Cognitive deficits in parkinson's disease are associated with neuronal dysfunction and not white matter lesions

Abstract: Background
Cognitive deficits considerably contribute to the patient's burden in Parkinson's disease (PD). While cognitive decline is linked to neuronal dysfunction, the additional role of white matter lesions (WML) is discussed controversially.

Objective
To investigate the influence of WML, in comparison to neuronal dysfunction, on cognitive deficits in PD.

Methods
We prospectively recruited patients with PD who underwent neuropsychological assessment using the Mattis Dementia Rating Scale 2 (DRS-2) or Parkinson Neuropsychometric Dementia Assessment (PANDA) and both MRI and PET with [18F]fluorodeoxyglucose (FDG). WML-load and PD cognition-related covariance pattern (PDCP) as a measure of neuronal dysfunction were read out. Relationship between cognitive performance and rank-transformed WML was analyzed with linear regression, controlling for the patients’ age. PDCP subject scores were investigated likewise and in a second step adjusting for age and WML load.

Results
Inclusion criteria were met by 76 patients with a mean (± SD) age of 63.5 ± 9.0 years and disease duration of 10.7 ± 5.4 years. Neuropsychological testing revealed front executive and parietal deficits and a median DRS-2 score of 137 (range 119–144)/144 and PANDA score of 22 (range 3–30)/30. No association between WML and cognition was observed, whereas PDCP subject scores showed a trend-level negative correlation with the DRS-2 (P = 0.060) as well as a negative correlation with PANDA (P = 0.049) which persisted also after additional correction for WML (P = 0.039).

Conclusion
The present study indicates that microangiopathic WML do not have a relevant impact on neurocognitive performance in PD whereas neuronal dysfunction does

Standort
Deutsche Nationalbibliothek Frankfurt am Main
Umfang
Online-Ressource
Sprache
Englisch
Anmerkungen
Movement disorders clinical practice. - 10, 7 (2023) , 1066-1073, ISSN: 2330-1619

Ereignis
Veröffentlichung
(wo)
Freiburg
(wer)
Universität
(wann)
2023

DOI
10.1002/mdc3.13792
URN
urn:nbn:de:bsz:25-freidok-2371205
Rechteinformation
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Letzte Aktualisierung
25.03.2025, 13:43 MEZ

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  • 2023

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