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+-signalling-based molecular communications framework. A feed-forward and feedback control technique is used to manipulate IP 3 values to stabilize the concentration of Ca 2+ inside the astrocytes. The theoretical analysis of the given model aims i) to stabilize the Ca 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+ signalling, and maintain gliotransmitters' regulation remotely. It shows that the refractory periods from Ca 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+ signalling in astrocytes, ultimately improving neuronal activity.