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dc.contributor.authorAarsland, D
dc.contributor.authorBatzu, L
dc.contributor.authorHalliday, GM
dc.contributor.authorGeurtsen, GJ
dc.contributor.authorBallard, C
dc.contributor.authorRay Chaudhuri, K
dc.contributor.authorWeintraub, D
dc.date.accessioned2021-10-21T09:18:08Z
dc.date.issued2021-07-01
dc.description.abstractParkinson disease (PD) is the second most common neurodegenerative disorder, affecting >1% of the population ≥65 years of age and with a prevalence set to double by 2030. In addition to the defining motor symptoms of PD, multiple non-motor symptoms occur; among them, cognitive impairment is common and can potentially occur at any disease stage. Cognitive decline is usually slow and insidious, but rapid in some cases. Recently, the focus has been on the early cognitive changes, where executive and visuospatial impairments are typical and can be accompanied by memory impairment, increasing the risk for early progression to dementia. Other risk factors for early progression to dementia include visual hallucinations, older age and biomarker changes such as cortical atrophy, as well as Alzheimer-type changes on functional imaging and in cerebrospinal fluid, and slowing and frequency variation on EEG. However, the mechanisms underlying cognitive decline in PD remain largely unclear. Cortical involvement of Lewy body and Alzheimer-type pathologies are key features, but multiple mechanisms are likely involved. Cholinesterase inhibition is the only high-level evidence-based treatment available, but other pharmacological and non-pharmacological strategies are being tested. Challenges include the identification of disease-modifying therapies as well as finding biomarkers to better predict cognitive decline and identify patients at high risk for early and rapid cognitive impairment.en_GB
dc.identifier.citationVol. 7, article 47en_GB
dc.identifier.doi10.1038/s41572-021-00280-3
dc.identifier.urihttp://hdl.handle.net/10871/127533
dc.language.isoenen_GB
dc.publisherNature Researchen_GB
dc.rights.embargoreasonUnder embargo until 1 January 2022 in compliance with publisher policyen_GB
dc.rights© Springer Nature Limited 2021en_GB
dc.titleParkinson disease-associated cognitive impairmenten_GB
dc.typeArticleen_GB
dc.date.available2021-10-21T09:18:08Z
dc.descriptionThis is the author accepted manuscript. The final version is available from Nature Research via the DOI in this recorden_GB
dc.identifier.eissn2056-676X
dc.identifier.journalNature Reviews Disease Primersen_GB
dc.rights.urihttp://www.rioxx.net/licenses/all-rights-reserveden_GB
dcterms.dateAccepted2021-05-27
rioxxterms.versionAMen_GB
rioxxterms.licenseref.startdate2021-07-01
rioxxterms.typeJournal Article/Reviewen_GB
refterms.dateFCD2021-10-21T09:14:51Z
refterms.versionFCDAM
refterms.panelAen_GB


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