VDR and Alzheimer disease: The rapid increase in LVSCC-A1C expression and NGF down-regulation as a response to VDR silencing indicates that neurons could be vulnerable to aging and neurodegeneration when there is a long-term, or permanent, inefficient utilization of vitamin D. Because both Aβ [25] and VDR siRNA-dependent supression of VDR (current study) have very similar effects on neurons, we speculate that insufficient vitamin D levels in AD patients, in addition to depletion of VDR protein by Aβ, could give rise to a series of deleterious effects.