Objectives: Restless legs syndrome (RLS) can lead to severe clinical consequences, thus negatively impacts on patients’ overall health and quality of life. Nevertheless, the pathophysiology of RLS is still unclear, resulting in underestimate, incorrect, or ignored diagnosis and in limited management and treatment. The aim of this study was to compare the plasma proteome of RLS patients and healthy controls, in the search of diagnostic biomarkers related to the disease severity.Materials and Methods: Two‐dimensional gel electrophoresis coupled with liquid chromatography‐mass spectrometry was employed to analyze plasma samples of 34 patients with primary RLS, divided into two subgroups according to the disease severity: MMS group (mild‐moderate symptoms) and HS group (severe and very severe symptoms), and 17 age‐ and sex‐matched control subjects. Sleep quality, daytime sleepiness, and the level of depression were also evaluated.Results: We identified eight upregulated spots, corresponding to five unique proteins, in both RLS group vs. controls (alpha‐1B‐glycoprotein, alpha‐1‐acid glycoprotein 1, haptoglobin, complement C4‐A, and immunoglobulin kappa constant); five increased spots, consistent with three unique proteins, only in HS‐RLS (kininogen‐1, immunoglobulin heavy constant alpha 1, and immunoglobulin lambda constant 2); one downregulated spot in both patient's groups (complement C3) and another one only in HS‐RLS (alpha‐1‐antitrypsin).Conclusions: The significantly different plasma proteins detected in RLS were mainly associated with inflammation, immune response, and cardiovascular disorders. Particularly, the gradual increasing in immunoglobulins could be indicative of the disease severity and evolution. Accordingly, these proteins may represent a valid set of useful biomarkers for RLS diagnosis, progression and treatment.

Background Multiple sclerosis (MS) is a neuroinflammatory disease and inflammation and oxidative stress play important roles in its pathology. Thiol/disulphide homeostasis (TDH) is a special oxidative stress biomarker that has been found to be affected in several disorders including MS. There is no study demonstrating the effects of attack status of the relapsing‐remitting multiple sclerosis (RRMS) patients on TDH levels. Our aim was to determine TDH levels in three different periods of RRMS patients and healthy individuals. Methods The study was carried out in 29 patients with RRMS without a prior attack in the last twelve months (MS Control), 21 RRMS patients having a clinical acute attack within the last week (MS relapse), 12 of 21 MS relapse patients one month after the onset of attack and following 1000 mg methylprednisolone for 7 days (MS Remission) and 30 age‐ and sex‐matched healthy individuals. TDH status was determined using an automated spectrophotometric analysis method. TDH levels in all patient groups and control subjects were compared with each other. Results The lowest native thiol, total thiol levels and native thiol/total thiol ratio were found in the MS relapse patients in comparison to the MS control, MS remission groups and healthy controls. In contrast, disulphide levels, disulphide/native thiol and disulphide/total thiol ratios were highest in the MS relapse group compared to the other patient groups and healthy subjects. Conclusion Our findings indicate that increased oxidative stress in RRMS patients is reflected with decreased native and total thiol and increased disulphide levels. Since the formation of disulphide bonds is reversible, the progression of RRMS involving abnormal TDH may be controlled, converting disulphides to thiols. So, we suggest determining the dynamic TDH status as a novel and special biomarker in the diagnosis and prognosis of the RRMS patients.

Parkinson's disease (PD) is a neurodegenerative condition marked by the gradual depletion of dopaminergic neurons in the substantia nigra. Despite substantial strides in comprehending potential causative mechanisms, the validation of biomarkers with unequivocal evidence for routine clinical application remains elusive. Consequently, the diagnosis heavily relies on patients' clinical assessments and medical backgrounds. The imperative need for diagnostic and prognostic biomarkers arises due to the prevailing limitations of treatments, which predominantly address symptoms without modifying the disease course. This comprehensive review aims to elucidate the existing landscape of diagnostic and prognostic biomarkers for PD, drawing insights from contemporary literature.