Physical inactivity links depressive symptoms and cognitive functioning among individuals with Parkinson's disease.

OBJECTIVE: Parkinson's disease (PD) is a neurodegenerative disorder caused by disruption of dopamine-producing cells. PD is associated with motor symptoms and nonmotor symptoms including depression and cognitive impairment. Past research suggests an association between depression and cognitive impairment in PD. Physical activity may have a therapeutic effect on both depression and cognitive impairment. The present study investigates if physical activity mediates the association between depressive symptoms and cognition in a longitudinal sample of individuals with PD. METHOD: Participants include individuals newly diagnosed with PD (N = 487) enrolled in the Parkinson's Progression Marker Initiative (PPMI). Participants completed an array of neuropsychological tests over the course of 5 years, as well as questionnaires of depression and physical activity. Between-person and within-person effects of depression and cognition mediated through physical activity were analyzed using structural equation modeling. RESULTS: A significant direct effect demonstrated depression was associated with worse global cognitive functioning. Furthermore, there was a significant indirect within-person effect, indicating that physical activity fully mediated the association between depression and cognition. Individuals who became more depressed over time became less physically active and subsequently experienced cognitive decline over the 5-year period. CONCLUSIONS: Findings have implications for prognostic detection and/or the role of physical activity interventions to buffer effects of depression on cognitive impairment among individuals diagnosed with PD. Physical interventions may potentially be implemented among depressed persons to preserve cognitive functioning. Worsened depression early during PD may be a risk factor for inactivity and cognitive diminishment. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Gastrointestinal symptoms are predictive of trajectories of cognitive functioning in de novo Parkinson's disease.

INTRODUCTION: Non-motor symptoms such as cognitive and gastrointestinal (GI) symptoms are common in Parkinson's disease (PD). In PD, GI-symptoms often present prior to motor symptoms. It is hypothesized that GI-symptoms reflect disruptions of the microbiome-gut-brain axis, which leads to altered immune functioning, chronic neuroinflammation, and subsequent neurodegeneration. Initial evidence links gut-dysbiosis to PD pathology and motor symptom severity. The present study examines the longitudinal relationship between severity of GI-symptoms and cognitive impairment in newly diagnosed PD patients. METHODS: A secondary data analysis of the Parkinson's Progression Markers Initiative (PPMI) included 423 newly diagnosed PD patients who were followed for up to 5 years. Participants underwent neuropsychological tests of processing speed, attention, visuospatial functioning, verbal learning and verbal delayed recall. Participant were classified as cognitive intact, mild cognitive impairment or Parkinson's disease dementia. Frequency of GI-symptoms were assessed with the Scales for Outcomes in Parkinson's Disease Autonomic (SCOPA-AUT). Multi-level models (MLM) examined the longitudinal relationship between GI symptoms and cognitive impairment. RESULTS: All cognitive outcomes were predicted by the main effect of GI symptoms, or the GI-symptom X Occasion interaction term. Specifically, more severe GI-symptoms were predictive of a less favorable trajectory of performance on tests of letter fluency, visuospatial, learning and memory. Cognitive performance was uniquely associated with GI-symptoms and unrelated to non-GI autonomic symptoms. CONCLUSIONS: The presence of GI symptoms may serve as an early marker of cognitive impairment in PD. Future studies should examine specific mechanisms underlying the relationship between gut-dysbiosis and cognitive impairment.

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

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).