YKL-40 and the Cellular Metabolic Profile in Parkinson's Disease.

Parkinson's disease (PD) is the second most common neurodegenerative disease worldwide. A growing body of evidence suggests that mitochondrial dysfunction and inflammation play a crucial role as a pathogenetic mechanism in PD. The glycoprotein YKL-40 (CHI3L1) is a potential biomarker involved in inflammation and tumor processes. The aim of the present study was to investigate the metabolic profile of PBMCs from PD patients and to search for a possible relationship between cellular bioenergetics and YKL-40. The study included 18 naïve PD patients and an age-matched control group (HC, n = 7). Patients were diagnosed according to the MDS-PD, the UPDRS, and the Hoen-Yahr scales. Mitochondrial activity was measured by a metabolic analyzer on isolated PBMCs from PD patients. Gene (qPCR) and protein (ELISA) expression levels of YKL40 were investigated. New data are reported revealing changes in the mitochondrial activity and YKL-40 levels in PD patients. Bioenergetic parameters showed increased respiratory reserve capacity in PD compared to HC. The protein levels of YKL-40 were threefold higher in PD. We found a correlation between the YKL-40 protein levels and basal respiration and between YKL-40 and ATP production. These observations suggest an interplay between YKL-40 and mitochondrial function in PD. We assume that the YKL-40 gene and protein levels in combination with changes in mitochondrial function might serve as an additional tool to monitor the clinical course of PD.

Neuromyelitis Optica and Systemic Lupus Erythematosus Association ­ the Chicken or the Egg Dilemma: a Case Repor.

We present a case report of a 32-year-old woman diagnosed with opticomyelitis of Devic (OMD) and systemic lupus erythematosus (SLE). The onset of neurological symptoms was with optic neuritis. Five months later the neurological deficit progressed within a few days to lower paraplegia and upper paraparesis, retention of urine and faeces, impaired somatic and deep sensation below the level of Th1 dermatome. The results from laboratory investigations confirmed anaemic syndrome, increased urea and creatinine, hypoproteinemia and severe proteinuria. The results from CSF investigations demonstrated hyperproteinorachia with extremely high Ig fractions. Serum and CSF oligoclonal bands and positive serum Aquaporin IgG 32 times higher than the upper referent limit were found. The association with SLE was confirmed by the increased levels of total ANA and anti-ds-DNA ANA. MRT visualized the spinal cord as non-homogenously hypointense on T1 and extremely hyperintense on FLAIR sequences through its whole length up to the bulbar-pontine region. The MRT findings and the serum Aquaporin IgG confirmed the diagnosis OMD. The patient was treated with intravenous immunomodulating agents. We consider the presented case of special interest because of the comorbidity of an aggressive autoimmune systemic and an organ-specific disease of the central nervous system.

25 Hydroxyvitamin D and Cytokines in Multiple Sclerosis.

INTRODUCTION: Clinical trials of patients with multiple sclerosis (MS) have produced inconsistent results for the profile of cytokine secretion in serum and cerebrospinal fluid in patients with multiple sclerosis during periods of relapse and remission. Epidemiological and clinical observations data reveal an association of the changes in vitamin D serum concentration with the risk of developing MS. AIM: To evaluate changes in serum concentrations of 25(OH)D, IL17, IFN-gamma, TGFß1, IL4, IL10 in relapse and remission and their correlation with the severity of disability. PATIENTS AND METHODS: Fifty-three persons (30 clinically healthy controls and 23 patients with relapsing-remitting multiple sclerosis) living between 41° and 42° northern latitude were registered during the astronomical winter period (October 2012- May 2013). -Patients were diagnosed according to Mc Donald 2010 criteria. The degree of neurological deficit was assessed by EDSS. Serum concentrations of 25(OH)D (nmol/l) and cytokines (pg/ml) were tested by ELISA - once for controls and twice for patients (during relapse and remission). RESULTS: In the studied population average levels of 25(OH)D were close to insufficiency, most pronounced in patients in relapse, as differences were not statistically significant. A reverse correlation was found between the levels of 25(OH)D and the deficit in relapse and remission. Concentrations of TGFß1 significantly increased in remission compared with exacerbation and controls. Serum level of IL4 was significantly lower in relapse compared with controls. In remission there was a marked tendency of increase compared with exacerbation. During clinical improvement IL17 and IFN-gamma tended to decrease compared to the average levels in relapse. In both periods, the average concentrations of IFN-gamma in patients were significantly lower compared with controls. No statistically significant differences were found comparing cytokine changes with those of 25(OH)D and deficit. CONCLUSION: Persistent cytokine imbalance in patients compared with controls is a marker for Th1-mediated CNS demyelination. Anti-inflammatory TGFß1, IL4 are indicators of immune response intensity. The deficit severity does not depend on changes of the tested cytokines, but correlates with 25(OH)D levels during periods of relapse and remission.

Female sex hormones and multiple sclerosis.

Multiple sclerosis is the most frequent debilitating neurological disease in young subjects. The autoimmune process predominantly affects females. This paper presents a review of experimental and clinical data about the effect of female sex hormones and conditions associated with hormonal alterations on the disease process. Specific consideration is given to the use of estrogens as a remedy influencing the disease course. There haven't been enough studies to indicate presence of either hormonal disbalance in females with multiple sclerosis or peculiarities in the hormone-cytokine profile during disease relapse and remission. Further investigations in this area are needed to provide more profound knowledge of the pathogenesis of this socially significant disease.