• Neuroscience · Dec 2023

    Orm1 arises as a shared altered protein in two models of Multiple Sclerosis.

    • Sonsoles Barriola, Delgado-GarcíaLina MaríaLMDepartment of Molecular, Cellular and Developmental Neurobiology, Instituto Cajal, Consejo Superior de Investigaciones Científicas-CSIC, Madrid 28002, Spain; Laboratory of Molecular Neurobiology, Department of Biochemistry, Unive, Paz Cartas-Cejudo, Ignacio Iñigo-Marco, Joaquín Fernández-Irigoyen, Enrique Santamaría, and Laura López-Mascaraque.
    • Department of Molecular, Cellular and Developmental Neurobiology, Instituto Cajal, Consejo Superior de Investigaciones Científicas-CSIC, Madrid 28002, Spain; Ph.D. Program in Neuroscience, Autónoma de Madrid University-Cajal Institute, Madrid 28029, Spain.
    • Neuroscience. 2023 Dec 15; 535: 203217203-217.

    AbstractMultiple sclerosis (MS) is a complex autoimmune and neurodegenerative disorder that affects the central nervous system (CNS). It is characterized by a heterogeneous disease course involving demyelination and inflammation. In this study, we utilized two distinct animal models, cuprizone (CPZ)-induced demyelination and experimental autoimmune encephalomyelitis (EAE), to replicate various aspects of the disease. We aimed to investigate the differential CNS responses by examining the proteomic profiles of EAE mice during the peak disease (15 days post-induction) and cuprizone-fed mice during the acute phase (38 days). Specifically, we focused on two different regions of the CNS: the dorsal cortex (Cx) and the entire spinal cord (SC). Our findings revealed varied glial, synaptic, dendritic, mitochondrial, and inflammatory responses within these regions for each model. Notably, we identified a single protein, Orosomucoid-1 (Orm1), also known as Alpha-1-acid glycoprotein 1 (AGP1), that consistently exhibited alterations in both models and regions. This study provides insights into the similarities and differences in the responses of these regions in two distinct demyelinating models.Copyright © 2023 IBRO. Published by Elsevier Ltd. All rights reserved.

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