{"id":5087,"date":"2015-05-14T13:52:24","date_gmt":"2015-05-14T13:52:24","guid":{"rendered":"http:\/\/www.neurodegenerationresearch.eu\/?p=5087"},"modified":"2015-05-26T16:06:42","modified_gmt":"2015-05-26T16:06:42","slug":"scientists-create-mice-with-a-major-genetic-cause-of-als-and-ftd","status":"publish","type":"post","link":"https:\/\/neurodegenerationresearch.eu\/cs\/2015\/05\/scientists-create-mice-with-a-major-genetic-cause-of-als-and-ftd\/","title":{"rendered":"Scientists create mice with a major genetic cause of ALS and FTD"},"content":{"rendered":"<p><strong><em>Scientists at Mayo Clinic, Jacksonville, Florida, USA have created a novel mouse that exhibits the symptoms and neurodegeneration associated with the most common genetic forms of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), both of which are caused by a mutation in the a gene called C9ORF72. The study was<a href=\"http:\/\/www.sciencemag.org\/content\/early\/2015\/05\/13\/science.aaa9344?explicitversion=true\"> published<\/a> in the journal Science.<\/em><\/strong><\/p>\n<p>ALS destroys nerves that control essential movements, including speaking, walking, breathing and swallowing. After Alzheimer\u2019s disease, FTD is the most common form of early onset dementia. It is characterized by changes in personality, behavior and language due to loss of neurons in the brain\u2019s frontal and temporal lobes. Patients with mutations in the chromosome 9 open reading frame 72 (C9ORF72) gene have all or some symptoms associated with both disorders.<\/p>\n<p>\u201cOur mouse model exhibits the pathologies and symptoms of ALS and FTD seen in patients with theC9ORF72 mutation,\u201d said the study\u2019s lead author, Leonard Petrucelli, Ph.D., chair and Ralph and Ruth Abrams Professor of the Department of Neuroscience at Mayo Clinic, and a senior author of the study. \u201cThese mice could greatly improve our understanding of ALS and FTD and hasten the development of effective treatments.\u201d<\/p>\n<p>To create the model, Ms. Jeannie Chew, a Mayo Graduate School student and member of Dr. Petrucelli\u2019s team, injected the brains of newborn mice with a disease-causing version of the C9ORF72 gene. As the mice aged, they became hyperactive, anxious, and antisocial, in addition to having problems with movement that mirrored patient symptoms. The brains of the mice were smaller than normal and had fewer neurons in areas that controlled the affected behaviors. The scientists also found that the mouse brains had key hallmarks of the disorders, including toxic clusters of ribonucleic acids (RNA) and TDP-43, a protein that has long been known to go awry in the majority of ALS and FTD cases.<\/p>\n<p>\u201cFinding TDP-43 in these mice was unexpected\u201d Dr. Petrucelli said. \u201cWe don\u2019t yet know how foci and c9RAN proteins are linked to TDP-43 abnormalities, but with our new animal model, we now have a way to find out.\u201d Dr. Petrucelli and his team think these results are an important step in the development of therapies for these forms of ALS and FTD and other neurodegenerative disorders.<\/p>\n<p>Chew et al. \u201cC9ORF72 Repeat Expansions in Mice Cause TDP-43 Pathology, Neuronal Loss and Behavioral Deficits,\u201d Science, May 14, 2015.\u00a0DOI: 10.1126\/science.aaa9344<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Scientists at Mayo Clinic, Jacksonville, Florida, USA have created a [&hellip;]<\/p>\n<a href=\"https:\/\/neurodegenerationresearch.eu\/cs\/2015\/05\/scientists-create-mice-with-a-major-genetic-cause-of-als-and-ftd\/\">View Post<\/a>","protected":false},"author":3,"featured_media":5002,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[22],"tags":[118,130,72,119,193,238],"class_list":["post-5087","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-research-news","tag-als","tag-animal-cell-models","tag-dementia","tag-ftd","tag-motor-neuron-disease","tag-mouse"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.6 - 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