the neuroprotective efficacy of GM1-OS in parkinsonian models through the implementation of mitochondrial function and reduction in oxidative stress.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10216367PMC
http://dx.doi.org/10.3390/biomedicines11051305DOI Listing

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