Abstract
It is widely known that vitamin D receptors have been found in neurons and glial cells, and their highest expression is in the hippocampus, hypothalamus, thalamus and subcortical grey nuclei, and substantia nigra. Vitamin D helps the regulation of neurotrophin, neural differentiation, and maturation, through the control operation of growing factors synthesis (i.e., neural growth factor [NGF] and glial cell line-derived growth factor (GDNF), the trafficking of the septohippocampal pathway, and the control of the synthesis process of different neuromodulators (such as acetylcholine [Ach], dopamine [DA], and gamma-aminobutyric [GABA]). Based on these assumptions, we have written this review to summarize the potential role of vitamin D in neurological pathologies. This work could be titanic and the results might have been very fuzzy and even incoherent had we not conjectured to taper our first intentions and devoted our interests towards three mainstreams, demyelinating pathologies, vascular syndromes, and neurodegeneration. As a result of the lack of useful therapeutic options, apart from the disease-modifying strategies, the role of different risk factors should be investigated in neurology, as their correction may lead to the improvement of the cerebral conditions. We have explored the relationships between the gene-environmental influence and long-term vitamin D deficiency, as a risk factor for the development of different types of neurological disorders, along with the role and the rationale of therapeutic trials with vitamin D implementation.
Highlights
Low levels of vitamin D, considering serum 25-hydroxyvitamin D (25(OH)D), have been recognized as a widespread health problem, affecting approximately one billion people worldwide [1]
The authors concluded that individuals with Clinically Isolated Syndrome (CIS)/relapsing-remitting multiple sclerosis (RRMS) with higher vitamin D levels have a lower risk of the subsequent development of new T2 lesions and
Vitamin D deficiency might relate with higher disease severity and adverse outcomes, including death; hypovitaminosis D is independently associated with larger ischemic infarct volume [126]; vitamin D deficiency is related to slower recovery after stroke
Summary
Low levels of vitamin D, considering serum 25-hydroxyvitamin D (25(OH)D), have been recognized as a widespread health problem, affecting approximately one billion people worldwide [1]. The congenital deficiency of vitamin D significantly reduces the activity of glutamic acid decarboxylase (GAD) 65/67 (critical enzymes in GABAergic inter-neurons) and the levels of glutamate and glutamine in the brain tissue [27]. For these reasons, we reckon that a vitamin D deficiency could contribute to the complex relationship between genetics and the environment, the two common poles that many neurological pathologies debate between.
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