Neutrophil-to-lymphocyte ratio and lymphocyte count reflect alterations in central neurodegeneration-associated proteins and clinical severity in Parkinson Disease patients

神经退行性变 医学 淋巴细胞 帕金森病 免疫系统 免疫学 炎症 中性粒细胞与淋巴细胞比率 疾病 内科学
作者
Piergiorgio Grillo,Giulia Maria Sancesario,Roberta Bovenzi,Henri Zenuni,Jacopo Bissacco,Davide Mascioli,Clara Simonetta,Paolo Forti,Giulia Rebecca Degoli,Massimo Pieri,Valerio Chiurchiù,Alessandro Stefani,Nicola Biagio Mercuri,Tommaso Schirinzi
出处
期刊:Parkinsonism & Related Disorders [Elsevier BV]
卷期号:112: 105480-105480 被引量:13
标识
DOI:10.1016/j.parkreldis.2023.105480
摘要

Introduction Peripheral inflammation has been recently associated to Parkinson disease (PD). However, how the peripheral inflammatory immune response could affect the clinical-pathological features of the disease is not fully understood. In this study, we assessed the peripheral immune profile of a well-characterized PD cohort, examining several correlations with CSF biomarkers of neurodegeneration and the main clinical parameters, aimed at better elucidating the complex dynamics of the brain-periphery interactions in PD. Methods The leukocyte populations counts (neutrophils, lymphocytes, monocytes, eosinophils, and basophils) and the neutrophil-to-lymphocyte ratio (NLR) were collected and compared in 61 PD patients and 60 sex/age matched controls (CTRLs). Immune parameters were correlated with CSF levels of total α-synuclein, amyloid-β-42, total and phosphorylated-tau and main motor and non-motor scores. Results PD patients had lower lymphocyte and higher NLR counts compared to CTRLs. In PD patients, the lymphocyte count directly correlated with CSF α-synuclein levels, whereas NLR displayed an inverse correlation with the CSF amyloid-β42 levels. The lymphocyte count also negatively correlated with HY stage, while NLR positively with the disease duration. Conclusions This study provided in vivo evidence that, in PD, changes in leukocytes in the periphery, assessed as relative lymphopenia and NLR increase, reflects in central neurodegeneration-associated proteins modifications, especially in α-synuclein and amyloid-β pathways, and greater clinical burden.
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