Cited by 1,027Parkinson's Disease Mechanisms and TreatmentsDementia and Cognitive Impairment ResearchNeurological diseases and metabolism

The DOI matches its Crossref record; 216 of the 216 references it cites were found in a registry or an index.

Cognitive decline in Parkinson disease

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Aarsland, Dag, Creese, Byron, Politis, Marios, Chaudhuri, K. Ray, ffytche, Dominic H., Weintraub, Daniel, Ballard, Clive·2017·Nature Reviews Neurology

Abstract

Dementia is a frequent problem encountered in advanced stages of Parkinson disease (PD). In recent years, research has focused on the pre-dementia stages of cognitive impairment in PD, including mild cognitive impairment (MCI). Several longitudinal studies have shown that MCI is a harbinger of dementia in PD, although the course is variable, and stabilization of cognition - or even reversal to normal cognition - is not uncommon. In addition to limbic and cortical spread of Lewy pathology, several other mechanisms are likely to contribute to cognitive decline in PD, and a variety of biomarker studies, some using novel structural and functional imaging techniques, have documented in vivo brain changes associated with cognitive impairment. The evidence consistently suggests that low cerebrospinal fluid levels of amyloid-β 42, a marker of comorbid Alzheimer disease (AD), predict future cognitive decline and dementia in PD. Emerging genetic evidence indicates that in addition to the APOE*ε4 allele (an established risk factor for AD), GBA mutations and SCNA mutations and triplications are associated with cognitive decline in PD, whereas the findings are mixed for MAPT polymorphisms. Cognitive enhancing medications have some effect in PD dementia, but no convincing evidence that progression from MCI to dementia can be delayed or prevented is available, although cognitive training has shown promising results.

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Metadata

Authors
Aarsland, D., Creese, B., Politis, M., Chaudhuri, K. R., ffytche, D. H., Weintraub, D., & Ballard, C.
Affiliations
King's College London (GB)
Corresponding author
Aarsland, Dag
Venue
Nature Reviews Neurology
Published
2017-03-03
Volume
13
Issue
4
Pages
217-231
ISSN
  • 1759-4758 (ISSN-L)
  • 1759-4766
OpenAlex
W2593272776
Cited by
1,027
References
216
Citations by year
2026: 102 · 2025: 99 · 2024: 138 · 2023: 104 · 2022: 105 · 2021: 171 · 2020: 116 · 2019: 89 · 2018: 68 · 2017: 33
FWCI
11.11
Type
journal article
Language
en
Open access
Locations
  • Nature Reviews Neurology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • Open Research Exeter (University of Exeter) (acceptedVersion)
  • Figshare (submittedVersion)
  • Research Portal (King's College London) (submittedVersion, other-oa)
Funders
  • South London and Maudsley NHS Foundation Trust
  • National Institute for Health and Care Research
  • King's College London
  • Institute of Psychiatry, Psychology and Neuroscience, King’s College London
  • National Institute of Neurological Disorders and Stroke (P50NS053488)
Topics
  • Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
Keywords
Parkinson's disease, cognitive decline, Parkinson's disease dementia, mild cognitive impairment, cerebrospinal fluid biomarkers, amyloid-beta 42, Lewy body pathology, APOE ε4, GBA mutations, cognitive training, nootropic drugs
MeSH terms
Dementia, Humans, Parkinson Disease, Cognitive Dysfunction

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