PubMed:1353340 JSONTXT

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{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/1353340","sourcedb":"PubMed","sourceid":"1353340","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/1353340","text":"Late-onset metachromatic leukodystrophy: molecular pathology in two siblings.\nWe report on a new allele at the arylsulfatase A (ARSA) locus causing late-onset metachromatic leukodystrophy (MLD). In that allele arginine84, a residue that is highly conserved in the arylsulfatase gene family, is replaced by glutamine. In contrast to alleles that cause early-onset MLD, the arginine84 to glutamine substitution is associated with some residual ARSA activity. A comparison of genotypes, ARSA activities, and clinical data on 4 individuals carrying the allele of 81 patients with MLD examined, further validates the concept that different degrees of residual ARSA activity are the basis of phenotypical variation in 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