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Could vitamin D deficiency have an impact on motor and cognitive function in Parkinson’s disease?

The Egyptian Journal of Neurology, Psychiatry and Neurosurgery volume 55, Article number: 34 (2019) Cite this article

Abstract

Background

Multiple epidemiological data showed a significant higher prevalence of hypovitaminosis D in patients with Parkinson’s disease (PD).

Objectives

To assess the serum vitamin D level in patients with Parkinson’s disease and to investigate the possible relationship between the serum vitamin D level and both motor and cognitive symptoms in Parkinson’s disease

Materials and methods

A case-control study was conducted on 25 patients who fulfilled the criteria for diagnosis of idiopathic Parkinson’s disease based on the British Brain Bank criteria, and 25 healthy volunteers. Selected PD patients were submitted for assessment of cognitive function using the PD - Cognitive Rating Scale (PD-CRS) and assessment of motor function using the Unified Parkinson’s Disease Rating Scale (UPDRS). Serum 25 hydroxy vitamin D level was measured for all the included patients and controls.

Results

PD patients were found to have a significantly lower level of serum vitamin D than controls (P value = 0.001). There was a statistically significant negative correlation between the serum vitamin D level and the scores of motor, mentation, activities of daily living, medication complication, other complications, and the total score of UPDRS (P value = 0.01, < 0.001, 0.012, 0.017, 0.039, and 0.002 respectively). There was a statistically significant positive correlation between the serum vitamin D level and the scores of attention, working memory, immediate recall, delayed recall, naming, visuoperceptual abilities, visuoconstructional abilities, alternating verbal fluency, action verbal fluency, and the total score of PD-CRS (P value < 0.001 in all parameters).

Conclusion

Vitamin D deficiency is evident in PD patient, and such deficiency significantly affected both motor and cognitive symptoms.

Introduction

Parkinson’s disease (PD) is the second most common neurodegenerative disease; it affects 1–2/1000 population at any time. The prevalence of PD increases with age; it affects 1% of the population over the age of 60 [1]. Compared to other Arab countries, the prevalence of PD disease is higher in Nile valley governorates of Upper Egypt [2]. Several epidemiologic studies have suggested an inverse relationship between circulating vitamin D levels and the risk of PD. Serum level of vitamin D is significantly lower in patients with PD compared to healthy controls [3,4,5], and serum 25 hydroxy vitamin D (25(OH)D) concentration progressively decreases with the increase in severity of motor symptoms of Parkinson’s disease [6].

In a meta-analysis on the relationship between the vitamin D level and PD that included 20 studies (1 interventional, 14 observational, and 5 rodent studies), serum levels of 25(OH)D in PD patients were lower than in controls and higher levels of vitamin D were associated with better motor functions in most of the included studies [7]. Moreover, higher levels of vitamin D in PD patients were associated with better mood and cognitive function [8].

Vitamin D was proposed to alter cholinergic, dopaminergic, and noradrenergic neurotransmitter pathways in the central nervous system (CNS) [9]. Furthermore, vitamin D may play a role in neuronal plasticity and axogenesis [10]. Several studies demonstrated that vitamin D ameliorates synthesis of neurotrophic factors and detoxification pathways which protect the integrity and structure of neurons [11].

Vitamin D enhances the synthesis of dopamine through increasing the level and activity of the enzyme tyrosine hydroxlase [12]. Furthermore, vitamin D was assumed to have a neuroprotective effect on dopaminergic pathways in the central nervous system. Animals which were pretreated with vitamin D for 1 week maintained dopaminergic functions after administration of 6-hydroxydopamine (a selective dopamine agonist (DA) toxin) [13]. Vitamin D was also found to preserve serotonin and dopamine systems in the brains of animals repeatedly administered neurotoxic doses of methamphetamine [14]. Accumulating studies reported that the distribution of vitamin D receptors (VDR) in the substantia nigra is altered in patients with Parkinson’s disease [15]. It has been demonstrated that vitamin D plays a role in dopamine synthesis through regulation of tyrosine hydroxylase gene expression [16]. VDR is also highly expressed in putamen and caudate [14]. Kim and colleagues reported in their study a significant relationship between VDR gene polymorphism and Parkinson’s disease [17].

Vitamin D receptors were demonstrated in the promoter regions of ret, GDNFR-α, and neurturin genes which are strongly linked to PD [18]. Furthermore, adult rats born to vitamin D-deficient mothers showed a permanent downregulation of Park 7 expression in the hippocampus [19].

Despite the accumulating biological and epidemiological data which revealed that vitamin D deficiency contributes in the development of Parkinson’s disease [20], it is a debate if this relation is a direct effect or that patients suffering from Parkinson’s disease mostly have decreased ambulation and sun exposure and, as a sequence, higher prevalence of vitamin D deficiency [15, 21].

Aim of the work

The aim of this study was to assess the serum vitamin D level in patients with Parkinson’s disease and to investigate the possible relationship between the serum vitamin D level and both motor and cognitive symptoms in Parkinson’s disease.

Methods

The present study is a case-control study which included 25 PD patients and 25 normal healthy controls. The patients were enrolled from the Neurology outpatient clinic of Beni-Suef University Hospital. The study was approved by the ethical committee in the Faculty of Medicine, Beni-Suef University (FWA00015574 in the ninth of October 2018), and all participants in this study signed a written informed consent.

All the included patients fulfilled the criteria for diagnosis of idiopathic PD based on the British Brain Bank criteria [22] and had the ability to read, write, and do simple calculations.

Exclusion criteria were as follows: patients with visual impairment or hearing loss affecting their ability to complete the tests, patients with stroke temporally related to the onset of the disease, patients with a history of alcohol intake or drug abuse, patients with any medical disease which affects cognition or the serum level of vitamin D or calcium, patients with major psychiatric disorders, patients with structural brain lesions in an MRI study, and patients on vitamin D supplements or medications that affect the vitamin D level.

Participants of this study were subjected to the following battery of assessment

Evaluation and staging of Parkinson’s disease

Evaluation and staging of Parkinson’s disease were done for all PD patients (during on state) using the Modified Hoehn and Yahr staging scale (H&Y staging) [23] and Unified Parkinson’s Disease Rating Scale (UPDRS) [24].

Modified H&Y staging scale was used for staging of PD patients based on clinical features and functional disability. The first stage is the mildest stage of the disease and stage 5 is the worst stage.

UPDRS includes five parts: part I: assessment of mentation, behavior, and mood; part II: evaluation of daily living activities including speech, swallowing, salivation, turning in bed, cutting food, handwriting, hygiene, dressing, freezing, walking, falling, tremor, and sensory complaints; part III: clinician-scored motor evaluation; part IV: complication of therapy; and part V: other complications.

Cognitive assessment

Cognitive assessment was done for all PD patients (on medications) using the Parkinson’s Disease - Cognitive Rating Scale (PD-CRS) [25]. The following cognitive domains were included in the test: sustained attention, working memory, immediate and delayed free recall verbal memory, confrontation naming, visuoconstructional and visuoperceptual skills, and alternating and action verbal fluency. The total score for the test is 134.

Laboratory assessment

Serum level of 25(OH) vitamin D was measured for all patients and controls using Stat Fax 303Plus equipment. Fasting early morning venous blood samples were collected from resting subjects in 6-ml plain tubes then centrifuged. The processed serum was stored at − 80 °C prior to analysis. In a first step, 25(OH) vitamin D contained in the sample has to be released from its vitamin D-binding protein. The undiluted sample is placed in a test tube and mixed with sample buffer containing a 25(OH) vitamin D tracer reagent and then with a vitamin D release reagent. Then 25(OH) vitamin D can be determined with the 25(OH) vitamin D ELISA assay. Calculation of results was done using data reduction software; a 4-Parameter-Fit with lin-log coordinates for optical density and concentration is the data reduction method of choice. Measuring range was 5–120 ng/ml. Patients were considered to have vitamin D deficiency if they had a vitamin D level below 30 ng/ml.

Statistical methods

The data were coded and entered using the Statistical Package for the Social Sciences (SPSS), version 15.0, released 2006, Chicago, USA. The demographic data, clinical characteristics, and serum vitamin D level for included PD patients and controls were reported as mean ± SD and number (%) for categorical variables. The Student t test was used for comparison between PD patients and controls in vitamin D serum level. Chi-square test was used for comparison between PD patients and controls in the frequency of vitamin D deficiency. The Pearson correlation coefficient (r) was used to describe the relationship between serum vitamin D level and Modified Hoehn and Yahr staging, score of UPDRS, and score of PD-CRS. P value equal to or less than 0.05 was considered significant.

Results

The demographic data for included PD patients and controls were demonstrated in Table 1. There was no statistically significant difference between patients and controls in age (P value = 0.553) or sex (P value = 1).

Table 1 Demographics of PD patients and controls
Full size table

Regarding clinical characteristics of PD patients, the disease duration ranged from 0.5–5 years with a mean value of 1.77 ± 1.27 years. The total score for Modified Hoehn and Yahr staging ranged from 1.5 to 4 with a mean value 2.7 ± 0.707. The total UPDRS score ranged from 12 to 76 with a mean value 33.92 ± 15.16 (Table 2). The total PD-CRS ranged from 52 to 122 with a mean value 93.12 ± 24.45 (Table 3).

Table 2 Modified Hoehn and Yahr staging and UPDRS score for PD patients
Full size table
Table 3 CRS-PD score for PD patients
Full size table

Regarding the incidence of vitamin D deficiency, 84% (n = 21) of PD patients were found to have vitamin D deficiency and 16% (n = 4) were found to have normal vitamin D. As for controls, 24% (n = 6) were found to have vitamin D deficiency and 76% (n = 19) have normal vitamin D. There was a statistically significant difference between patients and controls (P value < 0.001). There was also a statistically significant difference between patients and controls in the mean value for serum 25 hydroxy vitamin D level (P value = 0.001) (Table 4).

Table 4 Serum 25 hydroxy vitamin D level in patients and controls
Full size table

There was a statistically significant negative correlation between serum vitamin D level and Modified Hoehn and Yahr staging, scores of motor, mentation, activities of daily living, medication complication, other complications, and the total score of UPDRS (Table 5).

Table 5 Correlation between Modified Hoehn and Yahr staging and UPDRS and serum vitamin D level
Full size table

There was a highly statistically significant positive correlation between the serum level of vitamin D and the scores of attention, working memory, immediate recall, delayed recall, naming, visuoperceptual abilities, visuoconstructional abilities, action verbal fluency, alternating verbal fluency, and the total score of PD-CRS (P value < 0.001 in all parameters).

Discussion

There are accumulating evidences supporting the role of vitamin D deficiency in the pathogenesis of PD [2]. Long-standing low vitamin D levels may lead to chronic loss of dopaminergic neurons in the central nervous system and, as a consequence, the development of Parkinson’s disease [26].

In our study, PD patients were found to have a significantly lower level of serum vitamin D compared to the control group. In line with our finding, a previous cross-sectional study reported higher prevalence of vitamin D deficiency in PD patients compared to healthy controls [6].

Similarly, a cohort study carried out by Bischoff-Ferrariet and colleagues [27] showed that the risk of developing PD was higher in individuals with low serum vitamin D levels. In such study, after adjustment for the potential confounders, individuals with a serum vitamin D level equal to or more than 50 nmol/l were found to have a 65% lower risk of developing PD compared to individuals with values below 25 nmol/l.

The relation between vitamin D deficiency and PD can be explained by the accumulating evidences that long-standing vitamin D deficiency results in loss of dopaminergic neurons in the substantia nigra and, as a consequence, the development of Parkinson’s disease [28].

The proposed mechanisms by which vitamin D may help in protection against PD include neuronal calcium regulation, antioxidative mechanisms, detoxification mechanisms, immunomodulation, and enhancement of nerve conduction [29]. In the substantia nigra, the enzyme which controls the formation of the active form 1,25(OH)2D and vitamin D receptors was found in high levels [14].

On the other hand, a study carried out by Fullard and colleagues [30] assessed the vitamin D serum level in a population at risk for developing PD. They did not find any statistically significant difference between the high-risk group and the age- and sex-matched control group, suggesting that vitamin D deficiency is not considered a risk for developing PD.

In our study, there was a statistically significant negative correlation between serum vitamin D level and Hoehn and Yahr staging scale; the scores of motor, mentation, activities of daily living, other complication; and the total score of UPDRS. In line with our findings, Sleeman and colleagues [31] revealed a significant negative correlation between the serum level of 25(OH)D concentration and the severity of motor symptoms of PD assessed by UPDRS. Similarly, Sato and colleagues [21] reported a negative correlation between 25(OH)D with severity of PD as assessed by Hoehn and Yahr (H&Y) staging. The study revealed a higher prevalence of vitamin D deficiency in patients with advanced stage of the disease. Furthermore, Peterson and colleagues investigated the association between motor activity and serum level of 25(OH)D using five posturography tests (the sensory organization test, motor control test, sit and stand test, the unilateral stance test with eyes closed and eye opened, and the walk and turn test) in 40 PD patients. The study reported the presence of significant positive correlation between the serum level of vitamin D and the automatic postural responses [32].

Regarding the effect of vitamin D supplementation on PD progression, Suzuki and colleagues [28] conducted a double-blind placebo-controlled trial on the impact of vitamin D supplementation (1200 IU/day) on progression of motor symptoms in PD assessed by modified Hoehn and Yahr scale and UPDRS. In such trial, 104 PD patients were studied for 1 year, 56 of them received 1200 IU vitamin D per day and the remaining 58 received placebo. Surprisingly, they found that PD patients receiving placebo experienced worsening of motor symptoms, while the deterioration in motor symptoms was significantly milder in those receiving vitamin D supplementation.

Ahmad Chitsaz and colleagues [33] found that advanced stages of PD (H&Y stages 4 to 5) were associated with a lower level of 25(OH)D compared to the early stages of the disease (H&Y stages 1 to 1.5), but this difference was not statistically significant.

Several theories can explain the influence of vitamin D deficiency on automatic postural responses. The most common theory for the link between vitamin D deficiency and falls is the associated muscle weakness. It is well recognized that chronic vitamin D deficiency may lead to myopathy. The activation of vitamin D receptors in muscles enhances protein synthesis and muscle cell growth. In vitamin D-deficient individuals, it has been demonstrated that there was significant improvement in muscle power after correction of vitamin D deficiency [34].

In our study, we found a statistically significant positive correlation between serum level of vitamin D and the scores of attention, working memory, immediate recall, delayed recall, naming, visuoperceptual abilities, visuoconstructional abilities, action verbal fluency, alternating verbal fluency, and the total score of PD-CRS.

Similar to our findings, Peterson and colleagues [4] found a significant positive correlation between vitamin D levels and the scores of immediate and delayed recall and the verbal fluency in Parkinson’s disease patients without dementia. In the group of PD with dementia, no statistically significant correlation was reported between the scores of any of the psychometric tests and vitamin D levels.

There are many hypotheses that explain the impact of vitamin D on cognition. The postulated mechanisms include the effect of vitamin D on the CNS through stabilization of mitochondrial function, augmentation of neurotrophic factors, and anti-ischemic and antioxidant effects [35, 36]. Vitamin D also plays a role in the regulation of cholinergic pathways and clearance of the harmful amyloid beta peptides [9, 37]. Furthermore, hypovitaminosis D may increase the risk of diabetes mellitus [38], hypertension [39], and stroke [40]. These conditions are considered precipitating factors for cognitive impairment [41].

The limitation of this work is the relatively small number of patients due to financial issues and limitation of resources.

Further studies with a larger number of patients and for a longer duration to assess the effect of correction of vitamin D deficiency on motor and cognitive symptoms in Parkinson’s disease should be conducted. Further researches should be directed also towards studying the effect of VDR polymorphisms on both motor and cognitive symptoms in PD, evaluating the relationship between serum vitamin D level and psychiatric manifestations in PD and studying the relationship between different Parkinson’s disease medications and serum vitamin D level.

Conclusion

Parkinson’s disease patients have a significantly lower vitamin D level compared to healthy controls, and such vitamin D deficiency significantly affects both motor and cognitive functions.

Abbreviations

6OHDA:

6-Hydroxydopamine

CNS:

Central nervous system

DA:

Dopamine agonist

H&Y:

Hoehn and Yahr

PD:

Parkinson’s disease

PD-CRS:

Parkinson’s Disease - Cognitive Rating Scale

UPDRS:

Unified Parkinson’s Disease Rating Scale

VDR:

Vitamin D receptors

References

  1. 1.

    Tysnes OB, Storstein A. Epidemiology of Parkinson’s disease. J Neural Transm (Vienna). 2017;124(8):901–5.

    Article  Google Scholar 

  2. 2.

    Khedr EM, Fawi G, Abbas MA, Mohammed TA, El-Fetoh NA, Attar GA, Zaki AF. Prevalence of parkinsonism and Parkinson’s disease in Qena governorate/Egypt: a cross-sectional community-based survey. Neurol Res. 2015;37(7):607–18.

    Article  Google Scholar 

  3. 3.

    Rimmelzwaan LM, van Schoor NM, Lips P, Berendse HW, Eekhoff EM. Systematic review of the relationship between vitamin D and Parkinson’s disease. J Park Dis. 2016;6(1):29–37.

    CAS  Google Scholar 

  4. 4.

    Peterson AL, Murchison C, Zabetian C, Leverenz JB, Watson GS, Montine T, Carney N, Bowman GL, Edwards K, Quinn JF. Memory, mood, and vitamin D in persons with Parkinson’s disease. J Park Dis. 2013;3(4):547–55.

    CAS  Article  Google Scholar 

  5. 5.

    Topal K, Paker N, Bugdayci D, Ozer F, Tekdos D. Bone mineral density and vitamin D status with idiopathic Parkinson’s disease. Osteoporos Int. 2010;21:S141–2.

    Google Scholar 

  6. 6.

    Van den Bos F, Speelman A, van Nimwegen M, van der Schouw Y, Backx F, Bloem B, et al. Bone mineral density and vitamin D status in Parkinson’s disease patients. J Neurol. 2013;260:754–60.

    CAS  Article  Google Scholar 

  7. 7.

    Evatt M, Delong M, Khazai N, Rosen A, Triche S, Tangpricha V. Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease. Arch Neurol. 2008;65(10):1348–52.

    Article  Google Scholar 

  8. 8.

    Sleeman I, Aspray T, Lawson R, Coleman S, Duncan G, Khoo TK, Schoenmakers I, Rochester L, Burn D, Yarnall A. The Role of Vitamin D in Disease Progression in Early Parkinson's Disease. J Parkinsons Dis. 2017;7(4):669–75.

    CAS  Article  Google Scholar 

  9. 9.

    Sonnenberg J, Luine V, Krey L, Christakos S. 1,25-Dihydroxyvitamin D3 treatment results in increased choline acetyltransferase activity in specific brain nuclei. Endocrinology. 1986;118:1433–9.

    CAS  Article  Google Scholar 

  10. 10.

    Taniura H, Ito M, Sanada N, Kuramoto N, Ohno Y, Nakamichi N, et al. Chronic vitamin D3 treatment protects against neurotoxicity by glutamate in association with upregulation of vitamin D receptor mRNA expression in cultured rat cortical neurons. J Neurosci Res. 2006;83:1179–89.

    CAS  Article  Google Scholar 

  11. 11.

    Kang H, Schuman EM. Intracellular Ca (2+) signaling is required for neurotrophin-induced potentiation in the adult rat hippocampus. Neurosci Lett. 2000;282:141–4.

    CAS  Article  Google Scholar 

  12. 12.

    Puchacz E, Stumpf WE, Stachowiak EK, Stachowiak MK. Vitamin D increases expression of the tyrosine hydroxylase gene in adrenal medullary cells. Brain Res Mol Brain Res. 1996;36:193–6.

    CAS  Article  Google Scholar 

  13. 13.

    Smith MP, Fletcher-Turner A, Yurek DM, Cass WA. Calcitriol protection against dopamine loss induced by intracerebroventricularadministration of 6-hydroxydopamine. Neurochem Res. 2006;31:533–9.

    CAS  Article  Google Scholar 

  14. 14.

    Cass WA, Smith MP, Peters LE. Calcitriol protects against the dopamine- and serotonin-depleting effects of neurotoxic doses of methamphetamine. Ann N Y Acad Sci. 2006;1074:261–71.

    CAS  Article  Google Scholar 

  15. 15.

    Eyles D, Smith S, Kinobe R, Hewison M, McGrath J. Distribution of the vitamin D receptor and 1 alpha-hydroxylase in human brain. J Chem Neuroanat. 2005;29:21–30.

    CAS  Article  Google Scholar 

  16. 16.

    Evatt M, DeLong M, Kumari M, Auinger P, McDermott M, Tangpricha V. High prevalence of Hypovitaminosis D status in patients with early Parkinson disease. Neurology. 2011;68:314–9.

    Google Scholar 

  17. 17.

    Kim JS, Kim YI, Song C, Yoon I, Park JW, Choi YB, Kim HT, Lee KS. Association of vitamin D receptor gene polymorphism and Parkinson’s disease in Koreans. J Korean Med Sci. 2005;20(3):495–8.

    CAS  Article  Google Scholar 

  18. 18.

    Wang T, Tavera-Mendoza L, Laperriere D, Libby E, MacLeod N, Nagai Y, et al. Large-scale in silico and microarray-based identification of direct 1, 25-dihydroxyvitamin D3 target genes. Mol Endocrinol. 2005;19:2685–95.

    CAS  Article  Google Scholar 

  19. 19.

    Eyles D, Almeras L, Benech P, Patatian A, Mackay-Sim A, McGrath J, et al. Developmental vitamin D deficiency alters the expression of genes encoding mitochondrial, cytoskeletal and synaptic proteins in the adult rat brain. J Steroid Biochem Mol Biol. 2007;103:538.

    CAS  Article  Google Scholar 

  20. 20.

    Newmark H, Newmark J. Vitamin D and Parkinson's disease--a hypothesis. Mov Disord. 2007;22(4):461–8.

    Article  Google Scholar 

  21. 21.

    Sato Y, Honda Y, Iwamoto J, Kanoko T, Satoh K. Abnormal bone and calcium metabolism in immobilized Parkinson’s disease patients. Mov Disord. 2005;20:1598–603.

    Article  Google Scholar 

  22. 22.

    Hughes A, Ben-Shlomo Y, Daniel S, Lees A. What features improve the accuracy of clinical diagnosis in Parkinson’s disease: a clinicopathologic study. Neurology. 1992;42(6):1142–6.

    CAS  Article  Google Scholar 

  23. 23.

    Goetz C, Poewe W, Rascol O, Sampaio C, Stebbins G, Counsell C, et al. Movement Disorder Society Task Force report on the Hoehn and Yahr staging scale: status and recommendations. The Movement Disorder society Task Force on rating scales for Parkinson’s disease. Mov Disord. 2004;19(9):1020–8.

    Article  Google Scholar 

  24. 24.

    Fahn S, Elton R, members of the UPDRS Development Committee. Unified Parkinson’s Disease Rating Scale. In: Fahn S, Marsden C, Calne D, Goldstein M, editors. Recent developments in Parkinson’s disease; 1987. p. 153–63.

    Google Scholar 

  25. 25.

    Pagonabarraga J, Kulisevsky J, Llebaria G, García-Sánchez C, Pascual-Sedano B, Gironell A. Parkinson’s disease-cognitive rating scale: a new cognitive scale specific for Parkinson’s disease. Mov Disord. 2008;23(7):998–1005.

    Article  Google Scholar 

  26. 26.

    Knekt P, Kilkkinen A, Rissanen H, Marniemi J, Saaksjarvi K, Heliovaara M. Serum vitamin D and the risk of Parkinson disease. Arch Neurol. 2010;67(7):808–11.

    Article  Google Scholar 

  27. 27.

    Bischoff-Ferrari H, Giovannucci E, Willett W, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr. 2006;84(1):18–28.

    CAS  Article  Google Scholar 

  28. 28.

    Suzuki M, Yoshioka M, Hashimoto M, Murakami M, Noya M, Takahashi D, et al. Randomized, double-blind, placebo-controlled trial of vitamin D supplementation in Parkinson disease. Am J Clin Nutr. 2013;97:1004–13.

    CAS  Article  Google Scholar 

  29. 29.

    Buell J, Dawson-Hughes B. Vitamin D and neurocognitive dysfunction: preventing “D”ecline? Mol Asp Med. 2008;29(6):415–22.

    CAS  Article  Google Scholar 

  30. 30.

    Fullard M, Xie S, Marek K, Stern M, Jennings D, Siderowf A, et al. Vitamin D in the Parkinson associated risk syndrome (PARS) study. Mov Disord. 2017;2(11):1636–40.

    Article  Google Scholar 

  31. 31.

    Sleeman I, Che Z, Counsell C. Risk of fracture amongst patients with Parkinson’s disease and other forms of parkinsonism. Parkinsonism Relat Disord. 2016;29:60–5.

    Article  Google Scholar 

  32. 32.

    Peterson A, Mancini M, Horak F. The relationship between balance control and vitamin D in Parkinson’s disease-a pilot study. Mov Disord. 2013;28:1133–7.

    Article  Google Scholar 

  33. 33.

    Chitsaz A, Maracy M, Basiri K, Boroujeni MI, Tanhaei AP, et al. 25-Hydroxyvitamin D and severity of Parkinson’s disease. Int J Endocrinol. 2013;689149:4.

    Google Scholar 

  34. 34.

    Pfeifer M, Begerow B, Minne H. Vitamin D and muscle function. Osteoporos Int. 2002;13:187–94.

    CAS  Article  Google Scholar 

  35. 35.

    Chen H, Zhang S, Hernan M, Willett W, Ascherio A. Dietary intakes of fat and risk of Parkinson’s disease. Am J Epidemiol. 2003;157(11):1007–14.

    Article  Google Scholar 

  36. 36.

    Sanchez B, Relova J, Gallego R, Ben-Batalla I, Perez-Fernandez R. 1,25 Dihydroxyvitamin D3 administration to 6-hydroxydopamine-lesioned rats increases glial cell line-derived neurotrophic factor and partially restores tyrosine hydroxylase expression in substantianigra and striatum. J Neurosci Res. 2009;87:723–32.

    CAS  Article  Google Scholar 

  37. 37.

    Masoumi A, Goldenson B, Ghirmai S, Avagyan H, Zaghi J, Abel K, et al. 1alpha, 25- dihydroxyvitamin D3 interacts with curcuminoids to stimulate amyloid-beta clearance by macrophages of Alzheimer’s disease patients. J Alzheimers Dis. 2009;17:703–17.

    CAS  Article  Google Scholar 

  38. 38.

    Mathieu C, Gysemans C, Giulietti A, Bouillon R. Vitamin D and diabetes. Diabetologia. 2005;48(7):1247–57.

    CAS  Article  Google Scholar 

  39. 39.

    Forman J, Bischoff-Ferrari H, Willett W, Stampfer M, Curhan G. Vitamin D intake and risk of incident hypertension: results from three large prospective cohort studies. Hypertension. 2005;46(4):676–82.

    CAS  Article  Google Scholar 

  40. 40.

    Poole K, Loveridge N, Barker P. Reduced vitamin D in acute stroke. Stroke. 2006;37(1):243–5.

    CAS  Article  Google Scholar 

  41. 41.

    Hendrie HC, Albert MS, Butters MA. The NIH cognitive and emotional health project: report of the critical evaluation study committee. Alzheimers Dement. 2006;2:1):12–32.

    Article  Google Scholar 

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Acknowledgements

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Funding

Authors did not receive any funding for this work.

Availability of data and materials

The datasets used and/ or analyzed during the current study are available from the corresponding author on reasonable request with permission from the Faculty of Medicine, Beni-Suef University, Egypt.

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  1. Neurology Department, Beni-Suef University, Beni Suef, 62511, Egypt

    Rasha H. Soliman, Mohammed I. Oraby, Mona Hussein & Sara Mostafa

  2. Clinical and Chemical Pathology Department, Beni-Suef University, Beni Suef, Egypt

    Sanaa Abd El-Shafy

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  1. Rasha H. Soliman
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  2. Mohammed I. Oraby
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Contributions

RHS participated in the study design and sequence alignment and helped to draft the manuscript. SAE participated in the study design, performed the laboratory work, and helped to draft the manuscript. MIO participated in the study design and sequence alignment and helped to draft the manuscript. MH participated in the study design and collection and analysis of data and helped to draft the manuscript. SM participated in the sequence alignment, collection of data, and data analysis and helped to draft the manuscript. All authors read and approved the final manuscript.

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Correspondence to Mona Hussein.

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A written informed consent was obtained from each participant in this study or from one of his family members, and the study was approved by the local ethics committee in the Faculty of Medicine, Beni-Suef University (the number is FWA00015574, and the date is ninth of October 2018).

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Soliman, R.H., Oraby, M.I., Hussein, M. et al. Could vitamin D deficiency have an impact on motor and cognitive function in Parkinson’s disease?. Egypt J Neurol Psychiatry Neurosurg 55, 34 (2019). https://doi.org/10.1186/s41983-019-0084-9

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Keywords

  • Parkinson’s disease
  • Vitamin D
  • PD-CRS
  • UPDRS
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