Prevalence of Vitamin D Insufficiency in Patients With Parkinson Disease and Alzheimer Disease

Department of Neurology, Emory University School of Medicine, 1841 Clifton Road NE, Atlanta, GA 30329, USA.
Archives of neurology (Impact Factor: 7.42). 11/2008; 65(10):1348-52. DOI: 10.1001/archneur.65.10.1348
Source: PubMed


A role for vitamin D deficiency in Parkinson disease (PD) has recently been proposed.
To compare the prevalence of vitamin D deficiency in a research database cohort of patients with PD with the prevalence in age-matched healthy controls and patients with Alzheimer disease (AD).
Survey study and blinded comparison of plasma 25-hydroxyvitamin D (25[OH]D) concentrations of stored samples in a clinical research database at Emory University School of Medicine.
Referral center (PD and AD patients), primary care clinics, and community setting (controls).
Participants were recruited into the study between May 1992 and March 2007. Every fifth consecutively enrolled PD patient was selected from the clinical research database. Unrelated AD (n = 97) and control (n = 99) participants were randomly selected from the database after matching for age, sex, race, APOE genotype, and geographic location.
Prevalence of suboptimal vitamin D and mean 25(OH)D concentrations.
Significantly more patients with PD (55%) had insufficient vitamin D than did controls (36%) or patients with AD (41%; P = .02, chi(2)test). The mean (SD) 25(OH)D concentration in the PD cohort was significantly lower than in the AD and control cohorts (31.9 [13.6] ng/mL vs 34.8 [15.4] ng/mL and 37.0 [14.5] ng/mL, respectively; P = .03).
This report of 25(OH)D concentrations in a predominantly white PD cohort demonstrates a significantly higher prevalence of hypovitaminosis in PD vs both healthy controls and patients with AD. These data support a possible role of vitamin D insufficiency in PD. Further studies are needed to determine the factors contributing to these differences and elucidate the potential role of vitamin D in pathogenesis and clinical course of PD.

Download full-text


Available from: Vin Tangpricha,
  • Source
    • "In our previous study, intracranial volume was inversely related with vitamin D (Plózer et al., 2014), the low serum level of which is a correlate or predictor of a wide variety of neurological and psychiatric conditions (Balion et al., 2012; Evatt et al., 2008; Holló et al., 2014). Vitamin D deficiency has been shown to promote cellular proliferation in the nervous system (Ko et al., 2004). "
    [Show abstract] [Hide abstract]
    ABSTRACT: The objective of this study was to investigate the relation between habitual milk and dairy consumption and brain morphology as assessed by magnetic resonance imaging (MRI) investigations in 119 young healthy university students. MRI measurements were performed on a Siemens Magnetom Trio Tim (3T) system while FreeSurfer software suite was used for volumetric segmentation. Dietary habits related to milk and dairy consumption were assessed by a structured questionnaire. Total cerebral cortex, total cerebral white matter, and total cerebral parenchyma were significantly related with cottage cheese and total protein intake from milk and dairy also when controlled for age and gender in the multivariate model. Our results indicate that dietary habits related with milk and dairy are proportionally associated with volumes of both cerebral cortex and cerebral white matter.
    International Journal of Food Sciences and Nutrition 10/2015; DOI:10.3109/09637486.2015.1093609 · 1.21 Impact Factor
  • Source
    • "The latest meta-analysis of all published observational studies that have measured vitamin D levels in schizophrenic patients confirms a strong association between vitamin D deficiency and schizophrenia (Valipour et al., 2014). Low levels of vitamin D have also been detected in patients with Parkinson's disease (Newmark and Newmark, 2007; Evatt et al., 2008, 2011; Knekt et al., 2010). Outcomes from a randomized clinical trial of vitamin D supplementation in patients with Parkinson disease is eagerly awaited (Suzuki et al., 2013). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Vitamin D is a neuroactive steroid. Its genomic actions are mediated via the active form of vitamin D, 1,25(OH)2D3, binding to the vitamin D receptor (VDR). The VDR emerges in rat mesencephalon at embryonic day 12, representing the peak period of dopaminergic cell birth. Our prior studies reveal that developmental vitamin D (DVD)-deficiency alters the ontogeny of dopaminergic neurons in the developing mesencephalon. There is also consistent evidence from others that 1,25(OH)2D3 promotes the survival of dopaminergic neurons in models of dopaminergic toxicity. In both developmental and toxicological studies it has been proposed that 1,25(OH)2D3 may modulate the differentiation and maturation of dopaminergic neurons; however, to date there is lack of direct evidence. The aim of the current study is to investigate this both in vitro using a human SH-SY5Y cell line transfected with rodent VDR and in vivo using a DVD-deficient model. Here we show that in VDR-expressing SH-SY5Y cells, 1,25(OH)2D3 significantly increased production of tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine synthesis. This effect was dose- and time-dependent, but was not due to an increase in TH-positive cell number, nor was it due to the production of trophic survival factors for dopamine neurons such as glial derived neurotrophic factor (GDNF). In accordance with 1,25(OH)2D3's anti-proliferative actions in the brain, 1,25(OH)2D3 reduced the percentage of dividing cells from approximately 15% to 10%. Given the recently reported role of N-cadherin in the direct differentiation of dopaminergic neurons, we examined here whether it may be elevated by 1,25(OH)2D3. We confirmed this in vitro and more importantly, we showed DVD-deficiency decreases N-cadherin expression in the embryonic mesencephalon. In summary, in our in vitro model we have shown 1,25(OH)2D3 increases TH expression, decreases proliferation and elevates N-cadherin, a potential factor that mediates these processes. Accordingly all of these findings are reversed in the developing brain in our DVD-deficiency model. Remarkably our findings in the DVD-deficiency model phenocopy those found in a recent model where N-cadherin was regionally ablated from the mesencephalon. This study has, for the first time, shown that vitamin D directly modulates TH expression and strongly suggests N-cadherin may be a plausible mediator of this process both in vitro and in vivo. Our findings may help to explain epidemiological data linking DVD deficiency with schizophrenia. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience 07/2015; 304. DOI:10.1016/j.neuroscience.2015.07.048 · 3.36 Impact Factor
  • Source
    • "studies were also reported. Low levels of plasma 25-dihydroxyvitamin D 3 (25-hydroxycholecalciferol, abbreviated as 25(OH)D) were suggested to be associated with mood disorders, dementia, mild cognitive impairment, PD, AD, and cognitive decline [40] [41] [42] [43] [44] [45] [46] [47] [48]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Scientists have worked for over a century to uncover the basis of Alzheimer's disease (AD) with the ultimate goal of discovering a treatment. However, none of the approaches utilized have defined the exact cause of the disease or an ultimate treatment for AD. In this review, we aim to define the role of vitamin D in AD from a novel and fundamental perspective and attempt to answer the following question: Why should we seriously consider "simple" vitamin D as a "fundamental factor" in AD? To answer this question, we explain the protective effects of vitamin D in the central nervous system and how the action of vitamin D and AD-type pathology overlap. Furthermore, we suggest that the role of vitamin D in AD includes not only vitamin D deficiency and vitamin D-related genes but also the disruption of vitamin D metabolism and action. This suggestion is supported by evidence that the disruption of vitamin D pathways mimic amyloid pathology. We define the term "inefficient utilization of vitamin D" as any alteration in vitamin D-related genes, including receptors, the enzymes related to vitamin D metabolism or the transporters of vitamin D, and we discuss the potential correlation of vitamin D status with the vulnerability of neurons to aging and neurodegeneration. Finally, in addition to the current knowledge that defines AD, we suggest that AD could be the result of a long-term hormonal imbalance in which the critical hormone is vitamin D, a secosteroid that has long been misnamed.
    Journal of Alzheimer's disease: JAD 01/2014; 40(2). DOI:10.3233/JAD-131970 · 4.15 Impact Factor
Show more