In conclusion, CAPE showed a protective effect on PON1 activity and levels of lipid profile, TSA, TAC and TOC in plasma and brain tissue and prevented the neurodegenerations in brain tissue in CPF-induced Parkinson's disease.
Exposure to pesticides increased the risk of alterations in different PD pathogenesis-related genes, such as GST (OR 1.97, 95% CI [1.41, 2.76]), PON-1 (OR 1.32, 95% CI [1.09, 1.6]), MDR1 (OR 2.06, 95% CI [1.58, 2.68]), and SNCA genes (OR 1.28, 95% CI [1.02, 1.37]).
To investigate whether ambient agricultural OP exposure and PON1L55M influence the rate of motor, cognitive, and mood-related symptom progression in PD.
The higher levels of PON2 in females may explain the lower frequency of neurological and cardiovascular diseases in females and the ability to identify males but not females with Parkinson's disease using a special PON1 status assay.
However, many studies suggest that the MM55 PON1 genotype is associated with a higher risk for Parkinson's disease in individuals exposed to organophosphates.
We performed a meta-analysis pooling data from all relevant studies in order to determine the effects of two PON 1 polymorphisms (L55M and Q192R) on Parkinson's disease.
Our results suggest that either these functional PON1 polymorphisms are not associated with AD and PD spectrum disorders, or that the relative risk conferred is small.
In this minireview we summarize the involvement of PON1 genotypes in the occurrence of Parkinson's disease, Alzheimer's disease and amyotrophic lateral sclerosis.
Carriers of the variant MM PON1-55 genotype exposed to organophosphates exhibited a greater than 2-fold increase in Parkinson disease risk compared with persons who had the wildtype or heterozygous genotype and no exposure (for diazinon, odds ratio = 2.2 [95% confidence interval = 1.1-4.5]; for chlorpyrifos, 2.6 [1.3-5.4]).
Our findings suggest that inherited interactive weakness of AChE and PON1 expression increases the insecticide-induced occurrence of Parkinson's disease.
Our findings suggest that inherited interactive weakness of AChE and PON1 expression increases the insecticide-induced occurrence of Parkinson's disease.
We performed a case--control association study in order to elucidate the possible contribution of variability within PON1 to the risk of sporadic PD in a Finnish population.
Therefore, the pooled results of the meta-analysis supported that there was an association between PON1-55M/L polymorphism and PD and that PON1-192Q/R polymorphism was unlikely to be a major risk factor for susceptibility to PD.
We have showed the frequency of the Met 54 allele of PON1 to be significantly increased in patients with PD compared with the controls (chi(2)=8.63, df=1, P<0.003).
We investigated the Gln --> Arg 191 polymorphism in paraoxonase (PON1) in St. Petersburg population, in three clinically differentiated groups of patients with Parkinson's disease (PD) and in the symptomatic tremor group.
Our data suggest that environmental neurotoxins metabolized by PON1 might be responsible for neurodegeneration with aging and that the B (Arg) allele form might have genetic susceptibility to PD.