It has been known for more than 20 years that vitamin D exerts marked effects on immune
and neural cells. These non-classical actions of vitamin D have recently gained a
renewed attention since it has been shown that diminished levels of vitamin D induce
immune-mediated symptoms in animal models of autoimmune diseases and is a risk factor
for various brain diseases. For example, it has been demonstrated that vitamin D (i)
modulates the production of several neurotrophins, (ii) up-regulates Interleukin-4
and (iii) inhibits the differentiation and survival of dendritic cells, resulting
in impaired allo-reactive T cell activation. Not surprisingly, vitamin D has been
found to be a strong candidate risk-modifying factor for Multiple Sclerosis (MS),
the most prevalent neurological and inflammatory disease in the young adult population.
Vitamin D is a seco-steroid hormone, produced photochemically in the animal epidermis.
The action of ultraviolet light (UVB) on 7-dehydrocholesterol results in the production
of pre-vitamin D which, after thermo-conversion and two separate hydroxylations, gives
rise to the active 1,25-dihydroxyvitamin D. Vitamin D acts through two types of receptors:
(i) the vitamin D receptor (VDR), a member of the steroid/thyroid hormone superfamily
of transcription factors, and (ii) the MARRS (membrane associated, rapid response
steroid binding) receptor, also known as Erp57/Grp58. In this article, we review some
of the mechanisms that may underlie the role of vitamin D in various brain diseases.
We then assess how vitamin D imbalance may lay the foundation for a range of adult
disorders, including brain pathologies (Parkinson's disease, epilepsy, depression)
and immune-mediated disorders (rheumatoid arthritis, type I diabetes mellitus, systemic
lupus erythematosus or inflammatory bowel diseases). Multidisciplinary scientific
collaborations are now required to fully appreciate the complex role of vitamin D
in mammal metabolism.