{"id":9676,"date":"2016-04-26T12:33:42","date_gmt":"2016-04-26T19:33:42","guid":{"rendered":"https:\/\/vermont.salk.edu\/?post_type=disclosure&p=9676"},"modified":"2016-04-26T12:34:44","modified_gmt":"2016-04-26T19:34:44","slug":"tamping-down-neurons-energy-use-could-treat-neurodegeneration","status":"publish","type":"disclosure","link":"https:\/\/www.salk.edu\/zh\/news-release\/tamping-down-neurons-energy-use-could-treat-neurodegeneration\/","title":{"rendered":"Tamping down neurons\u2019 energy use could treat neurodegeneration"},"content":{"rendered":"

LA JOLLA\u2014Salk Institute scientists showed how an FDA-approved drug boosts the health of brain cells by limiting their energy use. Like removing unnecessary lighting from a financially strapped household to save on electricity bills, the drug\u2014called rapamycin\u2014prolongs the survival of diseased neurons by forcing them to reduce protein production to conserve cellular energy.<\/p>\n

Rapamycin has been shown to extend lifespan and reduce symptoms in a broad range of diseases and, at the cellular level, is known to slow down the rate at which proteins are made. But the new Salk research, published in the journal eLife<\/em><\/a>, suggests that rapamycin could also target the neural damage associated with Leigh syndrome, a rare genetic disease, and potentially other forms of neurodegeneration<\/a> as well.<\/p>\n

\"rapamycin-effect-on-MILS-neurons\"
Salk scientists show how the drug rapamycin (bottom) rescues Leigh syndrome neurons.<\/p>\n

Click here for a high-resolution image.<\/a><\/p>\n

Credit: Salk Institute<\/figcaption><\/figure>\n

\u201cOur study shows that protein production in neurons is one of the major utilizers of energy and that neurons of Leigh syndrome degenerate because they can\u2019t sustain a high enough level of energy,\u201d says Tony Hunter<\/a>, the Renato Dulbecco Chair and American Cancer Society Professor in Salk\u2019s Molecular and Cell Biology Laboratory, who led the research.<\/p>\n

Previous studies on rapamycin, which blocks a key energy sensor in cells, found that it can alter the immune system, extend lifespan and treat disorders, including lupus and Alzheimer\u2019s disease. Researchers assumed that the drug prevented the neurodegeneration seen in Alzheimer\u2019s by encouraging cells to degrade damaged components and aggregated proteins. But recent data hinted that the drug might also have an effect on the mitochondria, organelles that act as cells\u2019 powerhouses, producing energy in the form of adenosine triphosphate (ATP).<\/p>\n

Xinde Zheng, a research associate in the Hunter lab, was already studying the properties of cells affected by Leigh syndrome, whose inherited neurodegeneration is caused by a mutation in mitochondrial DNA that reduces ATP production. Zheng wondered how rapamycin would affect the neurons plagued by the diseased mitochondria. He and Hunter teamed up with the lab of \u9c81\u65af\u8482\u00b7\u76d6\u5947<\/a>, a professor in Salk\u2019s Laboratory of Genetics and holder of the Vi and John Adler Chair for Research on Age-Related Neurodegenerative Disease. Zheng, together with Leah Boyer, then a researcher in Gage\u2019s lab and now director of Salk\u2019s Stem Cell Core, generated diseased neurons by taking skin cells from patients with Leigh syndrome, reprogramming them into stem cells in culture and then coaxing them to develop into brain cells in a dish.<\/p>\n

Though cells must make proteins to survive, protein production is a highly energy-consuming process and, for diseased cells, the process leaves too few energy reserves to deal with cellular stress or other demands.<\/p>\n

\u201cReducing protein production in aging neurons allows more energy for the cell to put toward folding proteins correctly and handling stress,\u201d says Zheng, the first author of the new paper. \u201cThe impact of our finding is that modulation of protein synthesis could be a general approach to treating neurodegeneration.\u201d<\/p>\n

\"Xinde
From left: Xinde Zheng, Tony Hunter, Leah Boyer and Rusty Gage<\/p>\n

Click here<\/a> for a high-resolution image.<\/p>\n

Credit: Salk Institute<\/figcaption><\/figure>\n

In their study, the team found that Leigh syndrome neurons decayed in the dish and showed clear signs of energy depletion. Meanwhile, Leigh syndrome neurons exposed to rapamycin had more ATP and showed less degeneration. By turning down the dial on protein production, the diseased and damaged neurons were able to survive longer.<\/p>\n

“We are surprised and delighted that rapamycin\u2019s effect to reduce protein synthesis as an energy-austerity approach may lead to a potential treatment for mitochondria-related neurodegenerative diseases,” says Gage.<\/p>\n

This is a good example of the value of studying a disease in a dish, according to Hunter. \u201cIt\u2019s led to a lot of new insights into the underlying biology of this rare and understudied condition,\u201d he adds.<\/p>\n

More work is needed to determine whether the findings on rapamycin hold true in animal models of Leigh syndrome and other neurodegenerative diseases, and to ascertain how exactly rapamycin is altering the metabolism of the cells.<\/p>\n

Other researchers on the study were Mingji Jin, Youngsung Kim, Weiwei Fan, Cedric Bardy, Travis Berggren<\/a> \u548c Ronald M. Evans<\/a>, all of the Salk Institute.<\/p>\n

The work and the researchers involved were supported by grants from the National Institutes of Health<\/a>, the Howard Hughes Medical Institute<\/a>, a Calouste Gulbenkian Foundation<\/a> Fellowship, a California Institute for Regenerative Medicine<\/a> Postdoctoral Training Award, and the Helmsley Center for Genomic Medicine<\/a>.<\/p>","protected":false},"featured_media":9677,"template":"","faculty":[76,72],"disease-research":[124],"class_list":["post-9676","disclosure","type-disclosure","status-publish","has-post-thumbnail","hentry","faculty-rusty-gage","faculty-tony-hunter","disease-research-neuroscience-and-neurological-disorders"],"acf":[],"yoast_head":"\nTamping down neurons\u2019 energy use could treat neurodegeneration - Salk Institute for Biological Studies<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.salk.edu\/zh\/news-release\/tamping-down-neurons-energy-use-could-treat-neurodegeneration\/\" \/>\n<meta property=\"og:locale\" content=\"zh_CN\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Tamping down neurons\u2019 energy use could treat neurodegeneration - Salk Institute for Biological Studies\" \/>\n<meta property=\"og:description\" content=\"LA JOLLA\u2014Salk Institute scientists showed how an FDA-approved drug boosts the health of brain cells by limiting their energy use. 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