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The COVID-19 pandemic before mass vaccination can be restrained only by the limitation of contacts between people, which makes the digital economy a key condition for survival. More than half of the world’s population lives in urban areas, and many cities have already transformed into “smart” digital/virtual hubs. Digital services ensure city life safe without an economy lockout and unemployment. Urban society strives to be safe, sustainable, well-being, and healthy. We set the task to construct a hybrid sociological and technological concept of a smart city with matched solutions, complementary to each other. Our modeling with the elaborated digital architectures and with the bionic solution for ensuring sufficient data governance showed that a smart city in comparison with the traditional city is tightly interconnected inside like a social “organism”. Society has entered a decisive decade during which the world will change by moving closer towards SDGs targets 2030 as well as by the transformation of cities and their digital infrastructures. It is important to recognize the large vector of sociological transformation as smart cities are just a transition phase to human-centered personal space or smart home. The “atomization” of the world urban population raises the gap problem in achieving SDGs because of different approaches to constructing digital architectures for smart cities or smart homes in countries. The strategy of creating smart cities should bring each citizen closer to SDGs at the individual level, laying in the personal space the principles of sustainable development and wellness of personality.

Astrogliosis is a pathological process that affects the density, morphology, and function of astrocytes. It is a common feature of brain trauma, autoimmune diseases, and neurodegeneration including spinocerebellar ataxia type 1 (SCA1), a poorly understood neurodegenerative disease. S100β is a Ca2+ binding protein. In SCA1, excessive excretion of S100β by reactive astrocytes and its uptake by Purkinje cells has been demonstrated previously. Under pathological conditions, excessive extracellular concentration of S100β stimulates the production of proinflammatory cytokines and induces apoptosis. We modeled astrogliosis by S100β injections into cerebellar cortex in mice. Injections of S100β led to significant changes in Bergmann glia (BG) cortical organization and affected their processes. S100β also changed morphology of the Purkinje cells (PCs), causing a significant reduction in the dendritic length. Moreover, the short-term synaptic plasticity and depolarization-induced suppression of synaptic transmission were disrupted after S100β injections. We speculate that these effects are the result of Ca2+-chelating properties of S100β protein. In summary, exogenous S100β induced astrogliosis in cerebellum could lead to neuronal dysfunction, which resembles a natural neurodegenerative process. We suggest that astrocytes play an essential role in SCA1 pathology, and that astrocytic S100β is an important contributor to this process.

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