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Study Identifies 19 Genes Linked to Parkinson’s – Offers New Insights for Treatment Targets

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A new study has shed light on the complex genetic interplay contributing to both Parkinson’s disease (PD) and its accompanying non-motor symptoms, potentially paving the way for more targeted treatments.

Researchers have identified specific genes whose altered expression in the brain cortex is causally linked to Parkinson’s.

This comprehensive study, published in npj Parkinson’s Disease, utilised a disease-agnostic brain cortex gene regulatory network, integrated with Mendelian randomisation analyses, to pinpoint 19 genes causally related to PD.

Parkinson’s disease, known for its motor symptoms like tremors and stiffness, also involves various non-motor symptoms, including cognitive and psychiatric issues. This heterogeneity in symptoms, often challenging to manage clinically, is likely due to complex interactions between genetic, epigenetic, and environmental factors. The study’s use of a Brain Cortex Gene Regulatory Network (BC-GRN) and Mendelian randomisation (MR) is pivotal in uncovering these complexities.

Of the 19 genes identified, alterations in the expression of nine increase and ten decrease the odds ratio (OR) for Parkinson’s. Notably, increased expression of ARHGAP27 and RNF40 in the brain cortex was associated with a decreased OR of PD, suggesting a protective effect. In contrast, down-regulation of genes like FAM200B, GPNMB, and NUPL2 was linked to increased Parkinson’s risk.

The study’s focus extended to traits co-occurring with Parkinson’s. By employing extended protein interaction networks derived from PD-risk genes and PD-associated SNPs, the research identified shared biological pathways and phenotypes connecting PD with established non-motor symptoms. This understanding could lead to novel therapeutic strategies targeting untreated non-motor conditions associated with PD.

A key finding is the identification of regulatory loci within the 17q21.31 region, known for its importance in cognitive and mood-related traits. These loci predominantly regulate gene expression in this region, contributing to the relative risk of non-motor mood-related traits in PD. The results suggest that genetic variants in 17q21.31 might be instrumental in understanding the co-occurrence of PD and certain psychiatric or mood disorders.

These findings hold immense promise for developing therapies targeting subsets of largely untreated non-motor conditions associated with Parkinson’s. The study emphasises the need for clinical trials that include genetic stratification to confirm these findings and target non-motor symptoms of PD effectively, particularly in the prodromal phase.

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