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Double (plp−/−mag−/−) and triple (plp−/−mbp−/−mag−/−) null-allelic mouse lines deficient in proteolipid protein (PLP), myelin-associated glycoprotein (MAG), and myelin basic protein (MBP) were generated and characterized genetically, biochemically, and morphologically including their behavioral capacities. Theplp−/−mag−/− mutant develops a rapidly progressing axon degeneration in CNS with severe cognitive and motor coordinative deficits but has a normal longevity. CNS axons of theplp−/−mbp−/−mag−/− mouse are hypomyelinated and ensheathed by “pseudomyelin” with disturbed protein and complex lipid composition. Theshiverer trait in theplp−/−mbp−/−mag−/− similar to the plp−/−mbp−/− mutant is significantly ameliorated, and its lifespan is considerably prolonged. The longevity of these dysmyelinosis mouse mutants recommends them as suitable models for the long-term evaluation of stem cell therapeutic strategies.

the journal of neuroscience/the journal of neuroscience

Early Onset of Axonal Degeneration in Double (plp−/−mag−/−) and Hypomyelinosis in Triple (plp−/−mbp−/−mag−/−) Mutant Mice