With vitamin D deficiency reaching epidemic proportions worldwide, there is now concern that optimal levels of vitamin D in the bloodstream are also necessary to preserve the neurological development and protect the adult brain.
Classically, vitamin D has a recognized role in the regulation of bone health and calcium-phosphorus homeostasis, by acting at the level of the skeletal bone, intestine and kidney.
There is now consistent evidence showing that several “non-calcemic” effects of vitamin D metabolites occur, and increasing consideration is given to vitamin D status as a marker of general health, since low vitamin D levels are associated with the development and progress of autoimmunity, infectious diseases, diabetes mellitus, cardio-metabolic disorders, obesity, neuromuscular disorders, and cancer.
It appears that vitamin D plays a role in neurotransmission and synaptic plasticity, and a link has been described between Vit. D and dopaminergic neurotransmission.
Collectively, the physiological effects of vitamin D in brain functions include the promotion of neurotransmission, neurogenesis, synaptogenesis, amyloid clearance and the prevention of neuronal death. It is not surprising that observational studies have documented associations between higher serum vitamin D concentrations and healthier cognitive performance.
Another recent field of interest regards VDR gene polymorphisms. Preliminary data suggest that single nucleotide polymorphisms (SNPs) in the VDR gene may have roles in the development of multiple sclerosis, Parkinson’s disease, and Alzheimer’s disease.
Vitamin D deficiency has been mechanistically and clinically linked to neurological diseases and neuropsychological disorders, cognitive impairment and neurodegenerative diseases.
One key aspect related to vitamin D homeostasis and neurological disorders is the role of vitamin D supplementation in deficient patients. Endocrine Society, the International Osteoporosis Foundation, and the American Geriatric Society suggest that a minimum level of 30 ng/mL is needed to minimize the risk of falls and fracture in older adults.
In the context of PD, potential neuroprotective effects exerted by vitamin D include the notion that 1,25(OH)2D indirectly inhibits the synthesis of nitric oxide, a free radical that can damage cells; secondly, it indirectly stimulates the synthesis of the antioxidant glutathione, and; thirdly, vitamin D may act as a neurotrophic factor, through the stimulation of nerve growth factor (NGF), glial cell line-derived neurotrophic factor (GDNF) and neurotrophin 3 (NT3).
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