Astrocytes are important for maintaining cholesterol metabolism, glutamate uptake, and neurotransmission. Indeed, inflammatory processes and neurodegeneration contribute to the altered morphology, gene expression, and function of astrocytes. Astrocytes, in collaboration with numerous microRNAs, regulate brain cholesterol levels as well as glutamatergic and inflammatory signaling, all of which contribute to general brain homeostasis. Neural electrical activity, synaptic plasticity processes, learning, and memory are dependent on the astrocyte–neuron crosstalk. Here, we review the involvement of astrocytic microRNAs that potentially regulate cholesterol metabolism, glutamate uptake, and inflammation in Alzheimer’s disease (AD). The interaction between astrocytic microRNAs and long non-coding RNA and transcription factors specific to astrocytes also contributes to the pathogenesis of AD. Thus, astrocytic microRNAs arise as a promising target, as AD conditions are a worldwide public health problem. This review examines novel therapeutic strategies to target astrocyte dysfunction in AD, such as lipid nanodiscs, engineered G protein-coupled receptors, extracellular vesicles, and nanoparticles.

All networks, including biological networks, computer networks, social networks and more can be represented as graphs, which include a number of small module such as subgraph, also called as network motifs. Network motifs are subgraph which recur themselves in a specific network or different networks. In biological networks, these network motifs plays very important role to identify diseases in human beings. In this paper we have developed a module to identify common network motifs types from cancer pathways and Signal Transduction Networks (STNs). It also identifies the topological behaviors o f cancer networks and STNs. In this study, we have implemented five motif algorithms such as Auto-Regulation Loop (ARL), Feed Backward Loop (FBL), Feed Forward Loop (FFL), Single-Input Motif (SIM) and Bi-fan. These algorithms gives correct results in terms of network motifs for human cancer and STNs. Finding network motifs by using online tool is limited to three nodes, but our proposed work provides facility to find network motifs upto any number of nodes. We applied five motif algorithms to human cancer networks and Signal Transduction Networks (STNs) which are collected from KEGG database as a result we got “Frequent Occurrences of Network Motifs (FONMs)”. These FONMs acts as a references for an oncologist in order to find type o f cancer in human beings.

Transcription factors (TF) and microRNAs are regulatory factors in astrocytes and are linked to several Parkinson's disease (PD) progression causes, such as disruption of glutamine transporters in astrocytes and concomitant disrupted glutamine uptake and inflammation. REST, a crucial TF, has been documented as an epigenetic repressor that limits the expression of neuronal genes in non-neural cells. REST activity is significantly linked to its corepressors in astrocytes, specifically histone deacetylases (HDACs), CoREST, and MECP2. Another REST-regulating TF, YY1, has been studied in astrocytes, and its interaction with REST has been investigated. In this review, the molecular processes that support the astrocytic control of REST and YY1 in terms of the regulation of glutamate transporter EAAT2 were addressed in a more detailed and comprehensive manner. Both TFs' function in astrocytes and how astrocyte abnormalities cause PD is still a mystery. Moreover, microRNAs (short non-coding RNAs) are key regulators that have been correlated to the expression and regulation of numerous genes linked to PD. The identification of numerous miRs that are engaged in astrocyte dysfunction that triggers PD has been shown. The term "Gut-brain axis" refers to the two systems' mutual communication. Gut microbial dysbiosis, which mediates an imbalance of the gut-brain axis, might contribute to neurodegenerative illnesses through altered astrocytic regulation. New treatment approaches to modify the gut-brain axis and prevent astrocytic repercussions have also been investigated in this review.