The loss of dopaminergic (DA) neurons is a hallmark of Parkinson's disease(PD), a common human neurodegenerative disorder. Stem cell replacement therapy is a promising strategy for alleviating PD, but one current limitation is generating large enough numbers of DA neurons. Now, on , Eric Huang and co-workers reveal that several stages of DA neurogenesis depend onβ-catenin. The authors show, using conditional gene knockout approaches,that regionally deleting β-catenin in the neurogenic niche of the mouse ventral midbrain (vMB), which gives rise to DA progenitors, disrupts progenitor cell adherent junctions and radial glial cell integrity. This leads to reduced DA neurogenesis and defects in DA neuron polarity, migration and segregation. By contrast, removing β-catenin from DA neural progenitors does not perturb vMB structure, but rather reduces DA neurogenesis by impairing the later progression of committed progenitors to DA neurons. From these findings, the authors suggest that β-catenin-mediated regulation of DA differentiation could be exploited in the development of cell-based therapies for PD.
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