Neutrophil-to-lymphocyte ratio and lymphocyte count reflect alterations in central neurodegeneration-associated proteins and clinical severity in Parkinson Disease patients
Blood cell count
Settore BIOS-09/A - Biochimica clinica e biologia molecolare clinica
Amyloid beta-Peptides
Neutrophils
610
Parkinson Disease
tau Proteins
3. Good health
Lymphocytes count
Alpha-synuclein
Cerebrospinal fluid
alpha-Synuclein
Humans
Lymphocytes
Lymphocyte Count
Amyloid-beta
Neutrophil-to-lymphocyte ratio
Biomarkers
DOI:
10.1016/j.parkreldis.2023.105480
Publication Date:
2023-06-04T05:25:16Z
AUTHORS (14)
ABSTRACT
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.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.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.This study provided in vivo evidence that, in PD, changes in leukocytes in the periphery, assessed as relative lymphopenia and NLR increase, reflect in central neurodegeneration-associated proteins modifications, especially in α-synuclein and amyloid-β pathways, and greater clinical burden.
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CITATIONS (21)
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