Animal models have been paramount in contributing to our knowledge and understanding of the consequences of vitamin D deficiency on brain development www.selleckchem.com/products/dabrafenib-gsk2118436.html and its implications for adult psychiatric and neurological diseases. The conflation of in vitro, ex vivo, and animal model data provide compelling evidence that vitamin
D has a crucial role in proliferation, differentiation, neurotrophism, neuroprotection, neurotransmission, and neuroplasticity. Vitamin D exerts its biological function not only by influencing cellular processes directly, but also by influencing gene expression through vitamin D response elements. This review highlights the epidemiological, neuropathological, experimental and molecular genetic evidence implicating vitamin D as a candidate in influencing susceptibility to a number of psychiatric and neurological diseases. The strength of evidence varies for schizophrenia, autism, Parkinson’s disease, amyotrophic lateral sclerosis, Alzheimer’s disease, and is especially strong for multiple sclerosis. It is well established that the vitamin D endocrine system plays a critical role in calcium homeostasis and bone health; however, in recent decades, the broad range of physiological actions
of vitamin D has been increasingly recognized. In addition to its role in proliferation, differentiation and selleck inhibitor immunomodulation, there is mounting evidence to support an intricate role of vitamin D in brain development and function in health and disease. The current review will summarize key concepts in vitamin D metabolism in the brain, and explore the relationship of vitamin D and brain development. A survey of the role of vitamin D in several psychiatric and neurological disorders including schizophrenia, autism, Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), and multiple sclerosis (MS) will be presented. Smoothened Vitamin D is a seco-steroid hormone that comes in two major forms depending on the source, vitamin D2 (ergocalceiferol) of plant origin, and vitamin D3 (cholecalciferol) of
animal origin. Vitamin D3 can be either ingested or produced photochemically in the epidermis by action of ultraviolet light (UVB) on 7-dehydrocholesterol. In both instances, vitamin D2 and D3 are biologically inert and require two separate hydroxylations by 25-hydroxylase (liver) and 1-α-hydroxylase (primarily in the kidney) to give rise to the active form (1,25-dihydroxyvitamin D2 and 1,25-dihydroxyvitamin D3 or calcitriol, respectively) [1] (Figure 1). The potential role of 1,25-dihydroxyvitamin D3 in the brain was first suggested by the discovery of high affinity calcitriol receptors in the pituitary [2], and later in the forebrain, hindbrain, and spinal cord [3] of rats. The presence of vitamin D metabolites in the cerebrospinal fluid of healthy patients further implied a role for vitamin D in the brain [4].