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Depressive symptoms precede cognitive impairment in de novo Parkinson's disease patients: Analysis of the PPMI cohort.

ABSTRACT: INTRODUCTION:Nonmotor symptoms, including depression, anxiety, apathy, and cognitive dysfunction, are common in Parkinson's disease (PD). Although a link between mood symptoms and cognitive impairment in PD has been theorized vis-à-vis striatal dopamine depletion, studies have been inconsistent regarding the relationship between mood symptoms and cognitive function. Inconsistencies may reflect the cross-sectional nature of previous studies. The current study examined the bidirectional longitudinal relationship between mood and cognition. METHOD:Data were obtained from 310 individuals newly diagnosed with PD, who were followed up to 4 years (baseline, 1st, 2nd, 3rd, and 4th annual follow-ups). Apathy, anxiety, depressive symptoms, motor severity, and neurocognitive functioning were assessed at each annual assessment. The longitudinal relationship between apathy, anxiety, depressive symptoms, and cognition was analyzed with multilevel models. RESULTS:Over the 4-year period, more severe depressive symptoms were related to worse performance on tasks of processing speed, verbal learning, and verbal delayed recall. Additionally, there was a significant Depression × Time interaction, suggesting that individuals with more severe depressive symptoms experience more rapid declines in global cognitive functioning and verbal learning. Apathy and anxiety were not significantly related to performance in any cognitive test. Lagged models revealed that changes in depression precede declines in working memory, verbal learning, delayed verbal recall, and global cognition. CONCLUSION:Findings suggest depressive symptoms may be a harbinger for future cognitive decline among individuals with PD. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

SUBMITTER: Jones JD

PROVIDER: S-EPMC6823115 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature

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Depressive symptoms precede cognitive impairment in de novo Parkinson's disease patients: Analysis of the PPMI cohort.

Jones Jacob D JD Kurniadi Natalie E NE Kuhn Taylor P TP Szymkowicz Sarah M SM Bunch Joseph J Rahmani Elizabeth E

Neuropsychology 20190725 8

<h4>Introduction</h4>Nonmotor symptoms, including depression, anxiety, apathy, and cognitive dysfunction, are common in Parkinson's disease (PD). Although a link between mood symptoms and cognitive impairment in PD has been theorized vis-à-vis striatal dopamine depletion, studies have been inconsistent regarding the relationship between mood symptoms and cognitive function. Inconsistencies may reflect the cross-sectional nature of previous studies. The current study examined the bidirectional lo ...[more]

PMID: 31343240

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Project description:BackgroundAltered cholinergic innervation plays a putative role in cognitive impairment in Parkinson's disease (PD) at least in advanced stages. Identification of the relationship between cognitive impairment and cholinergic innervation early in the disease will provide better insight into disease prognosis and possible early intervention.ObjectiveThe aim was to assess regional cholinergic innervation status in de novo patients with PD, with and without cognitive impairment.MethodsFifty-seven newly diagnosed, treatment-naive, PD patients (32 men, mean age 64.6 ± 8.2 years) and 10 healthy controls (5 men, mean age 54.6 ± 6.0 years) were included. All participants underwent cholinergic [18 F]fluoroethoxybenzovesamicol positron emission tomography and detailed neuropsychological assessment. PD patients were classified as either cognitively normal (PD-NC) or mild cognitive impairment (PD-MCI). Whole brain voxel-based group comparisons were performed.ResultsResults show bidirectional cholinergic innervation changes in PD. Both PD-NC and PD-MCI groups showed significant cortical cholinergic denervation compared to controls (P < 0.05, false discovery rate corrected), primarily in the posterior cortical regions. Higher-than-normal binding was most prominent in PD-NC in both cortical and subcortical regions, including the cerebellum, cingulate cortex, putamen, gyrus rectus, hippocampus, and amygdala.ConclusionAltered cholinergic innervation is already present in de novo patients with PD. Posterior cortical cholinergic losses were present in all patients independent of cognitive status. Higher-than-normal binding in cerebellar, frontal, and subcortical regions in cognitively intact patients may reflect compensatory cholinergic upregulation in early-stage PD. Limited or failing cholinergic upregulation may play an important role in early, clinically evident cognitive impairment in PD. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Project description:IntroductionParkinson's disease (PD) is a neurodegenerative disorder that commonly results in cognitive impairments and dementia. Intraindividual variability of neuropsychological performance is a sensitive marker of cognitive decline in other neurologic populations. However, studies have not examined the longitudinal utility of intraindividual variability in predicting future cognitive impairments among individuals with PD. In the current study, we hypothesized that increased intraindividual variability would predict future cognitive decline independent of traditional neuropsychological markers of cognitive impairment.MethodsThe sample included 423 newly diagnosed PD patients and 175 healthy controls, who were followed up to 5 years (baseline, first, second, third, fourth, and fifth annual follow-up). Participants underwent tests of learning, memory, processing speed, attention, verbal fluency, and visuospatial functioning. Cognitive status (cognitive intact, mild cognitive impairment, and dementia) was classified based on previously established criteria. Multilevel models were computed to examine the longitudinal relationship between intraindividual variability, cognitive status, and general cognitive functioning.ResultsAnalyses revealed that increased intraindividual variability was predictive of incident cognitive decline among individuals with PD. Specifically, greater dispersion in neuropsychological performance was associated with greater risk of transitioning from cognitively intact to mild cognitive impairment or transitioning from mild cognitive impairment to dementia. Additional analyses revealed a significant Intraindividual Variability × Group (PD or control) interaction, meaning that intraindividual variability was predictive of declines in cognitive functioning among PD participants only but not healthy controls.ConclusionIntraindividual variability may be a harbinger for future cognitive decline among individuals with PD. (PsycINFO Database Record (c) 2020 APA, all rights reserved).

Project description:The accumulation of beta amyloid in the brain has a complex and poorly understood impact on the progression of Parkinson's disease pathology and much controversy remains regarding its role, specifically in cognitive decline symptoms. Some studies have found increased beta amyloid burden is associated with worsening cognitive impairment in Parkinson's disease, especially in cases where dementia occurs, while other studies failed to replicate this finding. To better understand this relationship, we examined a cohort of 25 idiopathic Parkinson's disease patients and 30 healthy controls from the Parkinson's Progression Marker Initiative database. These participants underwent [18F]Florbetaben positron emission tomography scans to quantify beta amyloid deposition in 20 cortical regions. We then analyzed this beta amyloid data alongside the longitudinal Montreal Cognitive Assessment scores across 3 years to see how participant's baseline beta amyloid levels affected their cognitive scores prospectively. The first analysis we performed with these data was a hierarchical cluster analysis to help identify brain regions that shared similarity. We found that beta amyloid clusters differently in Parkinson's disease patients compared to healthy controls. In the Parkinson's disease group, increased beta amyloid burden in cluster 2 was associated with worse cognitive ability, compared to deposition in clusters 1 or 3. We also performed a stepwise linear regression where we found an adjusted R2 of 0.495 (49.5%) in a model explaining the Parkinson's disease group's Montreal Cognitive Assessment score 1-year post-scan, encompassing the left gyrus rectus, the left anterior cingulate cortex, and the right parietal cortex. Taken together, these results suggest regional beta amyloid deposition alone has a moderate effect on predicting future cognitive decline in Parkinson's disease patients. The patchwork effect of beta amyloid deposition on cognitive ability may be part of what separates cognitive impairment from cognitive sparing in Parkinson's disease. Thus, we suggest it would be more useful to measure beta amyloid burden in specific brain regions rather than using a whole-brain global beta amyloid composite score and use this information as a tool for determining which Parkinson's disease patients are most at risk for future cognitive decline.

Dataset Information

Depressive symptoms precede cognitive impairment in de novo Parkinson's disease patients: Analysis of the PPMI cohort.

Publications

Depressive symptoms precede cognitive impairment in de novo Parkinson's disease patients: Analysis of the PPMI cohort.

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