An oligodendrocyte-specific protein (OSP) cDNA was recently identified and found to be expressed primarily in oligodendrocytes and has a deduced amino acid sequence similar to that of peripheral myelin protein 22 (PMP-22). We raised antibodies against a synthetic peptide corresponding to OSP amino acid residues 179-194 which reacted with a 22 kd protein in mouse CNS. OSP immunoreactivity localized to spinal cord white matter tracts using immunohistochemistry in a similar distribution to that of MBP. OSP localized to CNS myelin biochemically with more than a 30-fold enrichment measured in purified myelin. We further purified the proteolipid fraction of myelin and determined that OSP contributes approximately 7% of total myelin protein making it the third most abundant protein in CNS myelin. No binding was found to several agglutinins or a HNK1-specific antibody suggesting that OSP is not a glycoprotein.
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http://dx.doi.org/10.1002/(SICI)1097-4547(19971201)50:5<713::AID-JNR8>3.0.CO;2-K | DOI Listing |
Neuropsychiatr Dis Treat
January 2025
Department of Rehabilitation Medicine, The Affiliated Taian City Central Hospital of Qingdao University, Taian, 271000, People's Republic of China.
As the aging process accelerates and living conditions improve, central nervous system (CNS) diseases have become a major public health problem. Diseases of the CNS cause not only gray matter damage, which is primarily characterized by the loss of neurons, but also white matter damage. However, most previous studies have focused on grey matter injury (GMI), with fewer studies on white matter injury (WMI).
View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Department of Neurology, Division of Neuroimmunology, School of Medicine, Johns Hopkins University, Baltimore, MD, 21287, USA.
Chronic innate immune activation in the central nervous system (CNS) significantly contributes to neurodegeneration in progressive multiple sclerosis (MS). Using multiple experimental autoimmune encephalomyelitis (EAE) models, we discovered that NLRX1 protects neurons in the anterior visual pathway from inflammatory neurodegeneration. We quantified retinal ganglion cell (RGC) density and optic nerve axonal degeneration, gliosis, and T-cell infiltration in Nlrx1 and wild-type (WT) EAE mice and found increased RGC loss and axonal injury in Nlrx1 mice compared to WT mice in both active immunization EAE and spontaneous opticospinal encephalomyelitis (OSE) models.
View Article and Find Full Text PDFCNS Neurosci Ther
January 2025
Children's Medical Center, Department of Pediatric Neurology, Peking University First Hospital, Beijing, China.
Aims: Alexander disease (AxD) is a leukodystrophy caused by mutations in the astrocytic filament gene GFAP. There are currently no effective treatments for AxD. Previous studies have rarely established AxD models with the patient's original GFAP mutations.
View Article and Find Full Text PDFJ Biol Chem
January 2025
Department of Neurology, Henry Ford Health, Detroit, MI 48202, USA. Electronic address:
Multiple sclerosis (MS) is a prevalent inflammatory neurodegenerative disease in young people, causing neurological abnormalities and impairment. To investigate a novel therapeutic agent for MS, we observed the impact of maresin 1 (MaR1) on disease progression in a well-known, relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE) mouse model. Treatment with MaR1 accelerated inflammation resolution, reduced neurological impairment, and delayed disease development by reducing immune cell infiltration (CD4+IL-17+ and CD4+IFNγ+) into the central nervous system (CNS).
View Article and Find Full Text PDFCells
January 2025
Institute of Health Sciences, Department of Neuroscience, Acibadem Mehmet Ali Aydinlar University, 34684 Istanbul, Türkiye.
Epilepsy is a chronic neurological disorder marked by recurrent seizures, significantly impacting individuals worldwide. Current treatments are often ineffective for a third of patients and can cause severe side effects, necessitating new therapeutic approaches. Glial cells, particularly astrocytes, microglia, and oligodendrocytes, are emerging as crucial targets in epilepsy management.
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