The Internet of Bio-Nano-Things is a new paradigm that can bring novel remotely controlled actuation and sensing techniques inside the human body. Towards precise bionano sensing techniques in the brain, we investigate the challenges of modelling spatial distribution of astrocyte networks in developing a mathematical framework that lay the groundwork for future early-detection techniques of neurodegenerative disease. In this paper, we investigate the effect of the @math -amyloid plaques in astrocytes with the Alzheimer's disease. We developed a computation model of healthy and Alzheimer's diseases astrocytes networks from the state of the art models and results that account for the intracellular pathways, IP @math dynamics, gap junctions, voltage-gated calcium channels and astrocytes volumes. We also implemented different types of astrocytes network topologies including shortcut networks, regular degree networks, Erd "os R 'enyi networks and link radius networks. A proposed multi-scale stochastic computational model captures the relationship between the intracellular and intercellular scales. Lastly, we designed and evaluated a single-hop communication system with frequency modulation using metrics such as propagation extend, molecular delay and channel gain. The results show that the more unstable but at the same time lower level oscillations of Alzheimer's astrocyte networks can create a multi-scale effect on communication between astrocytes with increased molecular delay and lower channel gain compared to healthy astrocytes, with an elevated impact on Erd "os R 'enyi networks and link radius networks topologies.
 Recent years have witnessed an increasing interest in neuron–glia communication. This interest stems from the realization that glia participate in cognitive functions and information processing and are involved in many brain disorders and neurodegenerative diseases. An important process in neuron–glia communications is astrocyte encoding of synaptic information transfer—the modulation of intracellular calcium (Ca2 + ) dynamics in astrocytes in response to synaptic activity. Here, we derive and investigate a concise mathematical model for glutamate-induced astrocytic intracellular Ca2 + dynamics that captures the essential biochemical features of the regulatory pathway of inositol 1,4,5-trisphosphate (IP3). Starting from the well-known two-variable (intracellular Ca2 + and inactive IP3 receptors) Li–Rinzel model for calcium-induced calcium release, we incorporate the regulation of IP3 production and phosphorylation. Doing so, we extend it to a three-variable model (which we refer to as the ChI model) that could account for Ca2 + oscillations with endogenous IP3 metabolism. This ChI model is then further extended into the G-ChI model to include regulation of IP3 production by external glutamate signals. Compared with previous similar models, our three-variable models include a more realistic description of IP3 production and degradation pathways, lumping together their essential nonlinearities within a concise formulation. Using bifurcation analysis and time simulations, we demonstrate the existence of new putative dynamical features. The cross-couplings between IP3 and Ca2 + pathways endow the system with self-consistent oscillatory properties and favor mixed frequency–amplitude encoding modes over pure amplitude–modulation ones. These and additional results of our model are in general agreement with available experimental data and may have important implications for the role of astrocytes in the synaptic transfer of information. We describe a two-dimensional stochastic model of intercellular Ca2+ wave (ICW) spread in glia that includes contributions of external stimuli, ionotropic and metabotropic P2 receptors, exo- and ecto-nucleotidases, second messengers, and gap junctions. In this model, an initial stimulus evokes ATP and UTP release from a single cell. Agonists diffuse and are degraded both in bulk solution and at cell surfaces. Ca2+ elevation in individual cells is determined by bound agonist concentrations s and by number and features of P2 receptors summed with that generated by IP3 diffusing through gap junction channels. Variability of ICWs is provided by randomly distributing a predetermined density of cells in a rectangular grid and by randomly selecting within intervals values characterizing the extracellular compartment, individual cells, and interconnections with neighboring cells. Variability intervals were obtained from experiments on astrocytoma cells transfected to express individual P2 receptors and or the gap junction protein connexin43. The simulation program (available as Supplementary Material) permits individual alteration of ICW components, allowing comparison of simulations with data from cells expressing connexin43 and or various P2 receptor subtypes. Such modeling is expected to be useful for testing phenomenological hypotheses and in understanding consequences of alteration of system components under experimental or pathological conditions. Intercellular Ca 2+ waves in astrocytes are thought to serve as a pathway of long-range signaling. The waves can propagate by the diffusion of molecules through gap junctions and across the extracellular space. In rat striatal astrocytes, the gap-junctional route was shown to be dominant. To analyze the interplay of the processes involved in wave propagation, a mathematical model of this system has been developed. The kinetic description of Ca 2+ signaling within a single cell accounts for inositol 1,4,5-trisphosphate (IP 3 ) generation, including its activation by cytoplasmic Ca 2+ , IP 3 -induced Ca 2+ liberation from intracellular stores and various other Ca 2+ transports, and cytoplasmic diffusion of IP 3 and Ca 2+ . When cells are coupled by gap junction channels in a two-dimensional array, IP 3 generation in one cell triggers Ca 2+ waves propagating across some tens of cells. The spatial range of wave propagation is limited, yet depends sensitively on the Ca 2+ -mediated regeneration of the IP 3 signal. Accordingly, the term “limited regenerative signaling” is proposed. The gap-junctional permeability for IP 3 is the crucial permissive factor for wave propagation, and heterogeneity of gap-junctional coupling yields preferential pathways of wave propagation. Processes involved in both signal initiation (activation of IP 3 production caused by receptor agonist) and regeneration (activation of IP 3 production by Ca 2+ , loading of the Ca 2+ stores) are found to exert the main control on the wave range. The refractory period of signaling strongly depends on the refilling kinetics of the Ca 2+ stores. Thus the model identifies multiple steps that may be involved in the regulation of this intercellular signaling pathway.