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Review
. 2022;12(s1):S183-S200.
doi: 10.3233/JPD-223277.

Blood and Cerebrospinal Fluid Biomarkers of Inflammation in Parkinson's Disease

Milan Zimmermann  1   2 , Kathrin Brockmann  1   2
Affiliations
Review

Blood and Cerebrospinal Fluid Biomarkers of Inflammation in Parkinson's Disease

Milan Zimmermann et al. J Parkinsons Dis. 2022.

Abstract

Given the clear role of inflammation in the pathogenesis of Parkinson's disease (PD) and its impact on incidence and phenotypical characteristics, this review provides an overview with focus on inflammatory biofluid markers in blood and cerebrospinal fluid (CSF) in PD patient cohorts. In preparation for clinical trials targeting the immune system, we specifically address the following questions: 1) What evidence do we have for pro-inflammatory profiles in blood and in CSF of sporadic and genetic PD patients? 2) Is there a role of anti-inflammatory mediators in blood/CSF? 3) Do inflammatory profiles in blood reflect those in CSF indicative of a cross-talk between periphery and brain? 4) Do blood/CSF inflammatory profiles change over the disease course as assessed in repeatedly taken biosamples? 5) Are blood/CSF inflammatory profiles associated with phenotypical trajectories in PD? 6) Are blood/CSF inflammatory profiles associated with CSF levels of neurodegenerative/PD-specific biomarkers? Knowledge on these questions will inform future strategies for patient stratification and cohort enrichment as well as suitable outcome measures for clinical trials.

Keywords: Parkinson’s disease; blood; cerebrospinal fluid; chemokine; cytokine; inflammation; interleukin.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Fig. 1
Fig. 1
Inflammatory markers in blood and CSF that are associated with clinical trajectories, disease progression, and neurodegenerative/disease-specific protein levels. In line with evidence from post-mortem and cell studies, blood and CSF levels of inflammatory markers indicate a contribution of the innate and adaptive immune system in both CNS and periphery. Of these, the most frequently reported inflammatory markers in blood and CSF that are associated with clinical trajectories, disease progression and neurodegenerative/disease-specific protein levels are IL-1β, IL-6, INF-γ, MCP-1 and TNF-α. Notably, inflammation is maximized in the early disease stages and maintains a chronic profile during the course of the disease. Figure created in BioRender.com.
See this image and copyright information in PMC

Comment in

References

    1. Nalls MA, Pankratz N, Lill CM, Do CB, Hernandez DG, Saad M, DeStefano AL, Kara E, Bras J, Sharma M, Schulte C, Keller MF, Arepalli S, Letson C, Edsall C, Stefansson H, Liu X, Pliner H, Lee JH, Cheng R; , International Parkinson’s Disease Genomics Consortium (IPDGC); Parkinson’s Study Group (PSG) Parkinson’s Research: The Organized GENetics Initiative (PROGENI); 23andMe; GenePD; NeuroGenetics Research Consortium (NGRC); Hussman Institute of Human Genomics (HIHG); Ashkenazi Jewish Dataset Investigator; Cohorts for Health and Aging Research in Genetic Epidemiology (CHARGE); North American Brain Expression Consortium (NABEC); United Kingdom Brain Expression Consortium (UKBEC); Greek Parkinson’s Disease Consortium; Alzheimer Genetic Analysis Group Ikram MA, Ioannidis JP, Hadjigeorgiou GM, Bis JC, Martinez M, Perlmutter JS, Goate A, Marder K, Fiske B, Sutherland M, Xiromerisiou G, Myers RH, Clark LN, Stefansson K, Hardy JA, Heutink P, Chen H, Wood NW, Houlden H, Payami H, Brice A, Scott WK, Gasser T, Bertram L, Eriksson N, Foroud T, Singleton AB (2014) Large-scale meta-analysis of genome-wide association data identifies six new risk loci for Parkinson’s disease. Nat Genet 46, 989–993. - PMC - PubMed
    1. Halliday GM, Stevens CH (2011) Glia: Initiators and progressors of pathology in Parkinson’s disease. Mov Disord 26, 6–17. - PubMed
    1. Williams-Gray CH, Wijeyekoon R, Yarnall AJ, Lawson RA, Breen DP, Evans JR, Cummins GA, Duncan GW, Khoo TK, Burn DJ, Barker RA, ICICLE-PD study group (2016) Serum immune markers and disease progression in an incident Parkinson’s disease cohort (ICICLE-PD). Mov Disord 31, 995–1003. - PMC - PubMed
    1. Witoelar A, Jansen IE, Wang Y, Desikan RS, Gibbs JR, Blauwendraat C, Thompson WK, Hernandez DG, Djurovic S, Schork AJ, Bettella F, Ellinghaus D, Franke A, Lie BA, McEvoy LK, Karlsen TH, Lesage S, Morris HR, Brice A, Wood NW, Heutink P, Hardy J, Singleton AB, Dale AM, Gasser T, Andreassen OA, Sharma M, International Parkinson’s Disease Genomics Consortium (IPDGC) North American Brain Expression Consortium (NABEC) and United Kingdom Brain Expression Consortium (UKBEC) Investigators (2017) Genome-wide pleiotropy between Parkinson disease and autoimmune diseases. JAMA Neurol 74, 780–792. - PMC - PubMed
    1. Caldi Gomes L, Galhoz A, Jain G, Roser AE, Maass F, Carboni E, Barski E, Lenz C, Lohmann K, Klein C, Bahr M, Fischer A, Menden MP, Lingor P (2022) Multi-omic landscaping of human midbrains identifies disease-relevant molecular targets and pathways in advanced-stage Parkinson’s disease. Clin Transl Med 12, e692. - PMC - PubMed

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