Background Cognitive dysfunction is a major feature of Parkinson’s disease (PD), but the pathophysiology remains unknown. One potential mechanism is abnormal low-frequency cortical rhythms which engage cognitive functions and are deficient in PD. We tested the hypothesis that mid-frontal delta/theta rhythms predict cognitive dysfunction in PD.
Method We recruited 100 patients with PD and 49 demographically similar control participants who completed a series of cognitive control tasks, including the Simon, oddball and interval-timing tasks. We focused on cue-evoked delta (1–4 Hz) and theta (4–7 Hz) rhythms from a single mid-frontal EEG electrode (cranial vertex (Cz)) in patients with PD who were either cognitively normal, with mild-cognitive impairments (Parkinson’s disease with mild-cognitive impairment) or had dementia (Parkinson’s disease dementia).
Results We found that PD-related cognitive dysfunction was associated with increased response latencies and decreased mid-frontal delta power across all tasks. Within patients with PD, the first principal component of evoked electroencephalography features from a single electrode (Cz) strongly correlated with clinical metrics such as the Montreal Cognitive Assessment score (r=0.34) and with National Institutes of Health Toolbox Executive Function score (r=0.46).
Conclusions These data demonstrate that cue-evoked mid-frontal delta/theta rhythms directly relate to cognition in PD. Our results provide insight into the nature of low-frequency frontal rhythms and suggest that PD-related cognitive dysfunction results from decreased delta/theta activity. These findings could facilitate the development of new biomarkers and targeted therapies for cognitive symptoms of PD.
- PARKINSON'S DISEASE
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Contributors AS, RCC, AIE and NN acquired the data. AS, JRW, JFC and NN conceptualised and designed the study. AS, JFC and NN conducted the analyses. AS, RCC, JRW, JFC and NN interpreted the data. AS and NN wrote the first draft of the manuscript, accepted full responsibility for the work and/or the conduct of the study, had access to the data, and controlled the decision to publish.
Funding This data were supported by NIH P20NS123151 and R01NS100849 to NSN and NRSA F32 AG069445-01 (RCC).
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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