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

<div>Wnt/<i>β</i>-catenin signaling cascade in Parkinson’s disease. Upon insult, Wnt/<i>β</i>-catenin activation stimulates neurogenesis in mouse models of Parkinson’s and Alzheimer’s diseases. In mammalians, the signaling pathway is activated when the Wnt ligand binds to its Frizzled (FZD) receptor. The protein complex of FZD, LRP5/6, CK1, and GSK-3<i>β</i> marks <i>β</i>-catenin protein for degradation in the proteasome. Unless <i>β</i>-catenin undergoes degradation, it will be translocated to the nucleus to regulate the proliferation and survival of dopaminergic neurons.</div>

Neural Plasticity

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Figure 1

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