Background Cognitive decline is common in Parkinson's disease (PD). Although some of the aetiological factors are known, it is not yet known whether drugs with anticholinergic activity (AA) contribute to this cognitive decline. Such knowledge would provide opportunities to prevent acceleration of cognitive decline in PD.
Objective To study whether the use of agents with anticholinergic properties is an independent risk factor for cognitive decline in patients with PD.
Methods A community-based cohort of patients with PD (n=235) were included and assessed at baseline. They were reassessed 4 and 8 years later. Cognition was assessed using the Mini-Mental State Examination (MMSE). A detailed assessment of the AA of all drugs prescribed was made, and AA was classified according to a standardised scale. Relationships between cognitive decline and AA load and duration of treatment were assessed using bivariate and multivariate statistical analyses.
Results More than 40% used drugs with AA at baseline. During the 8-year follow-up, the cognitive decline was higher in those who had been taking AA drugs (median decline on MMSE 6.5 points) compared with those who had not taken such drugs (median decline 1 point; p=0.025). In linear regression analyses adjusting for age, baseline cognition and depression, significant associations with decline on MMSE were found for total AA load (standardised β=0.229, p=0.04) as well as the duration of using AA drugs (standardised β 0.231, p=0.032).
Conclusion Our findings suggest that there is an association between anticholinergic drug use and cognitive decline in PD. This may provide an important opportunity for clinicians to avoid increasing progression of cognitive decline by avoiding drugs with AA. Increased awareness by clinicians is required about the classes of drugs that have anticholinergic properties.
- Parkinson's disease
- cognitive decline
- anticholinergic burden
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CB has received honoraria from Novartis, Pfizer, Shire, Lundbeck, Myriad, Janssen, Astra Zeneca and Servier pharmaceutical companies, and research grants from Novartis, Lundbeck, Astra-Zeneca and Janssen pharmaceuticals. DA has received honoraria from Novartis, Lundbeck, GE Health and Merck Serono and received 9.5 mill NOK, 2003–2007 (Age Research programme 153480); Health Region Western Norway; 500 000 NOK/year, 2008–2010 for the project Neurochemistry for dementia and PD; unrestricted industry grants 100 000 NOK/year from Kavli fund. DA received honoraria from Novartis, Lundbeck, GE Health and Merck Serono.
Funding The study was funded by the Stavanger Hospital Trust, Norway. UE was supported by a grant from Helse Vest, Norway. The funders had no role in the planning of the study or interpretation of the results.
Competing interests None.
Ethics approval Ethics was approved by the Regional Committees for Medical and Health Research Ethics (REK), Western Norway.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
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