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SO069

Circadian activity rhythms and proteomic pathways mediate the association between depression and Parkinson’s disease: evidence from large-scale cohort analyses

CIRCADIAN–ACTIVITY RHYTHM AND PROTEOMIC PATHWAYS MEDIATE THE ASSOCIATION BETWEEN DEPRESSION AND PARKINSON’S DISEASE: EVIDENCE FROM LARGE-SCALE COHORT ANALYSES

Late-onset depression increases the risk of Parkinson’s disease approximately 2.6-fold, with sleep–activity rhythm measures accounting for the largest mediation effects in this association.

The study aimed to investigate the association between late-onset depression (LOD) and incident Parkinson’s disease (PD), along with the proteomic mechanisms underlying this association. The population-based cohort analysis included 484,590 UK Biobank participants after excluding those with a PD diagnosis preceding LOD, other relevant psychiatric conditions, or missing covariate data; restricted cubic splines and multivariable Cox proportional hazards models were used. In a proteomic subgroup of 52,878 individuals in whom 2,920 plasma proteins were measured, differential expression analysis, principal component analysis (PCA), orthogonal partial least squares discriminant analysis (OPLS-DA), mediation analysis, functional enrichment analysis, and machine learning methods were applied. In addition, a LASSO-Cox risk model was developed in 81,806 participants, including 3,456 with LOD, and validation was performed in 6,352 NHANES participants, 79 of whom had PD. After multivariable adjustment, LOD was significantly associated with incident PD risk (hazard ratio [HR] = 2.59; 95% confidence interval [CI]: 2.12 to 3.16; HR in the basic model = 2.45; 95% CI: 2.01 to 2.99); the association between depressive symptoms and PD was also confirmed in NHANES (adjusted HR = 3.36; 95% CI: 1.62 to 6.97). Proteomic mediation analysis identified 87 potential mediator proteins enriched in cytokine–cytokine receptor interaction, leukocyte transendothelial migration, and cell adhesion pathways; however, sleep–activity rhythm measures accounted for the highest proportions mediated: activity levels during the most active 10-hour period (M10), 15.6%; average daily acceleration, 12.3%; relative amplitude, 7.6%; and the cosinor midline level, 7.6%. The contribution of traditional inflammatory markers was relatively small. Participants classified as high-risk based on the LASSO-Cox score had a higher hazard of PD than those classified as low-risk, both in the overall sample (HR = 6.26; 95% CI: 5.12 to 7.66) and in the LOD subgroup (HR = 5.18; 95% CI: 3.02 to 8.89); the abstract reported that the time-dependent area under the curve (AUC) reached 0.825. The authors emphasize that sleep–activity rhythm characteristics may be modifiable targets, but that interventional studies and independent validation of the risk model are needed before clinical implementation.

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