| Literature DB >> 17616409 |
Nicolas Deconinck1, Anissa Messaaoui, France Ziereisen, Hazim Kadhim, Yves Sznajer, Karine Pelc, Marie Cécile Nassogne, Marie T Vanier, Bernard Dan.
Abstract
Metachromatic leukodystrophy (MLD) is an autosomal recessive neurodegenerative lysosomal disease characterized by accumulation of sulfatides, extensive white matter damage and loss of both cognitive and motor functions. In vivo, the catabolism of sulfatide requires both the enzyme arylsulfatase A and a specific sphingolipid activator protein, saposin-B, encoded by the PSAP gene. Arylsulfatase A activity is deficient in the classical forms of MLD, but exceedingly rare cases of MLD are due to saposin-B deficiency. We report here a detailed clinical, radiological and histological description of a new case in a 2-year-old Italian girl, who presented as a late infantile case of MLD with normal arylsulfatase A activity, urinary excretion of sulfatides and mutations in the PSAP gene.Entities:
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Year: 2007 PMID: 17616409 DOI: 10.1016/j.ejpn.2007.05.004
Source DB: PubMed Journal: Eur J Paediatr Neurol ISSN: 1090-3798 Impact factor: 3.140