What would happen if we found out how to repair neurons in your brain that were defective?

According to new research, and with the help of mouse and human tissue, it has been found that astrocytes in the brain direct the formation of building new connections for learning and memories (“Faulty brain circuits,” 2019).

Experiments on mice who were modified to have less neural pathways paved the way for discovering that astrocytes can deliver a certain protein to help rebuild neural connections (“Faulty brain circuits,” 2019).

“ ‘Although astrocytes appear to all look alike in the brain, we had an inkling that they might have specialized roles in the brain due to regional differences in the brain’s function and because of observed changes in certain diseases,’” stated Jeffrey Rothstein, M.D., Ph.D., Director of the Brain Science Institute and professor of neurology at the Johns Hopkins University School of Medicine (“Faulty brain circuits,” 2019).

To explore how astrocytes help with re-building neural pathways, researchers analyzed the protein, glutamate transporter-1 – this protein can be volatile if it lingers in the brain for too long, which is why astrocytes release and reabsorb the protein after it sends its message (“Faulty brain circuits,” 2019).

After analyzing DNA and astrocytes in various areas of the brain, the protein Norrin was found – mice that had Norrin in their system had more branches on their neurons. With this discovery, researchers utilized Norrin and injected the protein in other mice, where they again saw significant neural growth. They tested this on human neurons as well, and also found the same result. With this knowledge, it may be possible to use Norrin to treat neurodegenerative disorders (“Faulty brain circuits,” 2019).

Reference: Johns Hopkins Medicine. (2019, July 30). Faulty brain circuits repaired using nanotechnology: Possible new drug targets for dementia and intellectual disability. ScienceDaily. Retrieved August 4, 2019 from www.sciencedaily.com/releases/2019/07/190730092624.htm

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