Antioxidant Dimethyl Fumarate Temporarily but Not Chronically Improves Intracortical Microelectrode Performance.
Antioxidant Dimethyl Fumarate Temporarily but Not Chronically Improves Intracortical Microelectrode Performance.
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DOI：
10.3390/mi14101902
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发表时间：
2023-10-04
期刊：
影响因子：
3.4
通讯作者：
Capadona JR
中科院分区：
文献类型：
--
作者：
Hoeferlin GF;Bajwa T;Olivares H;Zhang J;Druschel LN;Sturgill BS;Sobota M;Boucher P;Duncan J;Hernandez-Reynoso AG;Cogan SF;Pancrazio JJ;Capadona JR
皮质内微电极阵列 (MEA) 可用于多种应用，从基础神经科学研究到作为脑机接口 (BCI) 系统的一部分提供与大脑的密切接口，旨在恢复神经系统疾病或损伤患者的功能。不幸的是，MEA 往往会过早失效，导致许多应用功能丧失。 MEA 失败的一个重要因素是植入部位周围慢性炎症激活的小胶质细胞和巨噬细胞释放活性氧 (ROS) 造成的氧化应激。抗氧化剂提供了一种减轻氧化应激、改善组织健康和 MEA 性能的方法。在这里，我们研究使用临床可用的抗氧化剂富马酸二甲酯 (DMF) 来减少大鼠 MEA 模型中的神经炎症反应并改善 MEA 性能。每日使用 DMF 治疗 16 周，使 MEA 装置在亚慢性（第 5-11 周）阶段的记录能力得到显着改善（活性电极产量为 42%，对照为 35%）。然而，这些亚慢性改善在慢性植入阶段就消失了，因为在植入后 16 周，DMF 治疗的动物中出现更严重的神经炎症反应。然而，在亚慢性阶段，治疗组和对照组之间的神经炎症是不加区别的。尽管长期使用会更糟糕，但 MEA 性能的暂时改善（<12 周）是有意义的。使用 DMF 对 MEA 装置进行短期改进可以改善有限期限研究的使用。应进一步努力探索 DMF 治疗动物在 16 周时间点神经炎症反应恶化的机制，并评估其在特定应用中的有用性。
Intracortical microelectrode arrays (MEAs) can be used in a range of applications, from basic neuroscience research to providing an intimate interface with the brain as part of a brain-computer interface (BCI) system aimed at restoring function for people living with neurological disorders or injuries. Unfortunately, MEAs tend to fail prematurely, leading to a loss in functionality for many applications. An important contributing factor in MEA failure is oxidative stress resulting from chronically inflammatory-activated microglia and macrophages releasing reactive oxygen species (ROS) around the implant site. Antioxidants offer a means for mitigating oxidative stress and improving tissue health and MEA performance. Here, we investigate using the clinically available antioxidant dimethyl fumarate (DMF) to reduce the neuroinflammatory response and improve MEA performance in a rat MEA model. Daily treatment of DMF for 16 weeks resulted in a significant improvement in the recording capabilities of MEA devices during the sub-chronic (Weeks 5–11) phase (42% active electrode yield vs. 35% for control). However, these sub-chronic improvements were lost in the chronic implantation phase, as a more exacerbated neuroinflammatory response occurs in DMF-treated animals by 16 weeks post-implantation. Yet, neuroinflammation was indiscriminate between treatment and control groups during the sub-chronic phase. Although worse for chronic use, a temporary improvement (<12 weeks) in MEA performance is meaningful. Providing short-term improvement to MEA devices using DMF can allow for improved use for limited-duration studies. Further efforts should be taken to explore the mechanism behind a worsened neuroinflammatory response at the 16-week time point for DMF-treated animals and assess its usefulness for specific applications.
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