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The neuroprotective effects and transdifferentiation of astrocytes into dopaminergic neurons of Ginkgolide K on Parkinson' disease mice. | LitMetric

The neuroprotective effects and transdifferentiation of astrocytes into dopaminergic neurons of Ginkgolide K on Parkinson' disease mice.

J Neuroimmunol

The Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology, Shanxi University of Chinese Medicine, Jinzhong 030619, China; Institute of Brain Science, Shanxi Key Laboratory of Inflammatory Neurodegenerative Disease, Shanxi Datong University, Datong 037009, China. Electronic address:

Published: March 2022

AI Article Synopsis

  • - Parkinson's disease (PD) is a movement disorder linked to the loss of specific neurons in the brain, and although treatments exist, researchers are looking for cures that can protect or regenerate nerve cells.
  • - A study found that Ginkgolide K (GK) provided neuroprotective benefits in mice exposed to a toxic substance (MPTP), improving their movement and reducing neuron loss.
  • - GK works by modulating the immune response, promoting neurotrophic factors, and facilitating the transformation of astrocytes into neurons, suggesting its potential as a therapy for PD, though further research is needed to understand the exact mechanisms involved.

Article Abstract

Parkinson's disease (PD) is a chronic and progressive movement disorder caused by the selective loss of midbrain dopaminergic neurons of unknown etiology. Up to now, although there is a great development on treatments of PD, cures with neuroprotective or nerve regenerative effects are underway for PD patients. Here we reported neuroprotective effects of Ginkgolide K (GK) when mice were upon acute MPTP exposure, in which GK ameliorated the gait dysfunction and dopaminergic neuron loss. GK exhibits its ability in immunomodulation, including switching microglia to M2 phenotype and decreasing the microglia-mediated inflammation, inhibiting peripheral CD4IFN-γ and CD4IL-17 T cells and α-synuclein specific autoantibodies. The expression of neurotrophic factors BDNF, GDNF and NT-3 was promoted with a treatment of GK in MPTP mice brains. Notably, GK enhanced the expression of nestin in GFAP astrocytes followed by the transdifferentiation of astrocyte-to-neuron independent on the Wnt signaling although GK induced the expression of Wnt signaling on astrocytes. Based on these results, our work implicates a therapeutic potential of GK for protecting TH neurons by multiple and intercellular pathways to modify nerve regeneration in MPTP mice. However, its exactly cellular and molecular mechanisms need to be further explored and confirmed.

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Source
http://dx.doi.org/10.1016/j.jneuroim.2022.577806DOI Listing

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