TY - JOUR
T1 - Parkinson disease-associated cognitive impairment
AU - Aarsland, Dag
AU - Batzu, Lucia
AU - Halliday, Glenda M.
AU - Geurtsen, Gert J.
AU - Ballard, Clive
AU - Ray Chaudhuri, K.
AU - Weintraub, Daniel
N1 - Funding Information: This paper represents independent research partly funded by the National Institute for Health Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King’s College London. The views expressed are those of the author and not necessarily those of the NHS, the NIHR or the Department of Health and Social Care. D.A. has received research support and/or honoraria from Astra-Zeneca, H. Lundbeck, Novartis Pharmaceuticals, Evonik, and GE Health and has served as paid consultant for H. Lundbeck, Eisai, Heptares, Mentis Cura, Eli Lilly, and Biogen. C.B. reports grants and personal fees from Acadia pharmaceutical company, grants and personal fees from Lundbeck, personal fees from Roche, personal fees from Otsuka, personal fees from Biogen, personal fees from Eli Lilly, personal fees from Novo Nordisk, personal fees from AARP, grants and personal fees from Synexus, and personal fees from Exciva outside the submitted work. K.R.C. is in the advisory board of AbbVie, UCB, GKC, Bial, Cynapsus, Lobsor, Stada, Medtronic, Zambon, Profile, Sunovion, Roche, Therevance, Scion, Britannia, Acadia and 4D, has received honoraria for lectures from AbbVie, Britannia, UCB, Zambon, Novartis, Boeringer Ingelheim and Bial, and reports grants for investigator-initiated studies from Britania Pharmaceuticals, AbbVie, UCB, GKC and Bial as well as academic grants from EU, IMI EU, Horizon 2020, Parkinson’s UK, NIHR, PDNMG, Kirby Laing Foundation, NPF, MRC, and Wellcome Trust. D.W. has received research funding or support from Michael J. Fox Foundation for Parkinson’s Research, Alzheimer’s Therapeutic Research Initiative (ATRI), Alzheimer’s Disease Cooperative Study (ADCS), the International Parkinson and Movement Disorder Society (IPMDS) and the National Institute on Ageing (NIA), honoraria for consultancy from Acadia, Aptinyx, CHDI Foundation, Clintrex LLC (Alkahest, Aptinyx, Avanir, Otsuka), Eisai, Enterin, Great Lake Neurotechnologies, Janssen, Sage, Scion, Signant Health, Sunovion and Vanda, and license fee payments from the University of Pennsylvania for the QUIP and QUIP-RS. L.B., G.H. and G.G. report no competing interests. Funding Information: D.A. is a Royal Society Wolfson Research Merit Award Holder and would like to thank the Wolfson Foundation and the Royal Society for their support. Publisher Copyright: © 2021, Springer Nature Limited.
PY - 2021/12/1
Y1 - 2021/12/1
N2 - Parkinson 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.
AB - Parkinson 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.
UR - http://www.scopus.com/inward/record.url?scp=85109154052&partnerID=8YFLogxK
U2 - https://doi.org/10.1038/s41572-021-00280-3
DO - https://doi.org/10.1038/s41572-021-00280-3
M3 - Article
C2 - 34210995
SN - 2056-676X
VL - 7
JO - Nature reviews. Disease primers
JF - Nature reviews. Disease primers
IS - 1
M1 - 47
ER -