Abstract
Guillain-Barré syndrome (GBS) is an autoimmune-mediated peripheral neuropathy of unknown cause. However, about a quarter of GBS patients have suffered a recent bacterial or viral infection, and axonal forms of the disease are especially common in these patients. Proteomics is a good methodological approach for the discovery of disease biomarkers. Until recently, most proteomics studies of GBS and other neurodegenerative diseases have focused on the analysis of the cerebrospinal fluid (CSF). However, serum represents an attractive alternative to CSF because it is easier to sample and has potential for biomarker discovery. The goal of this research was the identification of serum biomarkers associated with recovery from GBS. To address this objective, a quantitative proteomics approach was used to characterize differences in the serum proteome between a GBS patient and her healthy identical twin in order to lessen variations due to differences in genetic background, and with additional serum samples collected from unrelated GBS (N = 3) and Spinal Cord Injury (SCI) (N = 3) patients with similar medications. Proteomics results were then validated by ELISA using sera from additional GBS patients (N = 5) and healthy individuals (N = 3). All GBS and SCI patients were recovering from the acute phase of the disease. The results showed that Piccolo, a protein that is essential in the maintenance of active zone structure, constitutes a potential serological correlate of recovery from GBS. These results provided the first evidence for the Piccolo's putative role in GBS, suggesting a candidate target for developing a serological marker of disease recovery.
Highlights
Guillain-Barré syndrome (GBS) is an immunemediated peripheral neuropathy that has been identified as the main cause of the acute neuromuscular paralysis, with an annual incidence ranging from 0.81 to 1.89 cases per 100.000 people [1, 2]
These results identified new biomarkers associated with GBS recovery and suggested that early growth response gene-2 (EGR2) over-expression has a pivotal role in the down-regulation of cytokines implicated in the pathophysiology of this acute neuropathy [18]
Most proteomics studies of GBS and other neurodegenerative diseases such as multiple sclerosis have focused on the analysis of the cerebrospinal fluid (CSF) [19,20,21, 23]
Summary
Guillain-Barré syndrome (GBS) is an immunemediated peripheral neuropathy that has been identified as the main cause of the acute neuromuscular paralysis, with an annual incidence ranging from 0.81 to 1.89 cases per 100.000 people [1, 2]. GBS is considered to be an autoimmune disease with the involvement of both cellular and humoral immune responses [2], the precise cause of the syndrome is unknown [2, 5,6,7,8,9]. About a quarter of patients with GBS have suffered a recent bacterial or viral infection, and axonal forms of the disease are especially common in these patients [2, 10,11,12,13,14]. Recent results point at pathogen-derived proteins as triggers of molecular mimicry involved in the GBS [15,16,17]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
