Summary: Researchers have developed a drug-coated strategy for neural prosthetic implants that significantly reduces the body’s immune response and limits scar tissue formation. By chemically attaching the anti-inflammatory drug dexamethasone to the surface of flexible polyimide electrodes, the team achieved a slow local release that preserves biocompatibility and improves the long-term stability and function of electrodes used to connect prosthetic limbs to the peripheral nervous system.
The coating is designed to release the drug gradually at the implant site for at least nine weeks (more than two months), a critical window when the foreign body reaction is typically strongest. In vitro and animal experiments demonstrated reduced inflammatory signalling, lower infiltration of immune cells, and a thinner fibrotic capsule around the devices, without compromising the mechanical properties or neuronal viability of the implant material.
Key Facts:
- Drug coating innovation: Dexamethasone is covalently bound to the polyimide surface so it is released locally and continuously rather than delivered systemically.
- Reduced immune reaction: Functionalized implants produced fewer pro-inflammatory markers in immune cells and less scar tissue in preclinical models.
- Improved chronic stability: The treatment maintains biocompatibility and the mechanical integrity of ultrathin, flexible electrodes through the critical early weeks after implantation.
Source: UAB
An international research collaboration that includes the Institut de Neurociències at the Universitat Autònoma de Barcelona (UAB) has demonstrated a promising approach to improve the long-term performance of neural prostheses used after limb amputation or severe nerve injury.
Neural electrodes restore communication between prosthetic devices and the peripheral nervous system, enabling sensory feedback and motor control. However, when implanted long-term, these devices often trigger a foreign body reaction: immune cells surround the device, inflammatory signalling increases, and a fibrotic capsule forms. That scar tissue can electrically isolate the electrode, reducing signal quality and reliability.
To address this challenge, researchers focused on the electrically inert polymer component of flexible neural implants: a polyimide material known as BPDA-PDA. The team developed a surface functionalization method that enables covalent binding of dexamethasone directly to the polymer scaffold. Because the drug is chemically attached rather than merely adsorbed, it provides a sustained, localized release that targets the immune response at the implant interface without systemic side effects.
Laboratory assays showed that macrophages exposed to the dexamethasone-functionalized polyimide produced fewer pro-inflammatory markers, indicating a dampened innate immune response. At the same time, tests with dorsal root ganglion (DRG) neurons confirmed that the modified material remained biocompatible and supported neuronal viability. In vivo implantation in animal models corroborated these findings: implants releasing dexamethasone attracted fewer inflammatory cells and developed a thinner fibrotic capsule compared with untreated controls.
Because polyimide BPDA-PDA is widely used to make ultrathin, ultra-flexible implants, integrating a sustained-release anti-inflammatory coating on its electrically inactive scaffold is a practical strategy to improve chronic electrode function. Limiting the foreign body reaction at the implant surface helps maintain electrical contact with surrounding nerve tissue, which is essential for reliable long-term stimulation and recording.
“This is a main step that has to be complemented by the demonstration in vivo that this coating improves the functional performance of chronically implanted electrodes in the peripheral nerves, for stimulating and recording nerve signals,” says Dr. Xavier Navarro, principal investigator of the UAB team participating in the BioFINE project. Future work will evaluate how the coating affects signal stability and device longevity during long-term use in peripheral nerve interfaces.
About this neuroscience and neurotech research news
Author: Octavi Lopez
Source: UAB
Contact: Octavi Lopez – UAB
Image: The image is credited to Neuroscience News
Original Research: Open access. “Covalent Binding of Dexamethasone to Polyimide Improves Biocompatibility of Neural Implantable Devices” by Xavier Navarro et al., published in Advanced Healthcare Materials. DOI: 10.1002/adhm.202405004
Abstract
Covalent Binding of Dexamethasone to Polyimide Improves Biocompatibility of Neural Implantable Devices
Neural implants are commonly used to interact with the peripheral nervous system in prosthetic and neuromodulation applications, but their chronic performance is often limited by foreign body reactions. This study evaluates a surface functionalization approach for BPDA-PDA polyimide, the electrically inert, highly flexible polymer used in ultrathin neural devices.
The novelty of the method lies in covalently attaching dexamethasone to the polymer scaffold, enabling continuous local release of the anti-inflammatory drug for at least nine weeks. In vitro results show reduced production of pro-inflammatory markers by macrophages, while assays with dorsal root ganglion neurons confirm preserved neuronal viability and biocompatibility. In vivo implantation demonstrates decreased inflammatory cell infiltration and reduced fibrotic capsule thickness around treated substrates.
These results indicate that local delivery of dexamethasone from the electrically inactive scaffold of neural implants can mitigate foreign body reactions and potentially extend the functional stability and lifespan of chronically implanted neuroprosthetic devices.