genesis Compromise of blood–brain barrier function as a result of vascular endothelial growth factor production Cytotoxic edema during trauma and stroke through AQP4 overactivity Potential for chronic cytokine activation of astrocytes to contribute to chronic pain Reactive astrocytes have the potential to promote neural toxicity via the generation cytotoxic molecules such as nitric oxide radicals and other reactive oxygen species, which may damage nearby neurons. Reactive astrocytes may also promote secondary degeneration after CNS injury. Novel therapeutic techniques Due to the destructive effects of astrogliosis, which include altered molecular expression, release of inflammatory factors, astrocyte proliferation and neuronal dysfunction, researchers are currently searching for new ways to treat astrogliosis and neurodegenerative diseases. Various studies have shown the role of astrocytes in diseases such as Alzheimer's, amyotrophic lateral sclerosis (ALS), Parkinson's, and Huntington's. The inflammation caused by reactive astrogliosis augments many of these neurological diseases. Current studies are researching the possible benefits of inhibiting the inflammation caused by reactive gliosis in order to reduce its neurotoxic effects. Neurotrophins are currently being researched as possible drugs for neuronal protection, as they have been shown to restore neuronal function. For example, a few studies have used nerve growth factors to regain some cholinergic function in patients with Alzheimer's. Anti-gliosis function of BB14 One specific drug candidate is BB14, which is a nerve growth factor-like peptide that acts as a TrkA agonist. BB14 was shown to reduce reactive astrogliosis following peripheral nerve injuries in rats by acting on DRG and PC12 cell differentiation. Although further research is needed, BB14 has the potential to treat a variety neurological diseases. Further research of neurotrophins could potentially lead to the development of a highly selective, potent, and small neurotrophin that targets reactive gliosis to alleviate some neurodegenerative diseases. Regulatory function of TGFB TGFB is a regulatory molecule involved in proteoglycan production. This production is increased in the presence of bFGF or Interleukin 1. An anti-TGFβ antibody may potentially reduce GFAP upregulation after CNS injuries, promoting axonal regeneration. Ethidium bromide treatment Injection of ethidium bromide kills all CNS glia (oligodendrocytes and astrocytes), but leaves axons, blood vessels, and macrophages unaffected. This provides an environment conducive to axonal regeneration for about four days. After four days, CNS glia reinvade the area of injection and axonal regeneration is consequently inhibited. This method has been shown to reduce glial scarring following CNS trauma. Metalloprotinease activity Oligodendrocyte precursor cells and C6 glioma