scholarly journals A Case-Control Association Study of RANTES (-28C>G) Polymorphism as a Risk Factor for Parkinson’s Disease in Isparta, Turkey

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Nilufer Sahin-Calapoglu ◽  
Serpil Demirci ◽  
Mustafa Calapoglu ◽  
Baris Yasar
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Association Study ◽  
Chemokine Receptors ◽  
Case Control ◽  
Pcr Rflp ◽  
Genes Encoding ◽  
Inflammatory Processes ◽  
Control Association

Background. Recent studies have revealed that inflammatory processes are involved in the pathogenesis of Parkinson’s disease (PD). Multiple lines of evidence have suggested that chemokines and their receptors are involved in several neurodegenerative disorders. We have examined whether genetic polymorphisms at the genes encoding chemokines IL-8 (-251A>T), MCP-1 (-2518A/G), and RANTES (-28C>G) and chemokine receptors CCR2 (V64I) and CCR5 (-Δ32) were associated with sporadic PD risk in Isparta, Turkey. Method. The pilot case-control association study included 30 PD patients and 60 control subjects, who were all genotyped with PCR-RFLP for the five polymorphisms. Their genotype and haplotype frequencies were compared statistically. Results. One SNP (-28C>G) in RANTES revealed a significant association with PD (P (allele) < 0.0001, p-trend = 0.0007). The risk allele (G) in the homozygous and dominant models (OR = 17.29 and 32.10, 95% CI = 0.86–347.24 and 1.74–591.937, resp.) suggests additional PD risk. The haplotype TGCAN from the IL-8 (-251A>T), MCP-1 (-2518A>G), RANTES (-28C>G), CCR-2 (V64I), and CCR-5 (-Δ32) has protective effect (OR = 0.08 [CI = 0.01–0.63], p=0.019). Conclusions. Our data are the first indication of the role of RANTES (-28C>G) in PD risk.

scholarly journals LRRK2 is not a Significant Cause of Parkinson's Disease in French-Canadians

2007 ◽  
Vol 34 (3) ◽  
pp. 333-335 ◽  
Author(s):  
Nicolas Dupré ◽  
Jean-Baptiste Rivière ◽  
Richard H. Myers ◽  
Pierre Provencher ◽  
Emmanuelle Pourcher ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Association Study ◽  
Case Control ◽  
Quebec City ◽  
Sequencing Analysis ◽  
Founder Population ◽  
French Canadian ◽  
Single Marker ◽  
Control Association

Background:An old founder mutation (G2019S) was found with high frequency in the North African Arabs (30%) and Ashkenazi Jews (18%).Objective:Demonstrate if mutations in the LRRK2 gene are a significant cause of Parkinson's disease (PD) in the French-Canadian founder population.Methods:Cases were recruited through a designated movement disorder clinic in Quebec City. Every index case had to meet the Ward and Gibb criteria for PD. Controls consisted of a non-disease group of similar age and ethnicity as the cases. Exons 31 and 41 of LRRK2 were amplified by PCR with intronic primers in all 125 PD cases and directly sequenced on an ABI 3700 sequencer. Six single nucleotide polymorphism were typed in 125 PD cases and 95 normal controls. Associations between unrelated cases and matched controls were analyzed. Single marker analysis and haplotype association tests were performed.Results:Sequencing analysis did not reveal any reported or novel mutations in exons 31 and 41 of LRRK2. The G2019S mutation as well as mutations affecting amino acid 1441 were absent in the 125 patients. The case-control association study performed to detect the presence of a common variant in LRRK2 did not provide any positive signal. Single-marker and haplotype analyses systematically gave non-significant P values.Conclusions:We performed a case-control association study in 125 French-Canadian (FC) patients with PD and 95 FC controls and found that common variants in LRRK2 are unlikely to be a significant cause of late-onset PD in this founder population.

Role of serotonergic-related systems in suicidal behavior: Data from a case–control association study

2011 ◽  
Vol 35 (6) ◽  
pp. 1518-1524 ◽  
Author(s):  
Pilar A. Saiz ◽  
Paz García-Portilla ◽  
Begoña Paredes ◽  
Paul Corcoran ◽  
Celso Arango ◽  
...  
Keyword(s):  
Association Study ◽  
Suicidal Behavior ◽  
Case Control ◽  
Control Association

scholarly journals Role of DJ-1 and Apo A1 as biomarkers in Parkinson’s disease: an observational case-control study

2019 ◽  
Vol 2 (3) ◽  
pp. 109
Author(s):  
Sahil Mehta ◽  
Ritu Shree ◽  
Missamma Mulagala ◽  
Apurva Sood ◽  
Manish Modi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Case Control Study ◽  
Case Control ◽  
Control Study

A case-control association of RANTES (-28C >G) and CCR5-Delta32 polymorphisms with Parkinson’s disease in Indians

2020 ◽  
Vol 739 ◽  
pp. 135404
Author(s):  
Narayani Subramanian ◽  
Srishti Ramanathan ◽  
Solomon Franklin Durairaj Paul ◽  
Vettriselvi Venkatesan ◽  
Teena Koshy
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Case Control ◽  
Control Association

scholarly journals Kinin Peptides Enhance Inflammatory and Oxidative Responses Promoting Apoptosis in a Parkinson’s Disease Cellular Model

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Anna Niewiarowska-Sendo ◽  
Andrzej Kozik ◽  
Ibeth Guevara-Lora
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Receptor Expression ◽  
Cellular Model ◽  
Enhanced Production ◽  
Kinin Receptors ◽  
Kinin Receptor ◽  
Inflammatory Processes

Kinin peptides ubiquitously occur in nervous tissue and participate in inflammatory processes associated with distinct neurological disorders. These substances have also been demonstrated to promote the oxidative stress. On the other hand, the importance of oxidative stress and inflammation has been emphasized in disorders that involve the neurodegenerative processes such as Parkinson’s disease (PD). A growing number of reports have demonstrated the increased expression of kinin receptors in neurodegenerative diseases. In this study, the effect of bradykinin and des-Arg10-kallidin, two representative kinin peptides, was analyzed with respect to inflammatory response and induction of oxidative stress in a PD cellular model, obtained after stimulation of differentiated SK-N-SH cells with a neurotoxin, 1-methyl-4-phenylpyridinium. Kinin peptides caused an increased cytokine release and enhanced production of reactive oxygen species and NO by cells. These changes were accompanied by a loss of cell viability and a greater activation of caspases involved in apoptosis progression. Moreover, the neurotoxin and kinin peptides altered the dopamine receptor 2 expression. Kinin receptor expression was also changed by the neurotoxin. These results suggest a mediatory role of kinin peptides in the development of neurodegeneration and may offer new possibilities for its regulation by using specific antagonists of kinin receptors.

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