Background
Although depression is very common in patients with Parkinson disease (PD), only a few studies have investigated the longitudinal effects of initial depression on cognitive decline in these patients. The purpose of this study was to investigate the effect of depression on cognitive functions in patients with PD.
Methods
We used data from the Parkinson Progression Markers Initiative (PPMI) to investigate the relationship between depression and PD. Depressive symptoms were measured in patients with PD based on the Geriatric Depression Scale (GDS) or Neuropsychiatric Inventory‐Questionnaire (NPI‐Q) scores obtained at baseline. We evaluated cognitive decline as whether a patient with PD progressed to PD with mild cognitive impairment (MCI) during a 4‐year follow‐up period. Multivariate Cox regression analysis was done to know whether depression can predict the conversion to MCI. In addition, a voxel‐based morphometric analysis using volumetric brain magnetic resonance imaging was used to compare structural changes related to future cognitive decline as well as to reveal longitudinal effect of baseline depression on cortical atrophy.
Results
Data from 263 patients with cognitively normal de novo PD who were available for longitudinal cognitive testing were analysed. The multivariate Cox regression analysis revealed that the depressive symptoms were independent risk factors for conversion to MCI in patients with de novo PD after adjusting for covariates (hazards ratio (95% CI)) of depression defined by the GDS (1.753 (1.084–2.835)) and the NPI (1.815 (1.083–3.042)) scores, respectively. The significant structural changes in PD with MCI as well as longitudinal effect of baseline depression on subsequent cortical atrophy were found in multiple areas on the voxel‐based morphometric analysis (P < 0.001, family‐wise error rate corrected).
Conclusions
Our study indicates that the presence of depressive symptoms in patients with early PD is associated with a higher risk of progression to MCI and early depression may reflect subsequent cortical atrophy.