Department of Pediatrics, School of Medicine, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA.
Published: September 2005
AI Article Synopsis
Article Abstract
Demyelination is the hallmark of numerous neurodegenerative conditions, including multiple sclerosis. Oligodendrocyte progenitors (OPCs), which normally mature into myelin-forming oligodendrocytes, are typically present around demyelinated lesions but do not remyelinate affected axons. Here, we find that the glycosaminoglycan hyaluronan accumulates in demyelinated lesions from individuals with multiple sclerosis and in mice with experimental autoimmune encephalomyelitis. A high molecular weight (HMW) form of hyaluronan synthesized by astrocytes accumulates in chronic demyelinated lesions. This form of hyaluronan inhibits remyelination after lysolecithin-induced white matter demyelination. OPCs accrue and do not mature into myelin-forming cells in demyelinating lesions where HMW hyaluronan is present. Furthermore, the addition of HMW hyaluronan to OPC cultures reversibly inhibits progenitor-cell maturation, whereas degrading hyaluronan in astrocyte-OPC cocultures promotes oligodendrocyte maturation. HMW hyaluronan may therefore contribute substantially to remyelination failure by preventing the maturation of OPCs that are recruited to demyelinating lesions.
Spinal cord sarcoidosis, an uncommon manifestation of neurosarcoidosis, presents diagnostic and therapeutic challenges because the condition is rare and has diverse clinical manifestations that can mimic other conditions such as multiple sclerosis and neuromyelitis optica spectrum disorder. A middle-aged African American female with a history of idiopathic intracranial hypertension and hydrocephalus with ventriculoperitoneal shunt presented with progressive, predominantly left-sided gait instability, weakness, and paresthesia. Cerebrospinal fluid showed lymphocytosis, red blood cells, elevated oligoclonal bands, and elevated kappa free light chains, concerning for multiple sclerosis.
Multiple sclerosis (MS) is the most prevalent human inflammatory disease of the central nervous system with demyelination and glial scar formation as pathological hallmarks. Glial cells are key drivers of lesion progression in MS with roles in both tissue damage and repair depending on the surrounding microenvironment and the functional state of the individual glial subtype. In this review, we describe recent developments in the context of glial cell diversity in MS summarizing key findings with respect to pathological and maladaptive functions related to disease-associated glial subtypes.
Background: Upper limb dysfunction is a common debilitating feature of relapsing-remitting multiple sclerosis (RRMS). We aimed to examine the longitudinal trajectory of the iPad®-based Manual Dexterity Test (MDT) and predictors of change over time.
Methods: We prospectively enrolled RRMS patients (limited to Expanded Disability Status Scale (EDSS) < 4).
Background: In acquired immunodeficiency syndrome patients, Talaromyces marneffei infections are mostly disseminated and may involve the skin, mucosa, respiratory system, digestive system, lymphatic system, and as some reports indicate, the nervous system. Mp1p, a cell wall-specific polysaccharide in Talaromyces marneffei, is used for laboratory diagnosis of Talaromyces marneffei in blood and urine samples. However, Cerebrospinal fluid Mp1p diagnosis of Talaromyces marneffei central nervous system infection has not been reported.
Poor understanding of the cellular and molecular basis of clinical and genetic heterogeneity in progressive multiple sclerosis (MS) has hindered the search for new effective therapies. To address this gap, we analyzed 632,000 single-nucleus RNA sequencing profiles from 156 brain tissue samples of MS and control donors to examine inter- and intra-donor heterogeneity. We found distinct cell type-specific gene expression changes between MS gray and white matter, highlighting clear pathology differences.
