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Accumulation of sulfatide in neuronal and glial cells of arylsulfatase A deficient mice

Artikel i vetenskaplig tidskrift
Författare Marie Molander-Melin
Zarah Pernber
Sebastian Franken
Volkmar Gieselmann
Jan-Eric Månsson
Pam Fredman
Publicerad i J Neurocytol
Volym 33
Nummer/häfte 4
Sidor 417-27
ISSN 0300-4864 (Print)
Publiceringsår 2004
Publicerad vid Institutionen för klinisk neurovetenskap, Sektionen för laborativ neurovetenskap
Institutionen för klinisk neurovetenskap, Sektionen för kliniska nervsjukdomar
Sidor 417-27
Språk en
Länkar dx.doi.org/10.1007/s11068-004-4207-...
www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Brain Chemistry, Cerebellum/cytology, Cerebral Cortex/cytology, Cerebroside-Sulfatase/genetics/*metabolism, Immunohistochemistry, Lipids/chemistry, Male, Mice, Mice, Knockout, Neuroglia/*chemistry/cytology, Neurons/*chemistry/cytology, Sulfoglycosphingolipids/*analysis
Ämneskategorier Neurokemi

Sammanfattning

Arylsulfatase A (ASA) degrades sulfatide, seminolipid and lactosylceramide sulfate, glycolipids recognized by the Sulph I antibody although sulfatide is considered the main antigen. Sulfatide is myelin associated but studies have shown a minor distribution also in non-myelin forming cells. The aim of this work was to further study sulfatide in neurons and astrocytes by immunohistochemistry, facilitated by investigation of tissue from adult ASA deficient (ASA -/-) mice. Cells with a low presence of sulfatide might be detected due to lack of ASA activity and accumulation of Sulph I antigens. Sulfatide positive astrocytes and neurons were more numerous and intensely stained in ASA -/- mice, demonstrating a sulfatide accumulation compared to controls. Sulph I staining was especially increased in the molecular layer of cerebellum, in which Purkinje cell dendrites displayed an altered morphology, and in layer IV-VI of cerebral cortex. In hippocampus, immunostaining was found in neuronal cytoplasm in ASA -/- but in nuclear membranes of control mice. We observed a gray matter astrogliosis, which appeared to be associated to sulfatide accumulation. In addition, the developmental change (<20 months) of Sulph I antigens, galactosylceramide, phospholipids and cholesterol were followed by lipid analyses which verified sulfatide and seminolipid accumulation in adult ASA -/- mice, although no lactosylceramide sulfate could be detected. In addition to demonstrating sulfatide in neurons and astrocytes, this study supports the value of ASA -/- mice as a model for metachromatic leukodystrophy and suggests that accumulation of sulfatide beyond myelin might contribute to the pathology of this disease.

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