Predicting cognitive decline using neuropsychiatric symptoms in prodromal Lewy body dementia: A longitudinal study.
Cognition
Dementia
Lewy body
Neuropsychiatry
Parkinson's disease
Journal
Parkinsonism & related disorders
ISSN: 1873-5126
Titre abrégé: Parkinsonism Relat Disord
Pays: England
ID NLM: 9513583
Informations de publication
Date de publication:
08 2023
08 2023
Historique:
received:
16
03
2023
revised:
28
06
2023
accepted:
07
07
2023
medline:
8
8
2023
pubmed:
14
7
2023
entrez:
13
7
2023
Statut:
ppublish
Résumé
Neuropsychiatric symptoms (NPS) in Lewy body dementias (LBD) occur frequently and early in disease progression. Such symptoms are associated with worse quality of life, caregiver burden and functional limitations. Limited evidence exists, however, outlining the longitudinal relationship between NPS and cognitive decline in prodromal LBD. 123 participants were derived from three cohort studies. Patients with mild cognitive impairment (MCI) relating to probable dementia with Lewy bodies (MCI-LB, n = 67) and Parkinson's disease (PD-MCI, n = 56) completed comprehensive cognitive and neuropsychiatric assessment and were followed up longitudinally. Linear regression and mixed effects models assessed the relationship between baseline NPS and cognition at baseline and over time. In MCI-LB, overall NPS burden was associated with declines over time in executive function (p = 0.026) and processing speed (p = 0.028) and baseline aberrant motor behaviour was associated with declines in attention (p < 0.025). Anxiety was significantly associated with poorer visuospatial functioning (p = 0.016) at baseline and poorer attention both at baseline (p = 0.017) and across time points (p = 0.024). In PD-MCI, psychosis was associated with poorer executive functioning at baseline (p = 0.008) and across time points (p = 0.002) but had no association with changes longitudinally. Core neuropsychiatric components of LBD are not strongly associated with cognition in prodromal disease. This may suggest that neuropathological mechanisms underlying NPS may not be the same as those underlying cognitive impairment. Non-core NPS, however, may be more directly associated with cognitive change. Future studies utilising neuroimaging techniques are needed to explore the neuropathological basis of NPS in prodromal LBD.
Identifiants
pubmed: 37441886
pii: S1353-8020(23)00841-6
doi: 10.1016/j.parkreldis.2023.105762
pii:
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
105762Subventions
Organisme : Department of Health
ID : BH120812
Pays : United Kingdom
Organisme : Department of Health
ID : BH120878
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/W000229/1
Pays : United Kingdom
Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest Dr Paul Donaghy has received grant support by the Medical Research Council, the Lewy Body Society and Alzheimer's Research UK. Dr Donaghy has also received payment for lectures by the Neurology Academy and has an unpaid leadership role on the Lewy Body Society Specialist Advisory Committee. Professor John-Paul Taylor is supported by the NIHR Newcastle Biomedical Research Centre. Professor John O'Brien has received grant support from Alliance Medical and Merck, consulting fees from Roche and Biogen and lecture fees from GE Healthcare. Professor O'Brien also participates on advisory boards for TauRx, Novo Nordisk and chairs the research strategy board for UK Alzheimer's Society. Dr Alison Yarnall has received grant support from the Dunhill Medical Trust, EU IMI, NIHR, Parkinson's UK, Michael J Fox Foundation, Weston Brain Institute and Intercept pharmaceuticals. Dr Yarnall has also received funding and/or honoraria from Britannia, UCB, Abbvie, GSK, Teva-Lundbeck, GE Healthcare and Genus for attending educational events. The remaining authors have no competing interests to declare.