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Regarding the former, transgenic mice that exhibit delayed demyelination and white matter degeneration from a variety of causes (e.g., myelin gene defects, peroxisome-deficient or -synuclein overexpressing oligodendrocytes, or disruption of their gap junctions, to name a few) frequently show a secondary T- and occasionally a concomitant B-lymphocytic inflammation (Ip et al., 2006

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