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Computational Modeling for Neuropsychological Assessment of Bradyphrenia in Parkinson’s Disease
The neural mechanisms of cognitive dysfunctions in neurological diseases remain poorly understood. Here, we conjecture that this unsatisfying state-of-the-art is in part due to the non-specificity of the typical behavioral indicators for cognitive dysfunctions. Our study addresses the topic by advan...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7230210/ https://www.ncbi.nlm.nih.gov/pubmed/32325662 http://dx.doi.org/10.3390/jcm9041158 |
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author | Steinke, Alexander Lange, Florian Seer, Caroline Hendel, Merle K. Kopp, Bruno |
author_facet | Steinke, Alexander Lange, Florian Seer, Caroline Hendel, Merle K. Kopp, Bruno |
author_sort | Steinke, Alexander |
collection | PubMed |
description | The neural mechanisms of cognitive dysfunctions in neurological diseases remain poorly understood. Here, we conjecture that this unsatisfying state-of-the-art is in part due to the non-specificity of the typical behavioral indicators for cognitive dysfunctions. Our study addresses the topic by advancing the assessment of cognitive dysfunctions through computational modeling. We investigate bradyphrenia in Parkinson’s disease (PD) as an exemplary case of cognitive dysfunctions in neurological diseases. Our computational model conceptualizes trial-by-trial behavioral data as resulting from parallel cognitive and sensorimotor reinforcement learning. We assessed PD patients ‘on’ and ‘off’ their dopaminergic medication and matched healthy control (HC) participants on a computerized version of the Wisconsin Card Sorting Test. PD patients showed increased retention of learned cognitive information and decreased retention of learned sensorimotor information from previous trials in comparison to HC participants. Systemic dopamine replacement therapy did not remedy these cognitive dysfunctions in PD patients but incurred non-desirable side effects such as decreasing cognitive learning from positive feedback. Our results reveal novel insights into facets of bradyphrenia that are indiscernible by observable behavioral indicators of cognitive dysfunctions. We discuss how computational modeling may contribute to the advancement of future research on brain–behavior relationships and neuropsychological assessment. |
format | Online Article Text |
id | pubmed-7230210 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-72302102020-05-28 Computational Modeling for Neuropsychological Assessment of Bradyphrenia in Parkinson’s Disease Steinke, Alexander Lange, Florian Seer, Caroline Hendel, Merle K. Kopp, Bruno J Clin Med Article The neural mechanisms of cognitive dysfunctions in neurological diseases remain poorly understood. Here, we conjecture that this unsatisfying state-of-the-art is in part due to the non-specificity of the typical behavioral indicators for cognitive dysfunctions. Our study addresses the topic by advancing the assessment of cognitive dysfunctions through computational modeling. We investigate bradyphrenia in Parkinson’s disease (PD) as an exemplary case of cognitive dysfunctions in neurological diseases. Our computational model conceptualizes trial-by-trial behavioral data as resulting from parallel cognitive and sensorimotor reinforcement learning. We assessed PD patients ‘on’ and ‘off’ their dopaminergic medication and matched healthy control (HC) participants on a computerized version of the Wisconsin Card Sorting Test. PD patients showed increased retention of learned cognitive information and decreased retention of learned sensorimotor information from previous trials in comparison to HC participants. Systemic dopamine replacement therapy did not remedy these cognitive dysfunctions in PD patients but incurred non-desirable side effects such as decreasing cognitive learning from positive feedback. Our results reveal novel insights into facets of bradyphrenia that are indiscernible by observable behavioral indicators of cognitive dysfunctions. We discuss how computational modeling may contribute to the advancement of future research on brain–behavior relationships and neuropsychological assessment. MDPI 2020-04-18 /pmc/articles/PMC7230210/ /pubmed/32325662 http://dx.doi.org/10.3390/jcm9041158 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Steinke, Alexander Lange, Florian Seer, Caroline Hendel, Merle K. Kopp, Bruno Computational Modeling for Neuropsychological Assessment of Bradyphrenia in Parkinson’s Disease |
title | Computational Modeling for Neuropsychological Assessment of Bradyphrenia in Parkinson’s Disease |
title_full | Computational Modeling for Neuropsychological Assessment of Bradyphrenia in Parkinson’s Disease |
title_fullStr | Computational Modeling for Neuropsychological Assessment of Bradyphrenia in Parkinson’s Disease |
title_full_unstemmed | Computational Modeling for Neuropsychological Assessment of Bradyphrenia in Parkinson’s Disease |
title_short | Computational Modeling for Neuropsychological Assessment of Bradyphrenia in Parkinson’s Disease |
title_sort | computational modeling for neuropsychological assessment of bradyphrenia in parkinson’s disease |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7230210/ https://www.ncbi.nlm.nih.gov/pubmed/32325662 http://dx.doi.org/10.3390/jcm9041158 |
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