While 1,25(OH)2D3 can protect against progression of neu- rodegenerative disorders such as EAE through its effects on the immune system, recent evidence suggests that it can act directly on the central nervous system (CNS) itself. The VDR is widely expressed throughout the CNS, and is a strong in­ducer of nerve growth factor expression. Several studies have suggested that 1,25(OH)2D3 has neuroprotective effects. In vivo experiments in rodents have shown that 1,25(OH)2D3 retards age-related decreases in hippocampal neuronal density, and protects against neuronal cell death in a rodent model of stroke. Moreover, 1,25(OH)2D3 can act directly on primary cultures of rat hippocampal neurons to inhibit ex­pression of markers associated with neuronal aging. Part of the neuroprotective effects of 1,25(OH)2D3 in the CNS may also lie in its capacity to protect cells from ROS. Studies in cul­tured rat neurons showed that 1,25(OH)2D3 protected against the neurotoxic effects of agents that caused oxidative damage by increasing intracellular levels of glutathione, consis­tent with its effects on redox balance observed in cancer cells.

Conclusions

Vitamin D action is not only involved in bone metabolism. The broad expression pattern of the VDR, and the widespread ef­fects of its hormone on cellular differentiation and proliferation have opened up a number of new fields of investigation for ba­sic researchers interested in 1,25(OH)2D3 function as well as those more concerned with the therapeutic potential of its syn­thetic analogues as chemopreventive agents against cancer and neuronal aging, as well as their potential in combating a number of autoimmune disorders. Make your pharmacy dollar go further cialis 200mg