Synthetic MC via Biological Transmitters: Therapeutic Modulation of the Gut-Brain Axis
This work addresses the problem of designing personalized treatments for neurological diseases like drug refractory epilepsy, though it is incremental as it builds on existing therapeutic modulation concepts.
The paper tackles the challenge of generating synthetic molecular communication signals inside the human body by proposing to modulate the natural gut-brain axis using personal health data, achieving excellent accuracy in identifying modulators through a machine learning model.
Synthetic molecular communication (SMC) is a key enabler for future healthcare systems in which Internet of Bio-Nano-Things (IoBNT) devices facilitate the continuous monitoring of a patient's biochemical signals. To close the loop between sensing and actuation, both the detection and the generation of in-body molecular communication (MC) signals is key. However, generating signals inside the human body, e.g., via synthetic nanodevices, poses a challenge in SMC, due to technological obstacles as well as legal, safety, and ethical issues. Hence, this paper considers an SMC system in which signals are generated indirectly via the modulation of a natural in-body MC system, namely the gut-brain axis (GBA). Therapeutic GBA modulation is already established as treatment for neurological diseases, e.g., drug refractory epilepsy (DRE), and performed via the administration of nutritional supplements or specific diets. However, the molecular signaling pathways that mediate the effect of such treatments are mostly unknown. Consequently, existing treatments are standardized or designed heuristically and able to help only some patients while failing to help others. In this paper, we propose to leverage personal health data, e.g., gathered by in-body IoBNT devices, to design more versatile and robust GBA modulation-based treatments as compared to the existing ones. To show the feasibility of our approach, we define a catalog of theoretical requirements for therapeutic GBA modulation. Then, we propose a machine learning model to verify these requirements for practical scenarios when only limited data on the GBA modulation exists. By evaluating the proposed model on several datasets, we confirm its excellent accuracy in identifying different modulators of the GBA. Finally, we utilize the proposed model to identify specific modulatory pathways that play an important role for therapeutic GBA modulation.