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Consistent with these findings, microglia from TREM2-deficient animals under cuprizone-induced demyelination or in models of focal lysolecithin demyelination exhibit failure in their activation, showing less proliferation, resting morphology, lower expression levels of MHC class II and iNOS, deficits in phagocytosis of myelin debris and lipid metabolism (138), persistent demyelination after chronic use of cuprizone, more aggressive reduction of oligodendrocytes and clinical worsening (138, 139)

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