Dopamine D1 receptor activation improves adult hippocampal neurogenesis and exerts anxiolytic and antidepressant-like effect via activation of Wnt/β-catenin pathways in rat model of Parkinson's disease.
The present review focuses on the thermodynamic implications in the reprogramming of cellular energy metabolism enabling in Parkinson's disease (PD) through the contrasting interplay of the molecular signaling pathways WNT/ β-catenin and PPARγ.
Wnt/β-Catenin Signaling Pathway Governs a Full Program for Dopaminergic Neuron Survival, Neurorescue and Regeneration in the MPTP Mouse Model of Parkinson's Disease.
Dysregulation of Wnt/β-catenin pathway has been associated with various diseases, including cancer and neurodegenerative disorders, including Parkinson's disease (PD).
Moreover, modulators that interact with Nurr1 or regulate its function, such as retinoid X receptor, cyclic AMP-responsive element-binding protein, glial cell line-derived neurotrophic factor, and Wnt/β-catenin pathway, have the potential to enhance the effects of Nurr1-based therapies in PD.
Consistent with the DNA methylation changes, marked reduction of protein expression was observed for four Wnt and neurogenesis related genes (FOXC1, NEURG2, SPRY1, and CTNNB1) in midbrain dopaminergic (DA) neurons of PD.
It is well known that HIF-1α regulates Wnt/β-catenin signaling and that β-catenin protects neurons against misfolded protein-mediated disorders, including Alzheimer's and Parkinson's disease by preventing mitochondrial malfunction.