Soulika Lab - UC Davis
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Initiation and progression of axonopathy in experimental autoimmune encephalomyelitis.

Athena Soulika Lee, E Mccauley, E Miers, L Bannerman, P Pleasure, D

Published in Journal of Neuroscience

Axonal loss is the principal cause of chronic disability in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). In C57BL/6 mice with EAE induced by immunization with myelin oligodendrocyte glycoprotein peptide 35-55, the first evidences of axonal damage in spinal cord were in acute subpial and perivascular foci of infiltrating n...

Disruption of NMDA receptors in oligodendroglial lineage cells does not alter their susceptibility to experimental autoi...

Burns, T Itoh, T Shen, H Lee, E Sohn, J Pleasure, D Guo, F Maeda, Y Ko, Em Delgado, M ...

Published in Journal of Neuroscience

Pharmacological studies have suggested that oligodendroglial NMDA glutamate receptors (NMDARs) mediate white matter injury in a variety of CNS diseases, including multiple sclerosis (MS). We tested this hypothesis in experimental autoimmune encephalomyelitis (EAE), a model of human MS, by timed conditional disruption of oligodendroglial NR1, an ess...

Conditional ablation of astroglial CCL2 suppresses CNS accumulation of M1 macrophages and preserves axons in mice with M...

Moreno, Monica Bannerman, Peter Ma, Joyce Guo, Fuzheng Miers, Laird Soulika, Athena M Pleasure, David

Published in The Journal of neuroscience : the official journal of the Society for Neuroscience

Current multiple sclerosis (MS) therapies only partially prevent chronically worsening neurological deficits, which are largely attributable to progressive loss of CNS axons. Prior studies of experimental autoimmune encephalomyelitis (EAE) induced in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein peptide 35-55 (MOG peptide), ...

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