Increased Intracranial Pressure in Myelin-Oligodendrocyte Glycoprotein Antibody-Associated Disease.

Objectives: To assess characteristics of increased intracranial pressure (ICP) in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).

Methods: This is a multicenter retrospective review of 84 MOGAD cases at the University of Florida, Baylor College of Medicine, the University of California San Diego, and Providence Health and Services, Portland, Oregon, to identify cases with a documented increased opening pressure >25 cm H2O. A literature review was conducted to identify previously reported MOGAD cases with an opening pressure >25 cm H2O.

Analysis of Evusheld safety and efficacy in multiple sclerosis patients.

Background: In December 2021, the U.S. Food and Drug Administration issued emergency use authorization for the combination monoclonal antibodies tixagevimab and cilgavimab (Evusheld - AstraZeneca) for COVID-19 pre-exposure prophylaxis.

Frequency, characteristics, predictors and treatment of relapsing myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).

Background: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) may have a monophasic or relapsing disease course. To date, factors that may predict a relapsing disease course remain largely unknown and only limited data exist regarding the efficacy of different utilized immunotherapy regimens at preventing or reducing relapses.

Objectives: To assess the characteristics, predictors, and immunotherapy of relapsing MOGAD.

Senescence marker p16INK4a expression in patients with multiple sclerosis.

Objectives: Telomere attrition is associated with disability accumulation and brain atrophy in multiple sclerosis (MS). Downstream of telomere attrition is cellular senescence. We sought to determine differences in the cellular senescence marker p16INK4a expression between MS and healthy control participants and the association of p16INK4a expression with MS disability and treatment exposure.

Characterization of cortico-meningeal translocator protein expression in multiple sclerosis.

Compartmentalized meningeal inflammation is thought to represent one of the key players in the pathogenesis of cortical demyelination in multiple sclerosis. PET targeting the 18 kDa mitochondrial translocator protein (TSPO) is a molecular-specific approach to quantifying immune cell-mediated density in the cortico-meningeal tissue compartment in vivo. This study aimed to characterize cortical and meningeal TSPO expression in a heterogeneous cohort of multiple sclerosis cases using in vivo simultaneous MR-PET with 11C-PBR28, a second-generation TSPO radioligand, and ex vivo immunohistochemistry.