Inflammation in mild cognitive impairment due to Parkinson's disease, Lewy body disease, and Alzheimer's disease.


Journal

International journal of geriatric psychiatry
ISSN: 1099-1166
Titre abrégé: Int J Geriatr Psychiatry
Pays: England
ID NLM: 8710629

Informations de publication

Date de publication:
08 2019
Historique:
received: 08 06 2018
accepted: 05 04 2019
pubmed: 18 4 2019
medline: 28 2 2020
entrez: 18 4 2019
Statut: ppublish

Résumé

Inflammation appears to play a role in the progression of neurodegenerative diseases. However, little is known about inflammation during early stages of cognitive decline or whether this differs in different disease groups. We sought to investigate this by assessing the inflammatory profile in patients with Parkinson disease with the early stages of cognitive impairment (PD-MCI), patients with prodromal Alzheimer disease (MCI-AD), prodromal Lewy body disease (MCI-LB), and controls. We obtained venous blood samples from participants with PD-MCI (n = 44), PD-normal cognition (n = 112), MCI-LB (n = 38), MCI-AD (n = 21), and controls (n = 84). We measured 10 cytokines using Meso Scale Discovery V-Plex Plus including interferon gamma, interleukin (IL)-10, IL-12p70, IL-13, IL-1beta, IL-2, IL-4, IL-6, IL-8, and tumour necrosis factor alpha. High-sensitivity C-reactive protein was measured. There was a higher level of inflammation in patients with MCI-AD and MCI-LB compared with controls. PD noncognitively impaired had higher inflammatory markers than controls, but there was no difference between PD-MCI and controls. There was a decrease in inflammatory markers with increasing motor severity based on the Unified Parkinson's Disease Rating Scale. Inflammation may be involved in the onset of cognitive decline in patients with MCI-AD and MCI-LB but appears to be less prominent PD-MCI albeit in a small data set. This suggests that anti-inflammatory medications may have most benefit at the earliest stages of neurodegenerative diseases. For PD cases, this might be in advance of the development of MCI.

Sections du résumé

BACKGROUND
Inflammation appears to play a role in the progression of neurodegenerative diseases. However, little is known about inflammation during early stages of cognitive decline or whether this differs in different disease groups. We sought to investigate this by assessing the inflammatory profile in patients with Parkinson disease with the early stages of cognitive impairment (PD-MCI), patients with prodromal Alzheimer disease (MCI-AD), prodromal Lewy body disease (MCI-LB), and controls.
METHODS
We obtained venous blood samples from participants with PD-MCI (n = 44), PD-normal cognition (n = 112), MCI-LB (n = 38), MCI-AD (n = 21), and controls (n = 84). We measured 10 cytokines using Meso Scale Discovery V-Plex Plus including interferon gamma, interleukin (IL)-10, IL-12p70, IL-13, IL-1beta, IL-2, IL-4, IL-6, IL-8, and tumour necrosis factor alpha. High-sensitivity C-reactive protein was measured.
RESULTS
There was a higher level of inflammation in patients with MCI-AD and MCI-LB compared with controls. PD noncognitively impaired had higher inflammatory markers than controls, but there was no difference between PD-MCI and controls. There was a decrease in inflammatory markers with increasing motor severity based on the Unified Parkinson's Disease Rating Scale.
CONCLUSIONS
Inflammation may be involved in the onset of cognitive decline in patients with MCI-AD and MCI-LB but appears to be less prominent PD-MCI albeit in a small data set. This suggests that anti-inflammatory medications may have most benefit at the earliest stages of neurodegenerative diseases. For PD cases, this might be in advance of the development of MCI.

Identifiants

pubmed: 30993722
doi: 10.1002/gps.5124
doi:

Substances chimiques

Biomarkers 0
Cytokines 0
IL1B protein, human 0
Interleukin-1beta 0
C-Reactive Protein 9007-41-4

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1244-1250

Subventions

Organisme : Parkinson's UK
ID : J-0802
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/R007446/1
Pays : United Kingdom
Organisme : Parkinson's UK
ID : G-1507
Pays : United Kingdom
Organisme : Medical Research Council
ID : G1100540
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom

Informations de copyright

© 2019 John Wiley & Sons, Ltd.

Auteurs

Eleanor King (E)

Institute of Neuroscience, Campus for Aging and Vitality, Newcastle upon Tyne, UK.

John O'Brien (J)

Institute of Neuroscience, Campus for Aging and Vitality, Newcastle upon Tyne, UK.

Paul Donaghy (P)

Institute of Neuroscience, Campus for Aging and Vitality, Newcastle upon Tyne, UK.

Caroline H Williams-Gray (CH)

John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, Cambridge University, Cambridge, UK.

Rachael A Lawson (RA)

Institute of Neuroscience, Campus for Aging and Vitality, Newcastle upon Tyne, UK.

Christopher M Morris (CM)

Institute of Neuroscience, Campus for Aging and Vitality, Newcastle upon Tyne, UK.

Nicola Barnett (N)

Institute of Neuroscience, Campus for Aging and Vitality, Newcastle upon Tyne, UK.

Kirsty Olsen (K)

Institute of Neuroscience, Campus for Aging and Vitality, Newcastle upon Tyne, UK.

Carmen Martin-Ruiz (C)

Institute of Neuroscience, Campus for Aging and Vitality, Newcastle upon Tyne, UK.

David Burn (D)

Institute of Neuroscience, Campus for Aging and Vitality, Newcastle upon Tyne, UK.

Alison J Yarnall (AJ)

Institute of Neuroscience, Campus for Aging and Vitality, Newcastle upon Tyne, UK.

John-Paul Taylor (JP)

Institute of Neuroscience, Campus for Aging and Vitality, Newcastle upon Tyne, UK.

Gordan Duncan (G)

Department of Medicine for the Elderly, Western General Hospital, Edinburgh, UK.

Tien K Khoo (TK)

School of Medicine & Menzies Health Institute Queensland, Griffith University, Southport, Queensland, Australia.

Alan Thomas (A)

Institute of Neuroscience, Campus for Aging and Vitality, Newcastle upon Tyne, UK.

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Classifications MeSH