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A Johns Hopkins study finds BVRA protects brain cells by boosting antioxidant defenses independently of bilirubin, offering new hope for treating Alzheimer’s and Parkinson’s.
A Johns Hopkins study reveals that the enzyme BVRA protects brain cells from oxidative stress independently of its role in bilirubin production.
It shields neurons by directly regulating NRF2, a key protein controlling antioxidant defenses, and maintaining mitochondrial health and immune function.
In mice lacking BVRA, NRF2 failed to activate, weakening protection against damage linked to Alzheimer’s and Parkinson’s.
Surprisingly, BVRA variants unable to produce bilirubin still offered protection, confirming a separate, crucial role.
The findings, published in PNAS, suggest new therapeutic pathways for neurodegenerative diseases, though human applications remain years away.
Un estudio de Johns Hopkins encuentra que BVRA protege las células cerebrales al aumentar las defensas antioxidantes independientemente de la bilirrubina, ofreciendo nuevas esperanzas para el tratamiento de Alzheimer y Parkinson.