{"id":49630,"date":"2016-06-10T00:00:00","date_gmt":"2016-06-09T23:00:00","guid":{"rendered":"http:\/\/www.pcb.ub.edu\/discovery-of-molecular-protection-linked-to-a-degenerative-neuromuscular-disease\/"},"modified":"2020-11-18T14:56:04","modified_gmt":"2020-11-18T13:56:04","slug":"discovery-of-molecular-protection-linked-to-a-degenerative-neuromuscular-disease","status":"publish","type":"post","link":"https:\/\/www.pcb.ub.edu\/en\/discovery-of-molecular-protection-linked-to-a-degenerative-neuromuscular-disease\/","title":{"rendered":"Discovery of molecular protection linked to a degenerative neuromuscular disease"},"content":{"rendered":"<p>In Kennedy\u2019s disease, the muscle cells and motor neurons\u2014the latter linked to muscle function too\u2014are damaged as a result of the accumulation of androgen receptor fibers\u2014a process that causes them to die.&#8221;Many aspects of diseases involving aggregates, such as Alzheimer\u2019s and Parkinson\u2019s, are unknown. In this regard, Kennedy\u2019s disease is in a worse position because it is a rare condition,&#8221; explains Xavier Salvatella, head of the\u00a0<a href=\"http:\/\/www.irbbarcelona.org\/en\/research\/laboratory-of-molecular-biophysics\" target=\"_blank\" rel=\"noopener noreferrer\">Molecular Biophysics Lab<\/a>\u00a0at IRB Barcelona.<\/p>\n<p>The onset of this genetically inherited disease occurs in late adulthood, affecting one in every 40,000 men and causing progressive deterioration of all muscles. Although not fatal, the condition is debilitating, and 20% of those affected eventually need a wheel chair.<\/p>\n<p>The mutation carried by those affected by Kennedy\u2019s disease causes a repeated and excessively long chain of a specific amino acid, namely glutamine, which impairs the activity of the androgen receptor. This protein, which activates the hormone testosterone, is responsible for triggering the genetic programme that favours the differential characteristics of men: more hair, deep voice, larger hands, etc.<\/p>\n<p>During adolescence, and depending on the extent to which they are affected, boys with the mutation do not fully develop the male phenotype, but this is often not diagnosed. In a second stage, in adulthood, muscle degeneration begins.\u00a0&#8220;It is known that the longer the polyglutamine chain, the earlier the onset of muscle atrophy. What we don\u2019t know and what this study helps us to understand is whythe harmful effect is triggered when the length of the poly glutamine exceed 38 residues&#8221;.<\/p>\n<p>Thanks to access to one of the main Nuclear Magnetic Resonance facilities in Europe, located at the University of Florence, for the first time the scientists have studied the protein in a test tube. They have observed that right next to the glutamine chain there is a region comprised by four leucine residues that allay the effects of the mutation.<\/p>\n<p>Salvatella\u2019s work indicates that\u00a0in-depth knowledge of the different protein sequences and how they affect each other may reveal new therapeutic targets. The IRB Barcelona scientist is engaged in several research lines devoted to Kennedy\u2019s disease. His studies involve the development of techniques and studies with mice and with chaperones\u2014proteins that bind to any protein that is about to aggregate.\u00a0Backed by funding from the \u201cFundaci\u00f3n La Marat\u00f3 de TV3\u201d and a\u00a0Consolidator Grant\u00a0from the European Research Council, Salvatella studies the sequence of molecular events that causes the aggregation of androgen receptors. He and his team seek to determine the regions of the protein sequence responsible for aggregation in order to identify valid targets to direct therapies and to prevent this process. &#8220;This is the first article in a series in which we can slowly explain how we think Kennedy\u2019s disease develops and propose therapeutic solutions,&#8221; he explains.<\/p>\n<p>The Iranian researcher\u00a0Bahareh Eftekharzadeh\u00a0is the first author of the paper. She did her PhD at IRB Barcelona funded by an International \u201cla Caixa\u201d Fellowship and is currently doing postdoc work at the University of Harvard. Salvatella\u2019s lab also receives funding from the Ministry of the Economy and Competitiveness, complemented by support from the ERDF and the Government of Catalonia.<\/p>\n<p>\n\u2022\u00a0<strong>Reference article:<\/strong><br \/>\n<strong>Sequence Context influences the Structure and Aggregation Behavior of a PolyQ Tract.<\/strong>\u00a0B. Eftekharzadeh, A. Piai, G. Chiesa, D. Mungianu, J. Garc\u00eda, R. Pierattelli, E. C. Felli, and X. Salvatella. Biophysical Journal\u00a0(7 June 2016). Doi:\u00a0<a href=\"http:\/\/www.cell.com\/biophysj\/fulltext\/S0006-3495(16)30217-X\" target=\"_blank\" rel=\"noopener noreferrer\">10.1016\/j.bpj.2016.04.022<\/a><\/p>\n","protected":false},"excerpt":{"rendered":"<p>Xavier Salvatella, ICREA researcher at the Institute for Research in Biomedicine (<a href=\"http:\/\/www.pcb.ub.edu\/portal\/en\/cerca?p_p_id=cercador_WAR_empleatsempresesportlet&amp;p_p_lifecycle=0&amp;p_p_state=normal&amp;p_p_mode=view&amp;p_p_col_id=column-1&amp;p_p_col_count=1&amp;_cercador_WAR_empleatsempresesportlet_keywords=irb&amp;_cercador_WAR_empleatsempresesportlet_tab=1\" target=\"_blank\" rel=\"noopener noreferrer\">IRB Barcelona<\/a>) at PCB,\u00a0in collaboration with scientists from the University of Florence (Italy), has described a molecular system of protection that involves the androgen receptor protein, a molecule that is mutated in patients with Kennedy\u2019s disease and which cause progressive muscle wastage.<\/p>\n<p>\u00a0<\/p>\n","protected":false},"author":1,"featured_media":53638,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"inline_featured_image":false,"footnotes":""},"categories":[8],"tags":[],"class_list":["post-49630","post","type-post","status-publish","format-standard","has-post-thumbnail","category-uncategorized"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.5 - 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