Although there is an increase in oxidative damage and inflammation in the brains of neurodegenerative patients, their pathogenic relevance is yet unknown. The central nervous system has a built-in immune system, and glial cells inside it not only sustain and nourish neuronal cells but also take part in a number of inflammatory processes that protect the nervous system from pathogens and aid in its recovery from stress and injury. A promising target for the discovery or development of neurodegenerative disorders, such as Alzheimer's disease shielding neurons in the mixer culture from the harmful effect, can occasionally emerge from normal glial actions, and this point of view requires further research examination. By accelerating mitochondriogenesis, astrocytes shield neurons from oxidative stress while also effectively reducing inflammation. The significance of inflammatory problems spread by glial cells has been viewed as a bystander effect, or epiphenomenon, arising when injured neurons acquire a glial cell activation response. Wyss Corey and his associates revealed that astrocytes can remove and destroy A-peptide plates through phagocytosis, while the Valles group proved anti-inflammatory effects following A-induction in astrocytes. It is tough to kill astrocytes, and these cells have been transformed by evolution to be stronger in front of damage to safeguard all the cells in our brain. For us, astrocytes are the first differentiated cells to die following injury. In all viability assays conducted on us and others, astrocytes have consistently outperformed neurons. In comparison to neuron and other cells outside the brain, glia have undergone several alterations over many years. For instance, TFAM in astrocytes may play a variety of roles in defending mtDNA against harmful substances.

The entire region of the mtDNA might be covered by TFAM, a protein belonging to the high-mobility group, to create the nucleoid structure, shielding the mtDNA from oxidative or inflammatory changes. Second, by binding mtDNA in the form of the nucleoid structure, TFAM was able to sustain the copy number of mtDNA. Additionally, TFAM may start mtDNA transcription to promote mitochondrial biogenesis, which could help to successfully counteract mitochondrial malfunction and explain mitochondrial DNA instability and metabolic changes in human cancer. According to another viewpoint supported by recent studies, SIRT-1 affects stem cell maintenance, growth-factor responses, and lineage cell fate decisions via redox status. As a result, not only will differentiated astrocytes be crucial, but also the stem cells' ability to respond to damage inside the brain. Not to mention, astrocytes have the unique ability to revert to a quiescent phenotype and a non-differentiated state, allowing them to transform into neurons if necessary.

To recover from a brain illness, alterations in epigenetics and glia's reaction to injury will be essential. In a healthy brain, astrocytes remove all harmful products, maintain brain homeostasis, and are ready to fight off viruses and microbes at night, when they are mostly reactive and ready to attack. Why is the research community mainly interested in neuronal works? Why don't we look into the function of glia in the brain? There are many people who are considering it; let's examine the future of study brain. In the coming century, it's likely that we'll learn how crucial astrocytes are to the research community and perhaps comprehend just how qualified they are while searching for unqualified cells. A unique protein that is only found in astrocytes is called GFAP, or glial fibrillary acidic protein, which is only slightly expressed in radial glia. The protein, which is des-metilated in astrocytes when astrocytes begin to differentiate from radial glia, may or may not have the same function as vimentine, which is to transport proteins and ions between cells.