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. Author manuscript; available in PMC: 2016 Jan 31.

Published in final edited form as: Mol Genet Metab. 2014 Dec 6;114(2):274–280. doi: 10.1016/j.ymgme.2014.11.015

Fig. 1 — Among gangliosidosis (Gang) patients (left-side charts), five CSF analytes of inflammation were consistently elevated in patients with the infantile-onset disease in contrast to the normal levels found in patients with juvenile-onset disease. This relationship of severity of disease to analyte elevation is important, this correspondence reflecting the rate of disease progression.

CSF and serum inflammatory biomarkers from patients with MPS diseases (right-side charts) showed no abnormalities in either serum or CSF. The analyte differences between gangliosidosis disease and MPS disease emphasize the value of these inflammatory biomarkers, and illustrate that the analyte abnormalities are not general indicators of lysosomal storage or dysfunction, but reflect some other pathologic mechanism of gangliosidosis disease in the central nervous system.

Fig. 1 — Among gangliosidosis (Gang) patients (left-side charts), five CSF analytes of inflammation were consistently elevated in patients with the infantile-onset disease in contrast to the normal levels found in patients with juvenile-onset disease. This relationship of severity of disease to analyte elevation is important, this correspondence reflecting the rate of disease progression.

CSF and serum inflammatory biomarkers from patients with MPS diseases (right-side charts) showed no abnormalities in either serum or CSF. The analyte differences between gangliosidosis disease and MPS disease emphasize the value of these inflammatory biomarkers, and illustrate that the analyte abnormalities are not general indicators of lysosomal storage or dysfunction, but reflect some other pathologic mechanism of gangliosidosis disease in the central nervous system.