Johns Hopkins的研究发现BVRA通过提升抗氧化剂防御系统来保护脑细胞, 而不依赖bilirubin, 为治疗阿尔茨海默氏病和帕金森氏病带来新的希望。 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.

Johns Hopkins的一项研究表明,酶BVRA保护脑细胞不受氧化性压力的影响,而不管其在生菌生产中的作用如何。 A Johns Hopkins study reveals that the enzyme BVRA protects brain cells from oxidative stress independently of its role in bilirubin production. 它通过直接管制NRF2来保护神经元,后者是控制抗氧化剂的主要蛋白质防御系统,并保持米托氏体的健康和免疫功能。 It shields neurons by directly regulating NRF2, a key protein controlling antioxidant defenses, and maintaining mitochondrial health and immune function. 在缺乏BVRA的小鼠中,NRF2未能启动,削弱了对与阿尔茨海默氏病和帕金森氏病有关的损害的保护。 In mice lacking BVRA, NRF2 failed to activate, weakening protection against damage linked to Alzheimer’s and Parkinson’s. 令人惊讶的是，无法产生胆红素的 BVRA 变体仍然提供保护，证实了单独的关键作用。 Surprisingly, BVRA variants unable to produce bilirubin still offered protection, confirming a separate, crucial role. 这些研究结果公布在PNAS中,其中提出了神经退化性疾病的新治疗途径,尽管人类的应用还早于数年。 The findings, published in PNAS, suggest new therapeutic pathways for neurodegenerative diseases, though human applications remain years away.