Sustained Anti-inflammatory Release from Mechanically-Adaptive Neural Probes for Addressing Neuroinflammation

Event Date:
March 7th 9:00 AM - 10:00 AM

NEC SEMINAR

Speaker: Mali Ya Mungu Ocoko

Advisors: Dr. Allison Hess-Dunning and Dr. Jeffrey Capadona

Title: Sustained Anti-inflammatory Release from Mechanically-Adaptive Neural Probes for Addressing Neuroinflammation

Abstract: Brain-machine interfaces (BMIs) enable communication between the central nervous system and external devices and have applications in rehabilitation, including motor dysfunction and limb loss. Intracortical BMIs (iBMIs) detect action potentials with single- and multi-unit resolution. However, their long-term performance is limited by neuroinflammatory responses that degrade signal quality over time. Studies have identified biological failure, particularly chronic immune activation, as a primary contributor to intracortical microelectrode (IME) failure. Various strategies have been used to improve device integration, including the use of flexible materials and the delivery of therapeutic agents.

Here, we combine both approaches and investigate the integration of dexamethasone-loaded titania nanotube arrays (TNAs) into a mechanically adaptive material to mitigate neuroinflammation. TNAs are highly ordered nanostructured materials with tunable geometries that can be used to control drug release. The mechanically adaptive material consists of a polymer nanocomposite made of polyvinyl acetate reinforced with cellulose nanocrystals (PVAC-CNC). We developed a transfer process to integrate TNAs onto the mechanically adaptive material. The combined effects of mechanical compliance and sustained local dexamethasone release were evaluated in a mouse model at 2- and 4-week time points by quantifying gene expression using a 152-gene panel. Despite the 3x greater thickness of mechanically adaptive probes compared to industry-standard silicon probes, the effects on gene expression were similar. This study improves our understanding of how biomaterial modifications influence neuroinflammation and inform the future design of neural interfaces