To develop, apply and assess screening criteria for extended diagnostic workup in MS patients for improved detection of alternative disease cause.

Objective To determine the prevalence of antibodies to Epstein-Barr virus (EBV) in a large cohort of patients with early multiple sclerosis (MS). Methods Serum samples were collected from 901 patients with a clinically isolated syndrome (CIS) or early relapsing–remitting multiple sclerosis (RRMS) participating in the German National MS cohort, a prospective cohort of patients with early MS with stringent inclusion criteria. Epstein-Barr nuclear antigen (EBNA)-1 and viral capsid antigen (VCA) antibodies were measured in diluted sera by chemiluminescence immunoassays (CLIAs). Sera of EBNA-1 and VCA antibody-negative patients were retested undiluted by an EBV IgG immunoblot. For comparison, we retrospectively analysed the EBV seroprevalence across different age cohorts, ranging from 0 to >80 years, in a large hospital population (N=16 163) from Berlin/Northern Germany. Results EBNA-1 antibodies were detected by CLIA in 839 of 901 patients with CIS/RRMS. Of the 62 patients without EBNA-1 antibodies, 45 had antibodies to VCA as detected by CLIA. In all of the remaining 17 patients, antibodies to EBV were detected by immunoblot. Altogether, 901 of 901 (100%) patients with CIS/RRMS were EBV-seropositive. EBV seropositivity increased with age in the hospital population but did not reach 100% in any of the investigated age cohorts. Conclusion The complete EBV seropositivity in this large cohort of patients with early MS strengthens the evidence for a role of EBV in MS. It also suggests that a negative EBV serology in patients with suspected inflammatory central nervous system disease should alert clinicians to consider diagnoses other than MS.

Leukodystrophien (LDs) sind eine Gruppe seltener, genetisch bedingter Stoffwechselkrankheiten, bei welchen es durch Myelinisierungsstörungen/Demyelinisierung zum Schwund an weißer Hirnsubstanz (WM) kommt. Wir konnten jüngst zeigen, dass der Amyloid-PET-Tracer [18F]Florbetaben, welcher neben dem eigentlichen Target auch an Myelin bindet, großes Potential zur verbesserten Bildgebung von WM-Erkrankungen besitzt. Das Ziel dieser aktuellen Pilotstudie war, die Eignung der Hybrid-[18F]Florbetaben-PET/MRT (mMR Siemens) speziell bei LDs erstmals zu testen.

Objectives: Cardioplegic solutions undergo constant improvement to reduce ischemia/reperfusion injury (IRI) during cardiac surgery. Addition of antioxidants in the Custodiol N solution or of low-dose cyclosporine A (CsA), an inhibitor of the mitochondrial transition pore, diminishes IRI in cardiac tissue, but effects on other organs are often neglected. Therefore, we investigated the effects of substances added to cardioplegic solutions on the brain.

A polymorphism in the promoter region of the human serotonin transporter (5-HTT)-coding SLC6A4 gene (5-HTTLPR) has been implicated in moderating susceptibility to stress-related psychopathology and to possess regulatory functions on human in vivo 5-HTT availability. However, data on a direct relation between 5-HTTLPR and in vivo 5-HTT availability have been inconsistent. Additional factors such as epigenetic modifications of 5-HTTLPR might contribute to this association. This is of particular interest in the context of obesity, as an association with 5-HTTLPR hypermethylation has previously been reported. Here, we tested the hypothesis that methylation rates of 14 cytosine–phosphate–guanine (CpG) 5-HTTLPR loci, in vivo central 5-HTT availability as measured with [11C]DASB positron emission tomography (PET) and body mass index (BMI) are related in a group of 30 obese (age: 36±10 years, BMI>35 kg/m2) and 14 normal-weight controls (age 36±7 years, BMI<25 kg/m2). No significant association between 5-HTTLPR methylation and BMI overall was found. However, site-specific elevations in 5-HTTLPR methylation rates were significantly associated with lower 5-HTT availability in regions of the prefrontal cortex (PFC) specifically within the obese group when analyzed in isolation. This association was independent of functional 5-HTTLPR allelic variation. In addition, negative correlative data showed that CpG10-associated 5-HTT availability determines levels of reward sensitivity in obesity. Together, our findings suggest that epigenetic mechanisms rather than 5-HTTLPR alone influence in vivo 5-HTT availability, predominantly in regions having a critical role in reward processing, and this might have an impact on the progression of the obese phenotype.

Free accessAbstractFirst published online April 1, 2017The Niels Lassen Award Session and Oral SessionsVolume 37, Issue 1_supplhttps://doi.org/10.1177/0271678X17695978