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Recently, a hybrid model (βcuprizone autoimmune encephalitisβ or CAE) combining the myelin-toxic effects of cuprizone (Zirngibl et al., 2022) together with an immune stimulation identical to EAE but without extrinsic myelin peptides, provided proof-of-principle for the notion that a primary biochemical βdysmyelinationβ can result in a very typical inflammatory demyelinating white matter lesion in an immune-stimulated host (Caprariello et al., 2018)
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