Cell Rep: special protein or plays a key role in the pathogenesis of neurodegenerative diseases

October 18, 2019 / BIOON / -- recently, a report was published in the international journal Cell reports In the previous research report, scientists from Queen Mary College of London University and other institutions found a special protein or played a key role in regulating brain inflammation through research on mice Relevant research may help improve scientists' understanding of the pathogenesis of neurodegenerative diseases Photo source: Miguel burguillos, PhD, researcher of cc0 public domain, said that when the brain is under pressure, a special protein called tet2 may help regulate the immune response of immune cells (or microglia) in the brain Although neuroinflammation plays an important role in resisting infection and coping with brain damage, excessive or chronic inflammation may kill neurons around the affected area, and the death of such neurons may cause many neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease The researchers pointed out that the removal of tet2 from the mouse body can effectively inhibit the neuroinflammatory response; now researchers know that tet2 can remove special chemical markers from DNA, which can help determine whether the gene is activated; the researchers believe that tet2 can actually activate the key immune cells in the brain to express, compared with the cells in other parts of the body, it is more inflammatory The performance of brain cells seems to be different Finally, the researchers said that although this is an exploratory study, the relevant research results have opened a new way for further study of neurodegenerative diseases In these diseases, neuroinflammation driven by microglia can induce many pathological manifestations In the long run, it may help scientists to develop new therapies for a variety of neurodegenerative diseases Original source: Alejandro Carrillo Jimenez et al, tet2 regulations the neuroinformatics response in microglia, cell reports (2019) Doi: 10.1016/j.cellep.2019.09.013