Abstract
Vitamin D is a fat-soluble secosteroid, traditionally considered a key regulator of bone metabolism, calcium and phosphorous homeostasis. Its action is made possible through the binding to the vitamin D receptor (VDR), after which it directly and indirectly modulates the expression of thousands of genes. Vitamin D is important for brain development, mature brain activity and associated with many neurological diseases, including Parkinson’s disease (PD). High frequency of vitamin D deficiency in patients with Parkinson’s disease compared to control population was noted nearly twenty years ago. This finding is of interest given vitamin D’s neuroprotective effect, exerted by the action of neurotrophic factors, regulation of nerve growth or through protection against cytotoxicity. Vitamin D deficiency seems to be related to disease severity and disease progression, evaluated by Unified Parkinson’s Disease Rating Scale (UPDRS) and Hoehn and Yahr (H&Y) scale, but not with age of PD onset and duration of disease. Additionally, fall risk has been associated with lower vitamin D levels in PD. However, while the association between vitamin D and motor-symptoms seems to be possible, results of studies investigating the association with non-motor symptoms are conflicting. In addition, very little evidence exists regarding the possibility to use vitamin D supplementation to reduce clinical manifestations and disability in patients with PD. However, considering the positive balance between potential benefits against its limited risks, vitamin D supplementation for PD patients will probably be considered in the near future, if further confirmed in clinical studies.
Highlights
As consequence of the growth of global population and improvement of the average lifespan, prevalence of neurological disorders is increasing
1,25(OH)2D3 plays a role in limiting inflammation, and some studies observed how in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)induced preclinical animal model of Parkinson’s disease (PD), orally administered vitamin D reduced the immunoreaction of glial fibrillary acidic protein (GFAP) in striatum and substantia nigra pars compacta (SNpc), suggesting that vitamin D might protect against glia-mediated inflammation and nigrostriatal neurodegeneration [69]
We summarized the current literature concerning the possible role of vitamin D in numerous physiological functions, from the modulation of the immunological response to the regulation of brain development and aging (Table 1)
Summary
As consequence of the growth of global population and improvement of the average lifespan, prevalence of neurological disorders is increasing. The scientific community is focused on the research of treatment and prevention of brain aging. Many mechanisms are involved in degeneration: inflammation, oxidative stress, mitochondrial dysfunction, lysosomal depletion, metal dysregulation, impaired RNA homeostasis, misfolding and aggregation of specific proteins, such alpha-synuclein, amyloid β (Aβ), hyperphosphorylated tau [1]. Lower serum concentrations of vitamin D (or 25-hydroxyvitamin D) seems to be associated with psychiatric disorders such as depression, bipolar disorder and schizophrenia, as well as neurological disorders, including neurodegenerative disorders such as dementia and Parkinson’s disease (PD) [2]. It has been postulated that maintaining adequate vitamin D serum concentration might avoid disease onset and possibly improve clinical outcomes [2]. We review the role of vitamin D as protective factor against neurodegeneration, its changes in serum concentration during disease progression and its hypothetical therapeutic use
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