Cognitive impairment in Parkinson’s disease: a report from a multidisciplinary symposium on unmet needs and future directions to maintain cognitive health

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Abstract

People with Parkinson’s disease (PD) and their care partners frequently report cognitive decline as one of their greatest concerns. Mild cognitive impairment affects approximately 20–50% of people with PD, and longitudinal studies reveal dementia in up to 80% of PD. Through the Parkinson’s Disease Foundation Community Choice Research Award Program, the PD community identified maintaining cognitive function as one of their major unmet needs. In response, a working group of experts across multiple disciplines was organized to evaluate the unmet needs, current challenges, and future opportunities related to cognitive impairment in PD. Specific conference goals included defining the current state in the field and gaps regarding cognitive issues in PD from patient, care partner, and healthcare professional viewpoints; discussing non-pharmacological interventions to help maintain cognitive function; forming recommendations for what people with PD can do at all disease stages to maintain cognitive health; and proposing ideas for how healthcare professionals can approach cognitive changes in PD. This paper summarizes the discussions of the conference, first by addressing what is currently known about cognitive dysfunction in PD and discussing several non-pharmacological interventions that are often suggested to people with PD. Second, based on the conference discussions, we provide considerations for people with PD for maintaining cognitive health and for healthcare professionals and care partners when working with people with PD experiencing cognitive impairment. Furthermore, we highlight key issues and knowledge gaps that need to be addressed in order to advance research in cognition in PD and improve clinical care.

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Most cited references 81

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Caregiving as a risk factor for mortality: the Caregiver Health Effects Study.

R. Schulz, S Beach (1999)

There is strong consensus that caring for an elderly individual with disability is burdensome and stressful to many family members and contributes to psychiatric morbidity. Researchers have also suggested that the combination of loss, prolonged distress, the physical demands of caregiving, and biological vulnerabilities of older caregivers may compromise their physiological functioning and increase their risk for physical health problems, leading to increased mortality. To examine the relationship between caregiving demands among older spousal caregivers and 4-year all-cause mortality, controlling for sociodemographic factors, prevalent clinical disease, and subclinical disease at baseline. Prospective population-based cohort study, from 1993 through 1998 with an average of 4.5 years of follow-up. Four US communities. A total of 392 caregivers and 427 noncaregivers aged 66 to 96 years who were living with their spouses. Four-year mortality, based on level of caregiving: (1) spouse not disabled; (2) spouse disabled and not helping; (3) spouse disabled and helping with no strain reported; or(4) spouse disabled and helping with mental or emotional strain reported. After 4 years of follow-up, 103 participants (12.6%) died. After adjusting for sociodemographic factors, prevalent disease, and subclinical cardiovascular disease, participants who were providing care and experiencing caregiver strain had mortality risks that were 63% higher than noncaregiving controls (relative risk [RR], 1.63; 95% confidence interval [CI], 1.00-2.65). Participants who were providing care but not experiencing strain (RR, 1.08; 95 % CI, 0.61-1.90) and those with a disabled spouse who were not providing care (RR, 1.37; 95% CI, 0.73-2.58) did not have elevated adjusted mortality rates relative to the noncaregiving controls. Our study suggests that being a caregiver who is experiencing mental or emotional strain is an independent risk factor for mortality among elderly spousal caregivers. Caregivers who report strain associated with caregiving are more likely to die than noncaregiving controls.

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The distinct cognitive syndromes of Parkinson's disease: 5 year follow-up of the CamPaIGN cohort.

Caroline Williams-Gray, Jonathan Evans, An Goris … (2009)

Cognitive abnormalities are common in Parkinson's disease, with important social and economic implications. Factors influencing their evolution remain unclear but are crucial to the development of targeted therapeutic strategies. We have investigated the development of cognitive impairment and dementia in Parkinson's disease using a longitudinal approach in a population-representative incident cohort (CamPaIGN study, n = 126) and here present the 5-year follow-up data from this study. Our previous work has implicated two genetic factors in the development of cognitive dysfunction in Parkinson's disease, namely the genes for catechol-O-methyltransferase (COMT Val(158)Met) and microtubule-associated protein tau (MAPT) H1/H2. Here, we have explored the influence of these genes in our incident cohort and an additional cross-sectional prevalent cohort (n = 386), and investigated the effect of MAPT H1/H2 haplotypes on tau transcription in post-mortem brain samples from patients with Lewy body disease and controls. Seventeen percent of incident patients developed dementia over 5 years [incidence 38.7 (23.9-59.3) per 1000 person-years]. We have demonstrated that three baseline measures, namely, age >or=72 years, semantic fluency less than 20 words in 90 s and inability to copy an intersecting pentagons figure, are significant predictors of dementia risk, thus validating our previous findings. In combination, these factors had an odds ratio of 88 for dementia within the first 5 years from diagnosis and may reflect the syndrome of mild cognitive impairment of Parkinson's disease. Phonemic fluency and other frontally based tasks were not associated with dementia risk. MAPT H1/H1 genotype was an independent predictor of dementia risk (odds ratio = 12.1) and the H1 versus H2 haplotype was associated with a 20% increase in transcription of 4-repeat tau in Lewy body disease brains. In contrast, COMT genotype had no effect on dementia, but a significant impact on Tower of London performance, a frontostriatally based executive task, which was dynamic, such that the ability to solve this task changed with disease progression. Hence, we have identified three highly informative predictors of dementia in Parkinson's disease, which can be easily translated into the clinic, and established that MAPT H1/H1 genotype is an important risk factor with functional effects on tau transcription. Our work suggests that the dementing process in Parkinson's disease is predictable and related to tau while frontal-executive dysfunction evolves independently with a more dopaminergic basis and better prognosis.

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Mild Cognitive Impairment.

Ronald C. Petersen (2016)

As individuals age, the quality of cognitive function becomes an increasingly important topic. The concept of mild cognitive impairment (MCI) has evolved over the past 2 decades to represent a state of cognitive function between that seen in normal aging and dementia. As such, it is important for health care providers to be aware of the condition and place it in the appropriate clinical context.

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Author and article information

Contributors

Jennifer G. Goldman:

ORCID: http://orcid.org/0000-0001-5014-7535

+312 563 2900 , Jennifer_Goldman@rush.edu

Journal

Journal ID (nlm-ta): NPJ Parkinsons Dis

Journal ID (iso-abbrev): NPJ Parkinsons Dis

Title: NPJ Parkinson's Disease

Publisher: Nature Publishing Group UK (London )

ISSN (Electronic): 2373-8057

Publication date (Electronic): 26 June 2018

Publication date PMC-release: 26 June 2018

Publication date Collection: 2018

Volume: 4

Electronic Location Identifier: 19

Affiliations

[1 ]ISNI 0000 0001 0705 3621, GRID grid.240684.c, Department of Neurological Sciences, Section of Parkinson Disease and Movement Disorders, , Rush University Medical Center, ; Chicago, IL USA

[2 ]Parkinson’s Foundation, New York, NY USA

[3 ]GRID grid.17089.37, Department of Medicine, , University of Alberta, ; Edmonton, AB Canada

[4 ]ISNI 0000 0004 1936 8972, GRID grid.25879.31, Department of Neurology, , University of Pennsylvania, ; Philadelphia, PA USA

[5 ]ISNI 0000 0004 1936 8796, GRID grid.430387.b, Department of Psychiatry, , Rutgers The State University of New Jersey, ; New Brunswick, NJ USA

[6 ]ISNI 0000 0004 1936 7558, GRID grid.189504.1, Department of Physical Therapy and Athletic Training and Center for Neurorehabilitation, , Boston University, ; Boston, MA USA

[7 ]ISNI 0000 0004 0635 0263, GRID grid.255951.f, Charles E. Schmidt College of Medicine, , Florida Atlantic University, ; Boca Raton, FL USA

[8 ]ISNI 0000 0001 2157 2938, GRID grid.17063.33, Morton and Gloria Shulman Movement Disorders Centre and the Edmond J. Safra Program in Parkinson’s disease, Toronto Western Hospital, University Health Network, , University of Toronto, ; Toronto, ON Canada

[9 ]ISNI 0000 0001 2353 285X, GRID grid.170693.a, University of South Florida, ; Tampa, FL USA

[10 ]ISNI 0000 0004 0459 167X, GRID grid.66875.3a, Department of Psychiatry and Psychology, , Mayo Clinic, ; Rochester, MN USA

[11 ]ISNI 0000 0001 0705 3621, GRID grid.240684.c, Department of Health and Aging, , Rush University Medical Center, ; Chicago, IL USA

[12 ]ISNI 0000 0004 1936 8972, GRID grid.25879.31, Department of Medicine, , University of Pennsylvania, ; Philadelphia, PA USA

[13 ]ISNI 0000 0004 1936 8606, GRID grid.26790.3a, Department of Neurology, Division of Neuropsychology, , University of Miami, ; Miami, FL USA

[14 ]ISNI 0000 0001 2175 4264, GRID grid.411024.2, Department of Neurology, , University of Maryland School of Medicine, ; Baltimore, MD USA

[15 ]ISNI 0000 0004 1936 8091, GRID grid.15276.37, Department of Clinical and Health Psychology, , University of Florida, ; Gainesville, FL USA

[16 ]ISNI 0000 0001 0705 3621, GRID grid.240684.c, Department of Clinical Nutrition, College of Health Sciences, , Rush University Medical Center, ; Chicago, IL USA

[17 ]ISNI 0000 0004 1936 7558, GRID grid.189504.1, Department of Neurology, , Boston University Medical Campus, ; Boston, MA USA

[18 ]ISNI 0000 0001 0664 3531, GRID grid.427785.b, Department of Clinical Neuropsychology and Center for Neuromodulation, , Barrow Neurological Institute, ; Phoenix, AZ USA

[19 ]ISNI 0000 0004 1936 8294, GRID grid.214572.7, Department of Neurology, , University of Iowa, and Neurology Service, ; Iowa City, Veterans Affairs Health Care Systen, Iowa City, IA USA

[20 ]Illinois, USA

[21 ]Colorado, USA

Author information

Jennifer G. Goldman http://orcid.org/0000-0001-5014-7535

Alexander I. Tröster http://orcid.org/0000-0002-8898-3878

Article

Publisher ID: 55

DOI: 10.1038/s41531-018-0055-3

PMC ID: 6018742

PubMed ID: 29951580

SO-VID: f572151c-7eb3-42cf-96ab-9a74f620a944

License:

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

History

Date received : 26 August 2017

Date revision received : 29 April 2018

Date accepted : 10 May 2018

Funding

Funded by: FundRef https://doi.org/10.13039/100001288, Parkinson's Disease Foundation (Parkinson's Disease Foundation, Inc.);

Award ID: Community Choice Research Award

Award Recipient : Jennifer G. Goldman Beth A. Vernaleo Richard Camicioli Nabila Dahodwala Roseanne D. Dobkin Terry Ellis James E. Galvin Connie Marras Jerri Edwards Julie Fields Robyn Golden Jason Karlawish Bonnie Levin Lisa Shulman Glenn Smith Christine Tangney Cathi A. Thomas Ergun Y. Uc Noreen Coyan Crystal Ellman Charlie Hoffman Don Simmonds

Cognitive impairment in Parkinson’s disease: a report from a multidisciplinary symposium on unmet needs and future directions to maintain cognitive health

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New directions in predictive processing

Most cited references 81

Caregiving as a risk factor for mortality: the Caregiver Health Effects Study.

The distinct cognitive syndromes of Parkinson's disease: 5 year follow-up of the CamPaIGN cohort.

Mild Cognitive Impairment.

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