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Furthermore, mice with cardiac-specific overexpression of mutated human B-crystallin (hR120GCryAB) displayed increases in GSH levels and in activities of GR, glucose-6-phosphate dehydrogenase (G6PD), catalase, and GPx (indicative of reductive stress), which led to the development of cardiac hypertrophy and heart failure in these mice (77, 78)

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This pattern holds biological significance in PD in that it suggests that disease- or treatment-related effects may exert selective pressure on the microbial network in the gut without necessarily lowering the overall number of microbial species present, thereby exerting an influence on GBA signaling and L-DOPA metabolism