Robust motifs in 2-phenylethylammonium and related tetrahalometallates

The novel crystal structures of seven compounds which combine 2-phenylethylammonium cations and perhalometallate anions, all with the general formula (C8H9NH3 +)2 MX4 2 , were determined to establish the effect of metal atom and halogen ligand substitution on the structures and hydrogen bonding interactions. Five of the structures, bis(2-phenylethylammonium) tetrachlorozincate, (C8H9NH3 +)2 ZnCl4 2 , bis(2-phenylethylammonium) tetraiodozincate, (C8H9NH3 +)2 ZnI4 2 , bis(2- phenylethylammonium) tetrabromodichloroiodozincate, (C8H9NH3 +)2 ZnCl2BrI2 , bis(2- phenylethylammonium) tetrabromocadmate, (C8H9NH3 +)2 CdBr4 2 , and bis(2- phenylethylammonium) tetrabromomercurate, (C8H9NH3 +)2 HgBr4 2 , were found to be isostructural, while two of the compounds containing iodo ligands, bis(2-phenylethylammonium) tetraiodocadmate, (C8H9NH3 +)2 CdI4 2 , and bis(2-phenylethylammonium) tetraiodomercurate, (C8H9NH3 +)2 HgI4 2 , crystallize in a different, but related disordered structure. Strong N+–H/X –M hydrogen bonding interactions, as well as weaker C–H/p aromatic interactions occur in all seven structures, and two robust tetrameric hydrogen bonded zero-dimensional motifs are present in all seven structures. C–H/ Cl–M hydrogen bonding interactions are present in the structure of bis(2-phenylethylammonium) tetrachlorozincate, and result in the distortion of the geometry of the 2-phenylethylammonium cation. Comparison of the identified zero-dimensional hydrogen bonding motifs with those occurring in related structures reported in the literature shows that the motifs are robust and can tolerate changes in cation, metal and ligand to a large extent.www.rsc.org/crystengcom

Anti-MOG Positive Bilateral Optic Neuritis and Brainstem Encephalitis Secondary to COVID-19 Infection: A Case Report

(1) Introduction: There have been numerous reports on the neuroinvasive competence of SARS-CoV-2. Here, we present a case with anti-MOG positive bilateral optic neuritis and brainstem encephalitis secondary to COVID-19 infection. Additionally, we present a review of the current literature regarding the manifestation of anti-MOG positive optic neuritis as well as anti-MOG positive encephalitis after COVID-19 infection. (2) Case Report: A 59-year-old female patient, with a recent history of COVID-19 infection, presented a progressive reduction of visual acuity and bilateral retrobulbar pain for the last 20 days. An ophthalmological examination revealed a decreased visual acuity (counting fingers) and a bilateral papilledema. An MRI scan of the brain revealed a mild thickening of the bilateral optic nerves and high-intensity lesions in the medial and right lateral pons. A high titer of IgG and IgM antibodies against SARS-CoV-2 in serum and antibodies against myelin oligodendrocyte glycoprotein (anti-MOG) in serum and CSF were revealed. The diagnosis of anti-MOG brainstem encephalitis and optic neuritis was set. (3) Conclusions: The history of COVID-19 infection should raise awareness about these autoimmune and infection-triggered diseases, such as anti-MOG antibody disease

Multiple Sclerosis: Shall We Target CD33?

Background: Multiple sclerosis (MS) is a chronic disease of the central nervous system (CNS). Myeloid lineage cells (microglia and macrophages) may participate in the pathogenic mechanisms leading to MS. CD33 is a transmembrane receptor, mainly expressed by myeloid lineage cells. CD33 rs3865444 is a promoter variant previously associated with Alzheimer’s disease, whose role in MS remains obscure. Objective: To assess the role of CD33 rs3865444 in MS risk. Methods: We genotyped 1396 patients with MS and 400 healthy controls for the presence of the CD33 rs3865444 variant. Odds ratios (ORs) with the respective 95% confidence intervals (CIs), were calculated with the SNPStats software, assuming five genetic models (co-dominant, dominant, recessive, over-dominant, and log-additive), with the G allele as the reference allele. The value of 0.05 was set as the threshold for statistical significance. Results: CD33 rs3865444 was associated with MS risk in the dominant (GG vs. GT + TT; OR (95% C.I.) = 0.79 (0.63–0.99), p = 0.041) and the over-dominant (GG + TT vs. GT; OR (95% C.I.) = 0.77 (0.61–0.97), p = 0.03) modes of inheritance. Given that the GG genotype was more frequent and the GT genotype was less frequent in MS patients compared to controls—while the observed frequency of the TT genotype did not differ between the two groups—the observed difference in MS risk may be stemming from either the GG (as a risk factor) or the GT (as a protective factor) genotype of CD33 rs3865444. Conclusions: Our preliminary results suggest a possible contribution of CD33 rs3865444 to MS. Therefore, larger multiethnic studies should be conducted, investigating the role of CD33 rs3865444 in MS

Thinking Outside the Ischemia Box: Advancements in the Use of Multiple Sclerosis Drugs in Ischemic Stroke

Ischemic stroke (IS) is a major cause of death and disability, despite early intervention. Thrombo-inflammation, the inflammatory process triggered by ischemia, is a concept that ties IS with multiple sclerosis (MS), under the wider ‘umbrella’ of neuroinflammation, i.e., the inflammation of the nervous tissue. Drawing from this, numerous studies have explored the potential of MS disease-modifying drugs in the setting of IS. In this review, we present the available studies and discuss their potential in ameliorating IS outcomes. Based on our search, the vast majority of the studies have been conducted on animals, yielding mostly positive results. Two clinical trials involving natalizumab showed that it does not confer any benefits, but four human studies regarding fingolimod have showcased its potential in improving recovery prospects. However, concerns on safety and other issues are raised, and basic questions still need to be answered

Brain atrophy in multiple sclerosis: mechanisms, clinical relevance and treatment options

Multiple sclerosis (MS) is an immune-mediated disease of the central nervous system characterized by focal or diffuse inflammation, demyelination, axonal loss and neurodegeneration. Brain atrophy can be seen in the earliest stages of MS, progresses faster compared to healthy adults, and is a reliable predictor of future physical and cognitive disability. In addition, it is widely accepted to be a valid, sensitive and reproducible measure of neurodegeneration in MS. Reducing the rate of brain atrophy has only recently been incorporated as a critical endpoint into the clinical trials of new or emerging disease modifying drugs (DMDs) in MS. With the advent of easily accessible neuroimaging softwares along with the accumulating evidence, clinicians may be able to use brain atrophy measures in their everyday clinical practice to monitor disease course and response to DMDs. In this review, we will describe the different mechanisms contributing to brain atrophy, their clinical relevance on disease presentation and course and the effect of current or emergent DMDs on brain atrophy and neuroprotection