(I-357) Exploration Into the Future; Neural Interfaces and Accelerated Aging

Introduction:: A long list of neurodegenerative disorders exist, making life increasingly difficult, affecting approximately 1 billion people globally (WHO, 2005). In response, neural engineering research labs are working to fabricate thin-film implants that will record and stimulate neural signals as a means for researching new treatment methods. However, the immune response to implants in neural tissue is hostile, causing failure to liquid ingress or encapsulation in scar tissue. To save time, money, and reduce the use of animal subjects, researchers are utilizing a method called reactive accelerated aging that artificially accelerates the degradation of devices intending to mimic failure mechanisms of devices implanted in the neural tissue environment. In order to build the best suited device, we need to try different materials and methods of fabrication and then test each using neural tissue models to compare their performance. Testing in vivo takes a lot of time and money and poses risk for failure, potentially causing damage or loss to either the device or its carrier. A more practical and relatively riskless method of device development is to utilize reactive accelerated aging, which uses naturally harmful accelerant factors such as heat and chemicals. This method acts to mimic the destined neural tissue site with a benchtop experiment that allows us to study the predicted in vivo behavior without risking the in vivo environment.


Materials and Methods:: Using reactive accelerated aging, this study tests and examines the overall fabrication quality and durability of two neural interface devices with iridium oxide microelectrodes; one insulated with solely polyimide substrate and one with an amorphous silicon carbide (a-SiC) layer within the polyimide substrate. Similar a-SiC thin film devices were shown to improve electrical insulation and liquid ingress resistance (Deku et al, 2018). Initial device measurements were recorded in phosphate buffered saline (PBS) at room temperature, then devices were assigned to one of three groups for aging tests in PBS: at room temperature, at 37°C, or at 87°C. Heat leads to evaporation of the solution, so a timed pump was incorporated to account for volume loss. In 7 day intervals, impedance and charge storage capacity of each electrode were recorded until device failure. The expectation is that heat is a key accelerated aging factor, with higher temperatures leading to faster device failure. Our goal is to find potential failure mechanisms in our devices early, and facilitate fabrication of revised devices with improved performance and longevity to remain effective in vivo for a patient's lifetime.

Results, Conclusions, and Discussions:: Our first experiments showed that the device with the additional layer of a-SiC was less susceptible to failure than the device with solely polyimide substrate. For polyimide-only devices, the polyimide substrate layers delaminated from internal metal layers during aging and the electrode was degraded. The added layer of a-SiC:H indeed improved resistance to liquid ingress and prevented delamination and changes in impedance over time. However, we did run into sporadic fractures of the a-SiC layers, and future work plans to explore the origins of these fractures in detail.

Apart from temperature, various factors within the neural tissue environment contribute to failure mechanisms, such as varying chemical concentrations, electrical levels, and ROS presence. Likewise, various factors need to be considered to get the right material for maximum biocompatibility, especially for different characteristics like device charge-transfer properties, fluid ingress resistance, flexibility, size, etc. For the next steps in this project, we plan to explore the combined use of electrical pulsing, chemicals like hydrogen peroxide (a source of ROS) and other strategies in order to improve our accelerated aging experimental conditions and determine the best aging techniques for mimicking the neural tissue environment. Expanding our accelerated aging experiments will allow our lab to effectively test different fabrication methods and materials to determine the most suitable designs for any targeted therapeutic use.


Acknowledgements (Optional): : I am proud to acknowledge Sandra Castro, Feather Crawford and the entire DucksRISE community, as well as Dr. Felix Deku, Rebecca Frederick and the entirety of The Deku Lab, and finally the wonderous Lanch McCormick, for this spectacular opportunity and experience. Thank you all very deeply, I couldn't be more thankful to work on such great things with such spectacular people.


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