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may respond to aggressive management with corticosteroids and immunosuppressants such as azathioprine, which are safely administered during pregnancy and lactation. Emerging safety data on monoclonal antibodies during pregnancy, make these attractive options, while intravenous immunoglobulin, plasma exchange and immunoadsorption can be safely used to treat severe relapses. The complex interplay between NMOSD and pregnancy outcomes would be best understood through prospective analysis of data collected through an international registry. Disclosure Dalia Rotstein has served as a consultant or speaker for Alexion and Roche. She has received research support from Roche Canada. Rohan D'Souza has served as a consultant and speaker for Ferring Canada Inc and Ferring Global Inc, on topics unrelated to this manuscript. The other authors have no relevant relationships to disclose.Small vessel disease (SVD) is associated with cognitive impairment in older age and be implicated in vascular dementia. Post-mortem studies show proliferation of activated microglia in the affected white matter. However, the role of inflammation in SVD pathogenesis is incompletely understood and better biomarkers are needed. We hypothesized that expression of the 18 kDa translocator protein (TSPO), a marker of microglial activation, would be higher in SVD. Positron emission tomography (PET) was performed with the second-generation TSPO ligand [11C]PBR28 in 11 participants with SVD. TSPO binding was evaluated by a two-tissue compartment model, with and without a vascular binding component, in white matter hyperintensities (WMH) and normal-appearing white matter (NAWM). In post-mortem tissue, in a separate cohort of individuals with SVD, immunohistochemistry was performed for TSPO and a pan-microglial marker Iba1. Kinetic modeling showed reduced tracer volume and blood volume fraction in WMH compared with NAWM, but a significant increase in vascular binding. Vascular [11C]PBR28 binding was also increased compared with normal-appearing white matter of healthy participants free of SVD. Immunohistochemistry showed a diffuse increase in microglial staining (with Iba1) in sampled tissue in SVD compared with control samples, but with only a subset of microglia staining positively for TSPO. Intense TSPO staining was observed in the vicinity of damaged small blood vessels, which included perivascular macrophages. The results suggest an altered phenotype of activated microglia, with reduced TSPO expression, in the areas of greatest white matter ischemia in SVD, with implications for the interpretation of TSPO PET studies in older individuals or those with vascular risk factors.Most blast-induced traumatic brain injuries (bTBI) are mild in severity and culpable for the lingering and persistent neuropsychological complaints in affected individuals. There is evidence that the prevalence of symptoms post-exposure may be sex-specific. Our laboratory has focused on changes in the monoamine and the neuropeptide, galanin, systems in male rodents following primary bTBI. In this study, we aimed to replicate these findings in female rodents. Trimethoprim price Brainstem sections from the locus coeruleus (LC) and dorsal raphe nuclei (DRN) were processed for in situ hybridisation at 1 and 7 days post-bTBI. We investigated changes in the transcripts for tyrosine hydroxylase (TH), tryptophan hydroxylase two (TPH2) and galanin. Like in males, we found a transient increase in TH transcript levels bilaterally in the female LC. Changes in TPH2 mRNA were more pronounced and extensive in the DRN of females compared to males. Galanin mRNA was increased bilaterally in the LC and DRN, although this increase was not apparent until day 7 in the LC. Serum analysis revealed an increase in corticosterone, but only in exposed females. These changes occurred without any visible signs of white matter injury, cell death, or blood-brain barrier breakdown. Taken together, in the apparent absence of visible structural damage to the brain, the monoamine and galanin systems, two key players in emotional regulation, are activated deferentially in males and females following primary blast exposure. These similarities and differences should be considered when developing and evaluating diagnostic and therapeutic interventions for bTBI.Objective This review summarizes recent findings on the epigenetics of Alzheimer's disease (AD) and provides therapeutic strategies for AD. Methods We searched the following keywords "genetics," "epigenetics," "Alzheimer's disease," "DNA methylation," "DNA hydroxymethylation," "histone modifications," "non-coding RNAs," and "therapeutic strategies" in PubMed. Results In this review, we summarizes recent studies of epigenetics in AD, including DNA methylation/hydroxymethylation, histone modifications, and non-coding RNAs. There are no consistent results of global DNA methylation/hydroxymethylation in AD. Epigenetic genome-wide association studies show that many differentially methylated sites exist in AD. Several studies investigate the role of histone modifications in AD; for example, histone acetylation decreases, whereas H3 phosphorylation increases significantly in AD. In addition, non-coding RNAs, such as microRNA-16 and BACE1-antisense transcript (BACE1-AS), are associated with the pathology of AD. These epigenetic changes provide us with novel insights into the pathogenesis of AD and may be potential therapeutic strategies for AD. Conclusion Epigenetics is associated with the pathogenesis of AD, including DNA methylation/hydroxymethylation, histone modifications, and non-coding RNAs, which provide potential therapeutic strategies for AD.Objective To conduct an investigation into the reliability of assessing the olfactory function of patients with Parkinson's disease (PD) in a clinical setting of crowding patients in populated countries, such as China, by the hyposmia rating scale (HRS) and compare other non-motor features between patients with PD with olfactory dysfunction (PD-OD) and patients with PD without olfactory dysfunction (PD-NOD), according to the result of olfactory function assessed by the Sniffin' Sticks test. Methods A total of 320 patients with clinically confirmed or clinically possible PD were recruited. Olfactory function of all participants was assessed with the HRS and the Sniffin' Sticks test. Demographic data and clinical information were collected, and patients were evaluated using standardized assessment protocols. With reference to the Sniffin' Sticks test, the specificity, sensitivity, coincidence rate, and kappa value of the HRS was computed, and then its reliability was evaluated. We divided patients into PD-OD and PD-NOD groups based on the results of olfactory function assessed by the Sniffin' Sticks test.