We evaluated the in silico expression and circulating levels of interleukin (IL)37 in patients with different forms of multiple sclerosis (MS) and also upon treatment with different disease-modifying drugs. The combined interpretation of the resulting data strengthens and extends the current emerging concept that endogenous IL37 plays an important role in determining onset and progression of MS. The in silico analysis revealed that production of IL37 from cluster of differentiation (CD)4+ T cells from MS patients was reduced in vitro as compared to healthy controls. The analysis of the datasets also demonstrated that “higher” levels of IL37 production from PBMC entailed significant protection from MS relapses. In addition, the in vivo part of the study showed that IL37 was selectively augmented in the sera of MS patients during a relapse and that treatment with the high potency disease-modifying drug fingolimod significantly increased the frequency of patients with circulating blood levels of IL37 (6/9, 66%) as compared to patients receiving no treatment (n = 48) or platform therapy (n = 59) who had levels of IL37 below the limit of the sensitivity of the assay. This finding therefore anticipates that fingolimod may at least partially exert its beneficial effects in MS by upregulating the production of IL37.

One aspect marginally analysed in the diagnostic work-up of patients with clinically isolated syndrome (CIS) is the role of intracortical lesions (ICLs), which are a prominent feature of MS and contribute to disability and cognitive impairment.2 A single-centre study3 showed that inclusion of ICL for the evaluation of DIS in CIS increased the accuracy of MRI diagnostic criteria, with an improvement of specificity.3

Objective: Since astrocytes at the blood–brain barrier are targeted by neuromyelitis optica spectrum disorder (NMOSD), this study aims to assess whether patients with NMOSD have a subclinical accumulation of brain water and if it differs according to disease activity.Methods: Seventy-seven aquaporin-4-positive patients with NMOSD and 105 healthy controls were enrolled at two European centres. Brain dual-echo turbo spin-echo MR images were evaluated and maps of T2 relaxation time (T2rt) in the normal-appearing white matter (NAWM), grey matter and basal ganglia were obtained. Patients with a clinical relapse within 1 month before or after MRI acquisition were defined ‘active’. Differences between patients and controls were assessed using z-scores of T2rt obtained with age-adjusted and sex-adjusted linear models from each site. A stepwise binary logistic regression was run on clinical and MRI variables to identify independent predictors of disease activity.Results: Patients had increased T2rt in both white and grey matter structures (p range: 0.014 to <0.0001). Twenty patients with NMOSD were defined active. Despite similar clinical and MRI features, active patients had a significantly increased T2rt in the NAWM and grey matter compared with those clinically stable (p range: 0.010–0.002). The stepwise binary logistic regression selected the NAWM as independently associated with disease activity (beta=2.06, SE=0.58, Nagelkerke R²=0.46, p<0.001).Conclusions: In line with the research hypothesis, patients with NMOSD have increased brain T2rt. The magnitude of this alteration might be useful for identifying those patients with active disease.

Background: The aetiology of multiple sclerosis (MS) is unclear, but numerous studies suggest that differentexogenous factors can lead to the development of the disease in genetically susceptible individuals. Theobjective of this case-control study was to determine the role of food and dietary patterns in patients with MSin the population of Belgrade (Serbia).Methods: In this matched case-control study, we included 110 cases with definite MS according to McDonald’scriteria, in whom the onset symptoms occurred up to 2 years prior to the interview, who were followed-up atthe Institute of Neurology, Clinical Centre of Serbia, Belgrade. The identical number of controls from the sameinstitution, individually matched by sex, age and area of residence, was recruited from patients with variousnon-autoimmune neurological disorders. Dietary information was obtained by using a frequency historyapproach.Results: According to univariate conditional logistic regression analysis the following factors weresignificantly related to MS: body mass index (BMI) less than 25 (OR=2.2, p=0.009), frequent consumption ofbeef (OR=1.7, p=0.043), chicken (OR=2.0, p=0.045), meat of the lamb (OR=2.1, p=0.013), butter (OR=1.7,p=0.056) and ice-cream (OR=1.8, p=0.031), with dose-response relationship. Consumption of majority ofvarious fruit was more frequently reported by controls. According to multivariate conditional logisticregression analysis, BMI less than 25 (OR=2.3, p=0.008), consumption (weekly) of beef (OR=2.0, p=0.017)and butter (OR=1.9, p=0.027) was significantly related to MS, while regular consumption of cherry (OR=0.4,p=0.024) had protective role.Conclusions: This study might assist in potential defining of the dietary factors that could contribute to therisk of developing MS

Leber’s hereditary optic neuropathy (LHON) is a maternally inherited disorder that affects central vision in young adults and is typically associated with mitochondrial DNA (mtDNA) mutations. This study is based on a mutational screening of entire mtDNA in eight Serbian probands clinically and genetically diagnosed with LHON and four of their family members, who are asymptomatic mutation carriers. All obtained sequence variants were compared to human mtDNA databases, and their potential pathogenic characteristics were assessed by bioinformatics tools. Mitochondrial haplogroup analysis was performed by MITOMASTER. Our study revealed two well-known primary LHON mutations, m.11778G>A and m.3460G>A, and one rare LHON mutation, m.8836A>G. Various secondary mutations were detected in association with the primary mutations. MITOMASTER analysis showed that the two well-known primary mutations belong to the R haplogroup, while the rare LHON m.8836A>G was detected within the N1b haplogroup. Our results support the need for further studies of genetic background and its role in the penetrance and severity of LHON.