We detected overexpression of four miRNAs that have not been previously associated with progressive forms of MS. The increased expression of circulating miR-191-5p seems to be associated with progressive forms of MS, while miR-128-3p seems to be associated mostly with PPMS.
This study highlighted the connection of circulating miRNAs to MS. miR-24-3p and miR-128-3p showed a tendency of association with disability accumulation and disease activity, respectively. Further studies should evaluate their suitability for clinical use.
Parkinson's disease (PD) is a neurodegenerative disorder characterized by motor and non-motor symptoms and the selective loss of dopaminergic neurons. The etiology of idiopathic PD is likely a combination of genetic and environmental factors. Despite findings from mammalian studies that have provided significant insight into the disorder, the molecular mechanisms underlying its pathophysiology are still poorly understood. The nematode Caenorhabditis elegans (C. elegans) is a powerful system for genetic analysis. Considering C. elegans short lifespan, fully sequenced genome, high genetic and neurobiochemical conservation with humans, as well as the availability of facile genetic tools, the nematode represents a highly efficient and effective model system to explore the molecular basis of PD. In this review we describe the utility of C. elegans for PD research, and the opportunity the model system presents to identify therapeutic targets.
Objective The activation of autoreactive T cells is a major event in the initiation of autoimmune responses in multiple sclerosis (MS). In addition to the T cell receptor stimulation, optimal activation of T cells requires various costimulatory molecules, such as CD26 and CD30, which has not been extensively studied in MS. Our aim was to explore whether the circulating levels of CD26 and CD30 in sera are associated with MS subtypes, inflammatory disease activity and disability in MS patients. Methods The study included 195 participants: 39 relapsing-remitting MS patients, 19 secondary-progressive MS patients, 19 clinically isolated syndrome patients, 58 controls for sCD26 analysis and 60 for sCD30 analysis. The levels of sCD26 and sCD30 in sera were analyzed using enzyme-linked immunosorbent assay, and the levels of interleukin-10, tumor necrosis factor-a and interferon-c were analyzed with the Luminex assay. Results We observed increased levels of sCD26 and sCD30 in relapsingremitting MS, secondary-progressive MS, and clinically isolated syndrome patients compared with the controls (P < 0.05). Furthermore, elevated levels of sCD30 were noticed in treated relapsing-remitting MS patients than in untreated patients (P = 0.016), and also in converted CIS patients than in unconverted patients (P = 0.009). Although sCD26 and sCD30 could not associate with clinical measures, such as the disability score or disease activity, the levels of sCD30 correlated positively with interleukin-10 levels (r = 0.583, P < 0.0001) and sCD26 levels (r = 0.262, P = 0.046) in MS patients. Conclusion The present results suggest that the elevated levels of sCD30 are associated with the regulatory immune responses predisposing to clinically stable phase of MS.
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