scholarly journals Characterization of Gastrointestinal Symptom Type and Severity in Parkinson's Disease: A Case–Control Study in an Australian Cohort

Author(s):  
Jade E. Kenna ◽  
Megan C. Bakeberg ◽  
Anastazja M. Gorecki ◽  
Alfred Chin Yen Tay ◽  
Samantha Winter ◽  
...  
Author(s):  
Hamdy N. El-Tallawy ◽  
Tahia H. Saleem ◽  
Wafaa M. Farghaly ◽  
Heba Mohamed Saad Eldien ◽  
Ashraf Khodaery ◽  
...  

Abstract Background Parkinson’s disease is one of the neurodegenerative disorders that is caused by genetic and environmental factors or interaction between them. Solute carrier family 41 member 1 within the PARK16 locus has been reported to be associated with Parkinson’s disease. Cognitive impairment is one of the non-motor symptoms that is considered a challenge in Parkinson’s disease patients. This study aimed to investigate the association of rs11240569 polymorphism; a synonymous coding variant in SLC41A1 in Parkinson’s disease patients in addition to the assessment of cognitive impairment in those patients. Results In a case -control study, rs11240569 single nucleotide polymorphisms in SLC41A1, genes were genotyped in 48 Parkinson’s disease patients and 48 controls. Motor and non-motor performance in Parkinson's disease patients were assessed by using the Movement Disorder Society-Sponsored Revision of the Unified Parkinson’s Disease Rating Scale (MDS-UPDRS). The genotype and allele frequencies were compared between the two groups and revealed no significant differences between case and control groups for rs11240569 in SLC41A1 gene with P value .523 and .54, respectively. Cognition was evaluated and showed the mean ± standard deviation (SD) of WAIS score of PD patients 80.4 ± 9.13 and the range was from 61 to 105, in addition to MMSE that showed mean ± SD 21.96 ± 3.8. Conclusion Genetic testing of the present study showed that rs11240569 polymorphism of SLC41A1 gene has no significant differences in distributions of alleles and genotypes between cases and control group, in addition to cognitive impairment that is present in a large proportion of PD patients and in addition to the strong correlation between cognitive impairment and motor and non-motor symptoms progression.


2020 ◽  
Vol 79 ◽  
pp. e38
Author(s):  
C.A. Soto-Rincón ◽  
S.A. Castillo Torres ◽  
D.G. Marítnez-Roque ◽  
J. Duarte-Bravo ◽  
S. España-Pérez ◽  
...  

2010 ◽  
Vol 25 (15) ◽  
pp. 2587-2594 ◽  
Author(s):  
Michael Y. Shino ◽  
Valerie McGuire ◽  
Stephen K. Van Den Eeden ◽  
Caroline M. Tanner ◽  
Rita Popat ◽  
...  

2004 ◽  
Vol 19 (7) ◽  
pp. 807-811 ◽  
Author(s):  
Marco D'Amelio ◽  
Paolo Ragonese ◽  
Letterio Morgante ◽  
Antonio Epifanio ◽  
Graziella Callari ◽  
...  

2013 ◽  
Vol 333 ◽  
pp. e612
Author(s):  
L. Sellitti ◽  
M. Bigoni ◽  
L. Priano ◽  
G. Albani ◽  
R. Picconi ◽  
...  

2010 ◽  
Vol 104 (5) ◽  
pp. 757-764 ◽  
Author(s):  
Kentaro Murakami ◽  
Yoshihiro Miyake ◽  
Satoshi Sasaki ◽  
Keiko Tanaka ◽  
Wakaba Fukushima ◽  
...  

Increased homocysteine levels might accelerate dopaminergic cell death in Parkinson's disease (PD) through neurotoxic effects; thus, increasing intake of B vitamins involved in the regulation of homocysteine metabolism might decrease the risk of PD through decreasing plasma homocysteine. However, epidemiological evidence for the association of dietary B vitamins with PD is sparse, particularly in non-Western populations. We conducted a hospital-based case–control study in Japan to examine associations between dietary intake of folate, vitamin B6, vitamin B12 and riboflavin and the risk of PD. Patients with PD diagnosed using the UK PD Society Brain Bank criteria (n 249) and controls without neurodegenerative diseases (n 368) were recruited. Dietary intake during the preceding month was assessed at the time of study recruitment using a validated, self-administered, semi-quantitative, comprehensive diet history questionnaire. After adjustment for potential dietary and non-dietary confounding factors, intake of folate, vitamin B12 and riboflavin was not associated with the risk of PD (P for trend = 0·87, 0·70 and 0·11, respectively). However, low intake of vitamin B6 was associated with an increased risk of PD, independent of potential dietary and non-dietary confounders. Multivariate OR (95 % CI) for PD in the first, second, third and fourth quartiles of vitamin B6 were 1 (reference), 0·56 (0·33, 0·94), 0·69 (0·38, 1·25) and 0·48 (0·23, 0·99), respectively (P for trend = 0·10). In conclusion, in the present case–control study in Japan, low intake of vitamin B6, but not of folate, vitamin B12 or riboflavin, was independently associated with an increased risk of PD.


2020 ◽  
Author(s):  
ming xia ◽  
wenjuan Xiu ◽  
Xuliang Wang ◽  
Tingting Wu ◽  
Yingying Zheng ◽  
...  

Abstract Background: Previous cross-sectional studies have shown that Parkinson’s disease (PD) patients have lower serum 25- hydroxy vitamin D (25(OH)D) concentrations than controls. whether the research in other regions findings are generalizable to China populations remains untested in other studies. In this case-control study we examined the Correlation between 25-hydroxy-vitamin D and Parkinson's disease.Methods:We establish an association between deficiency of 25-hydroxy-vitamin D and PD in a case-control study of 100 PD patients and 100 control subjects free of neurologic disease in the First Affliated Hospital of Xinjiang Medical University.Results:Total 25-hydroxy-vitamin D levels, were deficient in 21% of patients with PD compared with 4% of controls. In univariate analyses Plasma levels of 25-hydroxy-vitamin D were associated with PD(p<0.001), respectively. In multivariate analyses, Vitamin D deficiency(25(OH)D <20 ng/mL) were significant associated with PD (p=0.008,OR=17.13,95% CI, 2.082-141.075). Individuals with levels in the lowest quartile of 25(OH)D values had the highest prevalence of PD(p =0.026,OR=11.786,95%CI,1.342-103.51)compared with individuals with values in the highest quartile.Conclusions:Our study reveals an association between 25-hydroxy-vitamin D and PD.Patients with incident PD had significantly lower serum 25(OH)D concentrations than age-matched controls, High-risk PD patients with vitamin D deficiency who have not yet developed exercise impairment, these populations should undergo vitamin D measurement and vitamin D treatment as soon as possible.


PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0130970 ◽  
Author(s):  
Xinglong Yang ◽  
Jing Xi ◽  
Quanzhen Zhao ◽  
Hua Jia ◽  
Ran An ◽  
...  

2006 ◽  
Vol 21 (10) ◽  
pp. 1688-1692 ◽  
Author(s):  
Roberta Frigerio ◽  
Kevin R. Sanft ◽  
Brandon R. Grossardt ◽  
Brett J. Peterson ◽  
Alexis Elbaz ◽  
...  

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