Role of Astrocytic Dysfunction in the Pathogenesis of Parkinson’s Disease Animal Models from a Molecular Signaling Perspective

<table class="table-group" id="tab1"><tr><td><table class="table"><tr><td class="thead-hr" colspan="3"><hr/></td></tr><tr class="thead"><td class="align_left">Molecule</td><td class="align_center">Proposed mechanism of action</td><td class="align_center">Tested PD models</td></tr><tr><td class="thead-hr" colspan="3"><hr/></td></tr><tr><td class="align_left">Capsaicin</td><td class="align_center">Activation of TRPV1 in astrocytes</td><td class="align_center">MPTP (mouse), 6-OHDA (rat)</td></tr><tr><td class="align_left">GDNF (vector transfection)</td><td class="align_center">GDNF overexpression in astrocytes</td><td class="align_center">MPTP (mouse), 6-OHDA (rat)</td></tr><tr><td class="align_left">Silibinin</td><td class="align_center">Suppression of astrocyte activation (via ERK/JNK phosphorylation)</td><td class="align_center">MPTP (mouse)</td></tr><tr class="table-tr"><td colspan="3"><hr class="tbody-hr"/></td></tr></table></td></tr><tr class="table-fn"><td><div>GDNF: glial cell line-derived neurotrophic factor; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; TRPV1: transient receptor potential vanilloid 1 channel; ERK/JNK: extracellular signal-regulated kinase/c-Jun N-terminal kinase.<br/></div></td></tr></table>

<div>Potentially neuroprotective molecules upon astrocytic behavior modification.</div>

Neural Plasticity

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Table 1

Table 1: Role of Astrocytic Dysfunction in the Pathogenesis of Parkinson’s Disease Animal Models from a Molecular Signaling Perspective 