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Peripheral inflammation is presumed to be one of the causes of Parkinson's disease (PD), especially when it exists in the gastrointestinal tract.
Currently, many types of TNF inhibitors have been approved for the treatment of systemic inflammatory diseases, including inflammatory bowel disease (IBD).
Mendelian randomization is a valuable method to help answer questions in drug epidemiology.
Due to the principle of Mendelian randomization, the association between this genetic variation and disease is not expected to produce confounding or reverse causality, thus facilitating causal inference.
prevention
In order to evaluate the effect of long-term tumor necrosis factor (TNF) inhibition on Parkinson's disease (PD) risk and age of onset, they conducted a 2-sample Mendelian randomized study using genome-wide association studies ( GWAS ) summary statistics.
GWAS
The genetic association with lower circulating C-reactive protein (CRP; GWAS n = 204,402) has determined the genetic variation near the gene encoding TNF receptor 1 (TNFR1) (TNFRSF1A), predicting that anti-TNF therapy drugs block TNFR1 signaling Sex.
They used International Parkinson's Disease Genomics Consortium and 23andMe's GWAS data to estimate the impact of TNF-TNFR1 inhibition on PD risk (ncases/controls = 37,688/981,372) and age of PD onset (n = 28,568).
medsci.
TNF-TNFR1 signal inhibition is not expected to affect the risk of PD or the age of onset.
The findings are consistent in different models using different genetic tools and Mendelian randomization estimators.
Original source:
https://n.
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