Feed-Forward and Feedback Control in Astrocytes for Ca2p-Based Molecular Communications Nanonetworks

Synaptic plasticity depends on the gliotransmitters' concentration in the synaptic channel. And, an abnormal concentration of gliotransmitters is linked to neurodegenerative diseases, including Alzheimer's, Parkinson's, and epilepsy. In this paper, a theoretical investigation of the cause of the abnormal concentration of gliotransmitters and how to achieve its control is presented through a Ca^{2+}2+-signalling-based molecular communications framework. A feed-forward and feedback control technique is used to manipulate IP_33 values to stabilize the concentration of Ca^{2+}2+ inside the astrocytes. The theoretical analysis of the given model aims i) to stabilize the Ca^{2+}2+ concentration around a particular desired level in order to prevent abnormal gliotransmitters' concentration (extremely high or low concentration can result in neurodegeneration), ii) to improve the molecular communication performance that utilizes Ca^{2+}2+ signalling, and maintain gliotransmitters' regulation remotely. It shows that the refractory periods from Ca^{2+}2+ can be maintained to lower the noise propagation resulting in smaller time-slots for bit transmission, which can also improve the delay and gain performances. The proposed approach can potentially lead to novel nanomedicine solutions for the treatment of neurodegenerative diseases, where a combination of nanotechnology and gene therapy approaches can be used to elicit the regulated Ca^{2+}2+ signalling in astrocytes, ultimately improving neuronal activity.