1 nale for the secondary deficiency of NEU1 in galactosialidosis.

2 tosomal recessive lysosomal storage disorder galactosialidosis.

3 y of lysosomal neuraminidase: sialidosis and galactosialidosis.

4 lls was assessed in PPCA-/- mice, a model of galactosialidosis.

5 nerative lysosomal disorders, sialidosis and galactosialidosis.

6 e treatment for nonneuropathic patients with galactosialidosis and possibly for others with LSDs that

7  wild-type protective protein/cathepsin A by galactosialidosis fibroblasts resulted in a significant

8                                              Galactosialidosis (GS) is a human neurodegenerative dise

9 neurodegenerative lysosomal storage disorder galactosialidosis (GS).

10 PCA) are the cause of the lysosomal disorder galactosialidosis (GS).

11  lysosomal storage disorders: sialidosis and galactosialidosis (GS).

12  in the neurodegenerative lysosomal disorder galactosialidosis (GS).

13 ral mutations in the neuraminidase gene, and galactosialidosis, in which a primary defect of protecti

14 ctural defect in the neuraminidase gene, and galactosialidosis, in which the loss of neuraminidase ac

15                                              Galactosialidosis is a human lysosomal storage disease c

16 of PPCA, as in the lysosomal storage disease galactosialidosis, NEU1 self-associates into chain-like

17  fibroblasts of a G(M1) gangliosidosis and a galactosialidosis patient.

18 ed in mutant PPCAs from clinically different galactosialidosis patients have now been modeled in the

19 he high incidence of PPCA folding mutants in galactosialidosis reflects the fact that a single point