Title of article :
Gaucher disease with parkinsonian manifestations: does glucocerebrosidase deficiency contribute to a vulnerability to parkinsonism?
Author/Authors :
Tayebi، N. نويسنده , , Walker، J. نويسنده , , Stubblefield، B. نويسنده , , Orvisky، E. نويسنده , , LaMarca، M. E. نويسنده , , Wong، K. نويسنده , , Rosenbaum، H. نويسنده , , Schiffmann، R. نويسنده , , Bembi، B. نويسنده , , Sidransky، E. نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2003
Abstract :
Among the phenotypes associated with Gaucher disease, the deficiency of glucocerebrosidase, are rare patients with early onset, treatment-refractory parkinsonism. Sequencing of glucocerebrosidase in 17 such patients revealed 12 different genotypes. Fourteen patients had the common "non-neuronopathic" N370S mutation, including five N370S homozygotes. While brain glucosylsphingosine levels were not elevated, Lewy bodies were seen in the four brains available for study. The shared clinical and neuropathologic findings in this subgroup suggest that the deficiency in glucocerebrosidase may contribute to a vulnerability to parkinsonism.
Keywords :
Gaucher disease , Glucocerebrosidase , Parkinsonism , Metaxin , Genotype/phenotype correlation , Lewy body , Modifier gene
Journal title :
MOLECULAR GENETICS AND METABOLISM
Journal title :
MOLECULAR GENETICS AND METABOLISM