Cognitive deficits in Parkinson's disease: A cognitive neuroscience perspective
Abstract
Progress in characterization of the nature, neural basis, and treatment of cognitive deficits in Parkinson's disease is reviewed from the perspective of cognitive neuroscience. An initial emphasis on fronto‐striatal executive deficits is surveyed along with the discoveries of disruption as well as remediation of certain impairments by dopaminergic mediation and their association with theories of reinforcement learning. Subsequent focus on large cohorts has revealed considerable heterogeneity in the cognitive impairments as well as a suggestion of at least two distinct syndromes, with the dopamine‐dependent fronto‐striatal deficits being somewhat independent of other signs commonly associated with Parkinson's disease dementia. The utility is proposed of a new, integrated cognitive neuroscience approach based on combining genetic and neuroimaging methodologies with neuropsychological and, ultimately, psychopharmacological approaches. © 2014 International Parkinson and Movement Disorder Society
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Flexibility deficits in Parkinson disease may result from dysfunction of frontostriatal loops due to dopamine depletion.
“Flexibility deficits observed in Parkinson disease may result from dysfunction of frontostriatal loops resulting from dopamine depletion102.”
From Cognitive and behavioural flexibility: Neural mechanisms and clinical considerations (2021) · cites this paper as [102]
In Parkinson disease, cognitive impairments such as slowed thinking and cognitive inflexibility parallel motor impairments, suggesting reduced flexibility might be an appropriate reaction to a world experienced as more stationary.
“In Parkinson disease, cognitive impairments such as slowed thinking and cognitive inflexibility parallel motor impairments102, suggesting that reduced flexibility might be an appropriate reaction to a world that is experienced as more stationary.”
From Cognitive and behavioural flexibility: Neural mechanisms and clinical considerations (2021) · cites this paper as [102]
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- Authors
- Robbins, T. W., & Cools, R.
- Affiliations
- University of Cambridge (GB)
- Radboud University Nijmegen (NL)
- Corresponding author
- Robbins, Trevor W.
- Venue
- Movement Disorders
- Publisher
- Wiley
- Published
- 2014-04-15
- Volume
- 29
- Issue
- 5
- Pages
- 597-607
- ISSN
- 0885-3185 (ISSN-L)
- 1531-8257
- OpenAlex
- W2149431833
- Cited by
- 235
- References
- 105
- Citations by year
- 2026: 12 · 2025: 17 · 2024: 14 · 2023: 9 · 2022: 24 · 2021: 18 · 2020: 24 · 2019: 14 · 2018: 24 · 2017: 29 · 2016: 22 · 2015: 24 · 2014: 4
- FWCI
- 3.62
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Movement Disorders (publishedVersion)
- PubMed (publishedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- Wellcome Trust
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- Parkinson's disease, cognitive impairment, executive function, frontostriatal circuits, dopaminergic modulation, reinforcement learning, Parkinson's disease dementia, cognitive heterogeneity, neuropsychological assessment, psychopharmacological treatment
- MeSH terms
- Animals, Cognition, Cognition Disorders, Dementia, Humans, Memory, Parkinson Disease
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