Increased YKL-40 but Not C-Reactive Protein Levels in Patients with Alzheimer's Disease.

Víctor Antonio Blanco-Palmero,Fernando Bartolome,Isidro Ferrer,Eva Carro,Marcos Rubio-Fernández,Desireé Antequera,Alberto Villarejo-Galende,José Antonio Molina

doi:10.3390/biomedicines9091094

Abstract

Neuroinflammation is a common feature in Alzheimer’s (AD) and Parkinson’s (PD) disease. In the last few decades, a testable hypothesis was proposed that protein-unfolding events might occur due to neuroinflammatory cascades involving alterations in the crosstalk between glial cells and neurons. Here, we tried to clarify the pattern of two of the most promising biomarkers of neuroinflammation in cerebrospinal fluid (CSF) in AD and PD. This study included cognitively unimpaired elderly patients, patients with mild cognitive impairment, patients with AD dementia, and patients with PD. CSF samples were analyzed for YKL-40 and C-reactive protein (CRP). We found that CSF YKL-40 levels were significantly increased only in dementia stages of AD. Additionally, increased YKL-40 levels were found in the cerebral orbitofrontal cortex from AD patients in agreement with augmented astrogliosis. Our study confirms that these biomarkers of neuroinflammation are differently detected in CSF from AD and PD patients.

Highlights

IntroductionPublisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations
A total of 34 subjects were clinically diagnosed with AD, 22 subjects were grouped as mild cognitive impairment (MCI), and 30 subjects were diagnosed with PD
Female sex was overrepresented in the AD and MCI groups, while males represented around 60% of controls and PD subjects

Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Neuroinflammation is widely accepted as a pathological hallmark of Alzheimer’s (AD) [1,2] and Parkinson’s (PD) [3,4,5] disease. Several damage signals appear to induce neuroinflammation, including β-amyloid (Aβ) oligomers, tau, and α-synuclein (α-syn), mediated by the progressive astrocyte and microglial cell activation with the consequent overproduction of proinflammatory agents that may leak toward cerebrospinal fluid (CSF) [6]. Despite the analysis of these agents in CSF being a tempting topic to study, levels of inflammatory markers in CSF from AD and PD patients have not been sufficiently investigated

Methods

Results

Conclusion