{"id":15397,"date":"2018-04-19T11:24:40","date_gmt":"2018-04-19T11:24:40","guid":{"rendered":"http:\/\/www.neurodegenerationresearch.eu\/?p=15397"},"modified":"2018-04-19T11:24:40","modified_gmt":"2018-04-19T11:24:40","slug":"uncovering-the-early-origins-of-huntingtons-disease","status":"publish","type":"post","link":"https:\/\/neurodegenerationresearch.eu\/cs\/2018\/04\/uncovering-the-early-origins-of-huntingtons-disease\/","title":{"rendered":"Uncovering the early origins of Huntington&#8217;s disease"},"content":{"rendered":"<p>A team has developed a system to model Huntington\u2019s in human embryonic stem cells for the first time. In a report published in <em>Development<\/em>, they describe early abnormalities in the way Huntington\u2019s neurons look, and how these cells form larger structures that had not previously been associated with the disease.<\/p>\n<p>Huntington\u2019s is one of the few diseases with a straightforward genetic culprit: One hundred percent of people with a mutated form of the Huntingtin (HTT) gene develop the disease. The mutation takes the form of extra DNA, and causes the gene to produce a longer-than-normal protein.<\/p>\n<p>Research on Huntington\u2019s has thus far relied heavily on animal models of the disease. Suspecting that the disease works differently in humans, the researchers developed a cell-based human system for their research. They used the gene editing technology CRISPR to engineer a series of human embryonic stem cell lines, which were identical apart from the number of DNA repeats that occurred at the ends of their HTT genes.<\/p>\n<p>When cells divide, they typically each retain one nuclei. However, some of these mutated cells flaunted up to 12 nuclei\u2014suggesting that neurogenesis, or the generation of new neurons, was affected.<\/p>\n<p>Treatments for Huntington\u2019s have typically focused on blocking the activity of the mutant HTT protein. However, this research shows that the brain disruption may actually be due to a lack of HTT protein activity. The researchers created cell lines that completely lacked the HTT protein. These cells turned out to be very similar to those with Huntington\u2019s pathology, corroborating the idea that a lack of the protein\u2014not an excess of it\u2014is driving the disease.<\/p>\n<p><strong>Article:\u00a0 <a href=\"http:\/\/dev.biologists.org\/content\/145\/2\/dev156844\">&#8222;Chromosomal instability during neurogenesis in Huntington&#8217;s disease.&#8220;<\/a><\/strong><br \/>\n<strong>Reprinted from materials provided by <a href=\"https:\/\/www.rockefeller.edu\/news\/21212-uncovering-early-origins-huntingtons-disease\/\">Rockefeller University<\/a>.<\/strong><\/p>\n","protected":false},"excerpt":{"rendered":"<p>A team has developed a system to model Huntington\u2019s in [&hellip;]<\/p>\n<a href=\"https:\/\/neurodegenerationresearch.eu\/cs\/2018\/04\/uncovering-the-early-origins-of-huntingtons-disease\/\">View Post<\/a>","protected":false},"author":3,"featured_media":4999,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[22],"tags":[],"class_list":["post-15397","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-research-news"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.5 - 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