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Description

A study on genetic linkages between aberrant lipid metabolism and PD directly demonstrates that glucocerebrosidase and sphingomyelin phosphodiesterase 1 mutations enhance PD risk in humans, and that galactosylceramide beta hydrolase function loss increases -synuclein aggregation and accumulation in experimental murine models

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In the current study, we utilized an adjuvant-triggered arthritic animal model and observed the manifestation of RA disease parameters (41)

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