Together, these results suggest the sufficiency of low level of VPS35-mCherry fusion protein to diminish the deficit in neuronal terminal differentiation, cell death, and gliosis at the neonatal age, and thus to prevent neonatal death, demonstrating the neuronal Vps35 function in stabilizing retromer complex proteins in an age dependent manner, and supporting the view for Vps35 as a potential therapeutic target for neurodegenerative diseases. Here, VPS35 is linked to neurodegenerative disease.