{"id":9411,"date":"2016-04-06T10:21:06","date_gmt":"2016-04-06T17:21:06","guid":{"rendered":"https:\/\/vermont.salk.edu\/?post_type=disclosure&#038;p=9411"},"modified":"2024-01-30T15:44:27","modified_gmt":"2024-01-30T23:44:27","slug":"brain-guardians-remove-dying-neurons","status":"publish","type":"disclosure","link":"https:\/\/www.salk.edu\/zh\/news-release\/brain-guardians-remove-dying-neurons\/","title":{"rendered":"Brain guardians remove dying neurons"},"content":{"rendered":"<p>LA JOLLA\u2014By adolescence, your brain already contains most of the neurons that you\u2019ll have for the rest of your life. But a few regions continue to grow new nerve cells\u2014and require the services of cellular sentinels, specialized immune cells that keep the brain safe by getting rid of dead or dysfunctional cells.<\/p>\n<p>Now, Salk scientists have uncovered the surprising extent to which both dying and dead neurons are cleared away, and have identified specific cellular switches that are key to this process. The work was detailed in <em><a href=\"http:\/\/www.nature.com\/nature\/journal\/vaop\/ncurrent\/full\/nature17630.html\" target=\"_blank\" rel=\"noopener\">Nature<\/a><\/em> on April 6, 2016.<\/p>\n<div class=\"row\" style=\"\"><div class=\"col-md-8 col-md-push-2\"><div class=\"video-anchor\" id=\"video-bevh2BSuI0U\"><\/div><div class=\"embed-responsive embed-responsive-16by9\"> <iframe class=\"embed-responsive-item\" src=\"\/\/www.youtube.com\/embed\/bevh2BSuI0U?rel=0\" webkitallowfullscreen mozallowfullscreen allowfullscreen><\/iframe><\/div><!-- .embed-responsive --><\/div><!-- .col-md-*size --><\/div><!-- .\/row -->\n<p>\u201cWe discovered that receptors on immune cells in the brain are vital for both healthy and injured states,\u201d says <a href=\"https:\/\/www.salk.edu\/zh\/scientist\/greg-lemke\/\">Greg Lemke<\/a>, senior author of the work, a Salk professor of molecular neurobiology and the holder of the Fran\u00e7oise Gilot-Salk Chair. \u201cThese receptors could be potential therapeutic targets for neurodegenerative conditions or inflammation-related disorders, such as <a href=\"https:\/\/www.salk.edu\/zh\/science\/research\/neuroscience-and-neurological-disorders\/\">Parkinson\u2019s disease<\/a>.\u201d<\/p>\n<figure id=\"attachment_8774\"  class=\"wp-caption alignright\"><img decoding=\"async\" class=\"img-responsive wp-image-8774 size-medium\" src=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2016\/04\/Death-in-the-brain-300x250.jpg\" alt=\"Mer and Axl\" \/><figcaption class=\"wp-caption-text\">An accumulation of dead cells (green spots) is seen in the subventricular zone (SVZ)\u2014a neurogenic region\u2014of the brain in a mouse lacking the receptors Mer and Axl. (Blue staining marks all cells.) No green spots are seen in the SVZ from a normal mouse. <\/p>\n<p><a href=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2016\/04\/Death-in-the-brain.jpg\" target=\"_blank\" rel=\"noopener\">Click here<\/a> for a high-resolution image <\/p>\n<p>Credit: Salk Institute<\/figcaption><\/figure>\n<p>Two decades ago, the Lemke lab discovered that immune cells express critical molecules called TAM receptors, which have since become a focus for autoimmune and cancer research in many laboratories. Two of the TAM receptors, dubbed Mer and Axl, help immune cells called macrophages act as garbage collectors, identifying and consuming the over 100 billion dead cells that are generated in a human body every day.<\/p>\n<p>For the current study, the team asked if Mer and Axl did the same job in the brain. Specialized central nervous system macrophages called microglia make up about 10 percent of cells in the brain, where they detect, respond to and destroy pathogens. The researchers removed Axl and Mer in the microglia of otherwise healthy mice. To their surprise, they found that the absence of the two receptors resulted in a large pile-up of dead cells, but not everywhere in the brain. Cellular corpses were seen only in the small regions where the production of new neurons \u2014neurogenesis\u2014is observed.<\/p>\n<p>Many cells die normally during adult neurogenesis, but they are immediately eaten by microglia. \u201cIt is very hard to detect even a single dead cell in a normal brain, because they are so efficiently recognized and cleared by microglia,\u201d says Paqui G. Trav\u00e9s, a co-first author on the paper and former Salk research associate. \u201cBut in the neurogenic regions of mice lacking Mer and Axl, we detected many such cells.\u201d<\/p>\n<p>When the researchers more closely examined this process by tagging the newly growing neurons in mice\u2019s microglia missing Mer and Axl, they noticed something else interesting. New neurons that migrate to the olfactory bulb, or smell center, increased dramatically without Axl and Mer around. Mice lacking the TAM receptors had a 70 percent increase in newly generated cells in the olfactory bulb than normal mice.<\/p>\n<div class=\"row\" style=\"\"><div class=\"col-md-8 col-md-push-2\"><div class=\"video-anchor\" id=\"video-jLAnUtCBUtU\"><\/div><div class=\"embed-responsive embed-responsive-16by9\"> <iframe class=\"embed-responsive-item\" src=\"\/\/www.youtube.com\/embed\/jLAnUtCBUtU?rel=0\" webkitallowfullscreen mozallowfullscreen allowfullscreen><\/iframe><\/div><!-- .embed-responsive --><\/div><!-- .col-md-*size --><\/div><!-- .\/row -->\n<p>How\u2014and to what extent\u2014this unchecked new neural growth affects a mouse\u2019s sense of smell is not yet known, according to Lemke, though it is an area the lab will explore. But the fact that so many more living nerve cells were able to migrate into the olfactory bulb in the absence of the receptors suggests that Mer and Axl have another role aside from clearing dead cells\u2014they may actually also target living, but functionally compromised, cells.<\/p>\n<figure id=\"attachment_8777\"  class=\"wp-caption alignright\"><img decoding=\"async\" class=\"img-responsive wp-image-8777 size-medium\" src=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2016\/04\/Greg-Lemke_Lawrence-Fourgeaud_e_IMG_0733-300x200.jpg\" alt=\"Greg Lemke and Lawrence Fourgeaud\" \/><figcaption class=\"wp-caption-text\">Greg Lemke and Lawrence Fourgeaud <\/p>\n<p><a href=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2016\/04\/Greg-Lemke_Lawrence-Fourgeaud_e_IMG_0733.jpg\" target=\"_blank\" rel=\"noopener\">Click here<\/a> for a high-resolution image <\/p>\n<p>Credit: Salk Institute<\/figcaption><\/figure>\n<p>\u201cIt appears as though a significant fraction of cell death in neurogenic regions is not due to intrinsic death of the cells but rather is a result of the microglia themselves, which are killing a fraction of the cells by engulfment,\u201d says Lemke. \u201cIn other words, some of these newborn neuron progenitors are actually being eaten alive.\u201d<\/p>\n<p>This isn\u2019t necessarily a bad thing in the healthy brain, Lemke adds. The brain produces more neurons than it can use and then prunes back the cells that aren\u2019t needed. However, in an inflamed or diseased brain, the destruction of living cells may backfire.<\/p>\n<p>The Lemke lab did one more series of experiments to understand the role of TAM receptors in disease: they looked at the activity of Axl and Mer in a mouse model of Parkinson\u2019s disease. This model produces a human protein present in an inherited form of the disease that results in a slow degeneration of the brain. The team saw that Axl was far more active in this setting, consistent with other studies showing that increased Axl is a reliable indicator of inflammation in tissues.<\/p>\n<figure id=\"attachment_8775\"  class=\"wp-caption alignleft\"><img decoding=\"async\" class=\"img-responsive wp-image-8775 size-medium\" src=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2016\/04\/Trail-of-death-covercropped-300x136.jpg\" alt=\"Trail-of-death-covercropped\" \/><figcaption class=\"wp-caption-text\">In the area of a brain lacking Mer and Axl a \u2018trail of death\u2019 is apparent from the migratory pathway from the neurogenic region to the olfactory bulb (smell center of the brain). Blue staining marks all cells, and green spots are dead cells. No green spots are seen in the same section from a normal mouse. <\/p>\n<p><a href=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2016\/04\/Trail-of-death-covercropped.jpg\" target=\"_blank\" rel=\"noopener\">Click here<\/a> for a high-resolution image <\/p>\n<p>Credit: Salk Institute<\/figcaption><\/figure>\n<p>But the researchers were in for a surprise when they removed Axl and Mer from the Parkinson\u2019s mice. Instead of being worse off compared to mice with the disease but with normal microglia, the mice missing Axl and Mer actually lived longer. This may be because Axl and Mer target and destroy sick, dysfunctional neurons. In the presence of disease, there could be more dysfunctional neurons than normal, so Axl and Mer may be prompting the destruction of too many neurons, in effect hastening the disease.<\/p>\n<p>\u201cIt seems that we can modify the course of the disease in an animal model by manipulating Axl and Mer,\u201d says Lawrence Fourgeaud, a co-first author on the paper and former Salk research associate. The team cautions that more research needs to be done to determine if modulating the TAM receptors could be a viable therapy for neurodegenerative disease involving microglia.<\/p>\n<p>Other researchers on the paper were Yusuf Tufail, Humberto Leal-Bailey, Erin D. Lew, Patrick G. Burrola, Perri Callaway, Anna Zag\u00f3rska and Axel Nimmerjahn of the Salk Institute; and Carla V. Rothlin of the Yale University School of Medicine.<\/p>\n<p>The work was supported by the <a href=\"http:\/\/www.nih.gov\/\" target=\"_blank\" rel=\"noopener\">National Institutes of Health<\/a>, the <a href=\"http:\/\/helmsleytrust.org\/\" target=\"_blank\" rel=\"noopener\">Leona M. and Harry B. Helmsley Charitable Trust<\/a>, the <a href=\"http:\/\/www.hhmi.org\/\" target=\"_blank\" rel=\"noopener\">Howard Hughes Medical Institute<\/a>, and the <a href=\"http:\/\/nomisfoundation.ch\/\" target=\"_blank\" rel=\"noopener\">Nomis<\/a>, <a href=\"http:\/\/www.hnberger.org\/\" target=\"_blank\" rel=\"noopener\">H.N. and Frances C. Berger<\/a>, Fritz B. Burns, HKT, <a href=\"http:\/\/waittfoundation.org\/\" target=\"_blank\" rel=\"noopener\">Waitt<\/a>, <a href=\"http:\/\/www.ritaallenfoundation.org\/\" target=\"_blank\" rel=\"noopener\">Rita Allen<\/a>, and <a href=\"http:\/\/www.hearstfdn.org\/\" target=\"_blank\" rel=\"noopener\">Hearst<\/a> foundations.<\/p>","protected":false},"featured_media":9409,"template":"","faculty":[96],"disease-research":[459,124],"class_list":["post-9411","disclosure","type-disclosure","status-publish","has-post-thumbnail","hentry","faculty-greg-lemke","disease-research-glial-biology","disease-research-neuroscience-and-neurological-disorders"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.3 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Brain guardians remove dying neurons - 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\/brain-guardians-remove-dying-neurons\/\" \/>\n<meta property=\"og:locale\" content=\"zh_CN\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Brain guardians remove dying neurons - Salk Institute for Biological Studies\" \/>\n<meta property=\"og:description\" content=\"LA JOLLA\u2014By adolescence, your brain already contains most of the neurons that you\u2019ll have for the rest of your life. 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