Working with fish, birds and mice, Johns Hopkins Medicine researchers report new evidence that some animals’ natural capacity to regrow neurons is not missing, but is instead inactivated in mammals. Specifically, the researchers found that some genetic pathways that allow many fish and other cold-blooded animals to repair specialized eye neurons after injury remain present in mammals as well, but are turned off, blocking regeneration and healing.
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A description of the study, published online by the journal Science on Oct. 1, offers a better understanding of how genes that control regeneration are conserved across species, as well as how they function. This may help scientists develop ways to grow cells that are lost due to hereditary blindness and other neurodegenerative diseases.
“Our research overall indicates that the potential for regeneration is there in mammals, including humans, but some evolutionary pressure has turned it off,” says Seth Blackshaw, Ph.D., professor of
Researchers at Penn State College of Medicine now better understand the role of a protein, interleukin-21 (IL-21), in the immune system response to infections in the nervous system. The results of their recent study support further investigation into using IL-21 as a therapeutic agent for persistent central nervous system infections.
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CD4 T cells in the immune system produce IL-21, which is critical for the development of CD8 tissue-resident-memory (TRM) cells during persistent viral infections of the central nervous system with polyomavirus.
Dr. Aron Lukacher, professor and chair of the Department of Microbiology and Immunology, said the results, published in Science Immunology, demonstrate that IL-21 is an important factor in the development of effective immune responses to chronic infections in the central nervous system including neurodegenerative HIV-AIDS and progressive multifocal leukoencephalopathy (PML), a fatal brain infection caused by JC polyomavirus. PML starts with symptoms including clumsiness, weakness or difficulty speaking