Role for OCT in Detecting Homonymous Ganglion Cell Layer Thinning in Patients with Demyelinating Disease

Thinning in the ganglion cell layer + the inner plexiform layer (GCIPL) on optical coherence tomography (OCT) can be quantified and used as a proxy for neurodegeneration. Additionally, studies have demonstrated that lesions in the optic radiations can lead to a characteristic homonymous pattern of degeneration in the retina. It is unknown whether lesions in demyelinating diseases including multiple sclerosis (MS), neuro-myelitis optica (NMO) and anti- myelin oligodendrocyte glycoprotein syndrome (anti-MOG) lead to these patterns on OCT. This study's purpose was to identify homonymous patterns of GCIPL thinning in a demyelinating diseasecohort

Legislative Documents

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Additional file 3: of Inhibition of 2-AG hydrolysis differentially regulates blood brain barrier permeability after injury

Figure S1. In vivo selectivity of CPD-4645. Levels of inhibition of MAGL, ABHD6, and FAAH in the brain after 10 mg/kg subcutaneous dose of CPD-4645 at given tie point as determined by activity-based protein profiling using the pan-serine hydrolase probe FP-rhodamine. Full MAGL inhibition was normalized by effect seen at 2 h post-subcutaneous administration of 16 mg/kg JZL-184. (TIFF 1521 kb

Additional file 1: of Inhibition of 2-AG hydrolysis differentially regulates blood brain barrier permeability after injury

Table S1. Differentially regulated genes. Differentially regulated genes (increased or decreased by at least twofold) and p values for LPS-vehicle vs sham-vehicle and LPS-CPD-4645 vs LPS-vehicle groups. (XLSX 294 kb