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: 7.01). 11/2008; 65(10):1348-52. DOI: 10.1001/archneur.65.10.1348
Source: PubMed

ABSTRACT 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.

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Available from: Vin Tangpricha, Aug 30, 2015
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    • "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]. "
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    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
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    • "Related to the role of vitamin D and PD, there are some cross-sectional studies in Japan indicating that serum levels of 25-hydroxyvitamin D (25OHD) as well as 1, 25-hydroxy- vitamin D (1, 25OHD) may have an inverse correlation with the severity of PD [12] [13], and higher circulating 25OHD levels are significantly related to milder form of PD [14]. This observation has been confirmed in a European Caucasian population showing a significant decline in vitamin D levels in patients with PD compared with healthy controls and patients with Alzheimer disease [15]. More recently, in a post hoc analysis of more than 3000 participants in Finland, higher serum vitamin D level was associated with lower risk for PD [8]. "
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    ABSTRACT: Introduction. A role for vitamin D deficiency in Parkinson's disease (PD) has recently been proposed. Given the growing body of evidence for the association of vitamin D with several neurodegenerative disorders and unavailability of any published study in the Middle East, the present study is aimed to determine the associations of circulating 25-hydroxyvitamin D (25OHD) levels with the severity of PD in an Iranian sample. Methods. In 109 patients, the severity of PD was evaluated by using Hoehn & Yahr (HR) stages and Unified Parkinson's Disease Rating Stage (UPDRS) Part III compared with 25OHD level in a double-blind and cross-sectional study. Results. Mean ± SD levels of 25OHD were 28.5 ± 1.4 and 27.1 ± 1.5, for males and females, respectively. Also, 38.4% of the patients showed deficiency levels of 25OHD (<20 ng/mL), and 72.8% had insufficient levels (<30 ng/mL). High prevalence of 25OHD insufficiency in subjects with early disease was not associated with HR stage and UPDRS scores even after multivariate adjustment for possible confounders including disease duration. Conclusions. These findings are consistent with the possibility that vitamin D status does not seem to deteriorate during the early disease stages of PD. Further studies are needed to reveal the natural role and significance of vitamin D insufficiency in PD.
    International Journal of Endocrinology 07/2013; 2013(3):689149. DOI:10.1155/2013/689149 · 1.52 Impact Factor
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    • "There is evidence to suggest that polymorphisms in the VDR gene confer susceptibility to PD [34], [35]. Additionally, low serum levels of vitamin D are associated with PD [36], [37]. Coupled with the observation that VDR expression is higher in the substantia nigra than other brain regions [33], these facts indicate that dopamine neurons could be more susceptible to alterations in vitamin D signaling. "
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    ABSTRACT: During development a tightly controlled signaling cascade dictates the differentiation, maturation and survival of developing neurons. Understanding this signaling mechanism is important for developing therapies for neurodegenerative illnesses. In previous work we have sought to understand the complex signaling pathways responsible for the development of midbrain dopamine neurons using a proteomic approach. One protein we have identified as being expressed in developing midbrain tissue is the vitamin D receptor. Therefore we investigated the effect of the biologically active vitamin D3 metabolite, calcitriol, on primary fetal ventral mesencephalic cultures of dopamine neurons. We observed a dose responsive increase in numbers of rat primary dopamine neurons when calcitriol was added to culture media. Western blot data showed that calcitriol upregulated the expression of glial derived neurotrophic factor (GDNF). Blocking GDNF signaling could prevent calcitriol's ability to increase numbers of dopamine neurons. An apoptosis assay and cell birth dating experiment revealed that calcitriol increases the number of dopamine neurons through neuroprotection and not increased differentiation. This could have implications for future neuroprotective PD therapies.
    PLoS ONE 04/2013; 8(4):e62040. DOI:10.1371/journal.pone.0062040 · 3.23 Impact Factor
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