Abstract
Parkinson's disease (PD) is the second most common form of neurodegeneration in the elderly population. Clinically, it is characterized by tremor, rigidity, slowness of movement, and postural imbalance. A significant association between low serum vitamin D and PD has been demonstrated, suggesting that elevated vitamin D levels might provide protection against PD. Genetic studies have helped identify a number of proteins linking vitamin D to PD pathology, including the major histocompatibility complex (MHC) class II, the vitamin D receptor (VDR), cytochrome P450 2D6 (CYP2D6), chromosome 22, the renin-angiotensin system (RAS), heme oxygenase-1 (HO-1), poly(ADP-ribose) polymerase-1 gene (PARP-1), neurotrophic factor (NTF), and Sp1 transcription factor. Vitamin D has also been implicated in PD through its effects on L-type voltage-sensitive calcium channels (L-VSCC), nerve growth factor (NGF), matrix metalloproteinases (MMPs), prostaglandins (PGs) and cyclooxygenase-2 (COX-2), reactive oxygen species (ROS), and nitric oxide synthase (NOS). A growing body of evidence suggests that vitamin D supplementation may be beneficial for PD patients. Among the different forms of vitamin D, calcitriol (1,25-dihydroxyvitamin D3) is best indicated for PD, because it is a highly active vitamin D3 metabolite with an appropriate receptor in the central nervous system (CNS).
Highlights
Parkinson’s disease (PD) is a movement disorder characterized by tremor, rigidity, slowness of movement, and postural imbalance
A vitamin D analogue was reported to reduce the expression of matrix metalloproteinases (MMPs)-2, MMP-9, VEGF, and parathyroid hormone-related protein in Lewis lung carcinoma cells [143]. These findings suggested that vitamin D plays a role in modulating MMP activation in PD
Recent studies have highlighted a possible relationship between vitamin D and PD
Summary
Parkinson’s disease (PD) is a movement disorder characterized by tremor, rigidity, slowness of movement, and postural imbalance. There is evidence of abnormalities in the vitamin D-endocrine system in PD patients, including low bone mineral density (BMD), decreased vitamin D levels, and increased bone turnover makers (bone alkaline phosphatase and urinary N-terminal telopeptide of type I collagen) compared to controls [1]. These factors, combined with balance problems, are the probable reasons for the high incidence of fractures, especially of the hip, reported in elderly women with PD [2]. We review the hypothesized roles of vitamin D in PD pathogenesis
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