泛酸激酶相关神经变性(pantothenate kinase-associated neurodegeneration,PKAN)是最常见的脑内铁沉积性神经变性病(neurodegeneration with brain iron accumulation,NBIA)之一,表现为进行性加剧的锥体外系和其他神经系统症状,具有高度临床和遗传异质性[1],在影像学上表现为铁离子异常沉积的特殊征象。PKAN国外的发病率为0.0001—0.0003%[2],约占NBIA的50%[3],国内尚无确切统计,是一种罕见的常染色体隐性遗传疾病。
近年来,脱硫弧菌(Desulfovibrio, DSV)与神经变性疾病(Neurodegenerative diseases, NDs)之间的潜在联系受到研究者的广泛关注。DSV是一种硫酸盐还原细菌,是人体内最主要的产H2S来源。研究表明,在阿尔茨海默病(Alzheimer’s disease, AD)、帕金森病(Parkinson’s disease, PD)和肌萎缩侧索硬化症(Amyotrophic lateral sclerosis, ALS)等NDs患者中,DSV的丰度和代谢活性与健康人群存在显著差异。DSV可能通过影响神经炎症、氧化应激反应以及神经递质的平衡参与NDs的发病机制。因此,调节DSV的数量和代谢活性可能为NDs的干预提供新的治疗靶点。本文综述了DSV与NDs之间的相关性研究进展,旨在为进一步探索DSV在NDs中的作用机制和开发新的治疗策略提供科学依据。In recent years, the potential link between Desulfovibrio (DSV) and neurodegenerative diseases (NDs) has garnered significant attention from researchers. DSV, a sulfate-reducing bacterium, is the primary source of hydrogen sulfide (H2S) production in the human body. Studies have shown that the abundance and metabolic activity of DSV in patients with Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) differ significantly from those in healthy individuals. DSV may contribute to the pathogenesis of NDs by influencing neuroinflammation, oxidative stress, and the balance of neurotransmitters. Therefore, regulating the quantity and metabolic activity of DSV may provide new therapeutic targets for the intervention of NDs. This review summarizes the progress in research on the relationship between DSV and NDs, aiming to provide scientific evidence for further exploration of the mechanisms of DSV in NDs and the development of new therapeutic strategies.
