{"id":126366,"date":"2025-06-11T20:00:00","date_gmt":"2025-06-11T18:00:00","guid":{"rendered":"https:\/\/ibecbarcelona.eu\/?p=126366"},"modified":"2025-06-11T16:37:26","modified_gmt":"2025-06-11T14:37:26","slug":"scientists-map-the-first-step-in-alzheimers-protein-aggregation-and-discover-clues-for-future-therapies","status":"publish","type":"post","link":"https:\/\/ibecbarcelona.eu\/ca\/creen-un-mapa-del-primer-pas-en-l%27agregacio-de-proteines-de-l%27alzheimer-que-dona-pistes-per-a-futures-terapies","title":{"rendered":"Creen un mapa del primer pas en l’agregaci\u00f3 de prote\u00efnes de l’alzheimer que dona pistes per a futures ter\u00e0pies"},"content":{"rendered":"\n

Es tracta d’una an\u00e0lisi a una escala sense precedents: van estudiar m\u00e9s de 140.000 versions del p\u00e8ptid A\u03b242, que forma plaques nocives en el cervell.<\/strong> \u00c9s el primer mapa que revela com les mutacions afecten una prote\u00efna en el seu estat de transici\u00f3, una fase ef\u00edmera i dif\u00edcil d’estudiar.<\/strong> La troballa obre noves vies per a prevenir l’alzheimer i suggereix un m\u00e8tode aplicable a l’estudi d’altres prote\u00efnes implicades en diferents patologies.<\/strong> L’estudi, publicat en la revista cient\u00edfica Science Advances<\/em>, ha estat una col\u00b7laboraci\u00f3 entre l’Institut Wellcome Sanger, del Regne Unit, l’Institut de Bioenginyeria de Catalunya i el Centre de Regulaci\u00f3 Gen\u00f2mica, a Barcelona.<\/strong><\/p>\n\n\n\n

\"\"
Benedetta Bolognesi (IBEC) i Ben Lehner (Wellcome Sanger Institute and CRG).<\/figcaption><\/figure>\n\n\n\n

Un nou estudi a gran escala ha mapat els primers esdeveniments moleculars que impulsen la formaci\u00f3 dels nocius agregats de prote\u00efnes amiloides presents en la malaltia d’Alzheimer, apuntant cap a un potencial nou objectiu terap\u00e8utic.<\/p>\n\n\n\n

\n

L’escala a la qual analitzem els p\u00e8ptids amiloides no tenia precedents: \u00e9s una cosa que no s’havia fet abans i hem demostrat que \u00e9s un nou m\u00e8tode molt efica\u00e7 que cal continuar desenvolupant.<\/p>\n\n\n\n

Ben Lehner<\/p>\n<\/blockquote>\n\n\n\n

Investigadors i investigadores de l’Institut Wellcome Sanger<\/a>, l’Institut de Bioenginyeria de Catalunya (IBEC)<\/a> i el Centre de Regulaci\u00f3 Gen\u00f2mica (CRG)<\/a> han utilitzat la gen\u00f2mica a gran escala i l’aprenentatge autom\u00e0tic (machine learning<\/em>) per a estudiar m\u00e9s de 140.000 versions d’un p\u00e8ptid anomenat A\u03b242, que forma plaques nocives en el cervell i se sap que exerceix un paper central en l’alzheimer.<\/p>\n\n\n\n

“L’enfocament que fem servir en aquest estudi obre la porta a revelar les estructures d’altres estats de transici\u00f3 de prote\u00efnes, inclosos els implicats en altres malalties neurodegeneratives. L’escala a la qual analitzem els p\u00e8ptids amiloides no tenia precedents: \u00e9s una cosa que no s’havia fet abans i hem demostrat que \u00e9s un nou m\u00e8tode molt efica\u00e7 que cal continuar desenvolupant.\u201d Comenta El professor Ben Lehner<\/strong>, coautor principal de l’estudi, cap de Gen\u00f2mica Generativa i Sint\u00e8tica en l’Institut Wellcome Sanger i professor de recerca ICREA en el CRG. \u201cEsperem que aix\u00f2 ens acosti un pas m\u00e9s al desenvolupament de tractaments contra la malaltia d’Alzheimer i altres malalties neurodegeneratives”, afegeix Lehner.<\/p>\n\n\n\n

Aquesta recerca \u00e9s un pas significatiu per a ajudar els cient\u00edfics a trobar noves maneres de prevenir la malaltia d’Alzheimer. A m\u00e9s, els m\u00e8todes utilitzats en l’estudi podrien aplicar-se \u00e0mpliament a altres reaccions de prote\u00efnes.<\/p>\n\n\n\n

Comprendre l’origen de la neurodegeneraci\u00f3<\/strong><\/h4>\n\n\n\n

M\u00e9s de 55 milions de persones a tot el m\u00f3n pateixen dem\u00e8ncia i s’estima que entre el 60% i el 70\u202f% d’aquests casos s\u00f3n malaltia d’Alzheimer.[1]<\/a> La majoria dels tractaments actuals per a l’alzheimer no retarden ni detenen la malaltia, per\u00f2 ajuden a controlar els s\u00edmptomes.<\/p>\n\n\n\n

La beta amiloide (A\u03b2) \u00e9s un p\u00e8ptid, una cadena curta d’amino\u00e0cids. Els p\u00e8ptids beta amiloides tenen tend\u00e8ncia a agrupar-se i agregar-se, formant estructures allargades conegudes com a fibril\u00b7les amiloides. Amb el temps, aquestes fibril\u00b7les s’acumulen en plaques que s\u00f3n les caracter\u00edstiques patol\u00f2giques distintives de m\u00e9s de 50 malalties neurodegeneratives i, sobretot, exerceixen un paper central cr\u00edtic en la malaltia d’Alzheimer.[2]<\/a><\/p>\n\n\n\n

\n

El nostre m\u00e8tode d’estudi \u00e9s crucial per a comprendre els primers esdeveniments en el proc\u00e9s d’agregaci\u00f3 de prote\u00efnes que condueix a la dem\u00e8ncia, per\u00f2 tamb\u00e9 ofereix un marc poder\u00f3s per a disseccionar els passos inicials clau de moltes reaccions biol\u00f2giques, no nom\u00e9s les que hem estudiat fins ara.<\/p>\n\n\n\n

Benedetta Bolognesi<\/p>\n<\/blockquote>\n\n\n\n

Perqu\u00e8 els p\u00e8ptids A\u03b2 que flueixen lliurement es converteixin en fibril\u00b7les estables i estructurades, requereixen una certa quantitat d’energia. L’estat intermedi, de curta vida, just abans que els p\u00e8ptids comencin a formar una fibril\u00b7la es coneix com a “estat de transici\u00f3”: \u00e9s extremadament poc probable que es formi, ra\u00f3 per la qual les fibril\u00b7les mai es formen en la majoria de les persones.<\/p>\n\n\n\n

Comprendre aquestes estructures i reaccions \u00e9s essencial per a desenvolupar ter\u00e0pies que puguin tractar i prevenir malalties neurodegeneratives. No obstant aix\u00f2, \u00e9s molt dif\u00edcil estudiar estats de transici\u00f3 d’alta energia i curta durada utilitzant m\u00e8todes cl\u00e0ssics. \u00c9s per aquest motiu que continua sent un gran desafiament en la recerca de l’alzheimer comprendre com A\u03b2 comen\u00e7a a agregar-se.<\/p>\n\n\n\n

Per aix\u00f2, en aquest nou estudi, investigadors i investigadores de l’Institut Sanger, el Centre de Regulaci\u00f3 Gen\u00f2mica i l’Institut de Bioenginyeria de Catalunya han tractat d’entendre com afecta el canvi en la gen\u00e8tica del A\u03b2 a la velocitat de la reacci\u00f3 d’agregaci\u00f3. Espec\u00edficament, els investigadors van estudiar el A\u03b242, un tipus de p\u00e8ptid A\u03b2 amb 42 amino\u00e0cids que es troba comunament en les persones amb alzheimer.<\/p>\n\n\n\n

\u201cEl nostre m\u00e8tode d’estudi \u00e9s crucial per a comprendre els primers esdeveniments en el proc\u00e9s d’agregaci\u00f3 de prote\u00efnes que condueix a la dem\u00e8ncia, per\u00f2 tamb\u00e9 ofereix un marc poder\u00f3s per a disseccionar els passos inicials clau de moltes reaccions biol\u00f2giques, no nom\u00e9s les que hem estudiat fins ara. Espero amb inter\u00e8s veure totes les formes en qu\u00e8 s’aplicar\u00e0 aquesta estrat\u00e8gia en el futur\u201d, explica la Dra. Benedetta Bolognesi<\/strong>, coautora principal de l’estudi i l\u00edder del grup de Transicions de Fase de Prote\u00efnes en la Salut i la Malaltia<\/a> a l’IBEC.<\/p>\n\n\n\n

Una an\u00e0lisi a gran escala<\/strong><\/h4>\n\n\n\n

Els investigadors van utilitzar una combinaci\u00f3 de tres t\u00e8cniques per a manejar grans quantitats d’informaci\u00f3 sobre A\u03b242 al mateix temps. L’equip va fer servir la s\u00edntesi massiva en paral\u00b7lel d’ADN per a estudiar com els amino\u00e0cids canviants en el A\u03b2 afecten la quantitat d’energia necess\u00e0ria per a formar una fibril\u00b7la, i c\u00e8l\u00b7lules de llevat modificades gen\u00e8ticament per a mesurar aquesta taxa de reacci\u00f3.[3]<\/a> A continuaci\u00f3, van usar l’aprenentatge autom\u00e0tic, un tipus d’intel\u00b7lig\u00e8ncia artificial,[4]<\/a> per a analitzar els resultats i generar un panorama energ\u00e8tic complet de la reacci\u00f3 d’agregaci\u00f3 de la beta amiloide, mostrant l’efecte de totes les possibles mutacions d’aquesta prote\u00efna sobre la velocitat de formaci\u00f3 de les fibril\u00b7les.<\/p>\n\n\n\n

Aquestes t\u00e8cniques van permetre a l’equip de recerca realitzar l’estudi a gran escala: “Vam mesurar l’efecte de m\u00e9s de 140.000 mutacions de A\u03b242 i vam poder aplicar un tipus d’aprenentatge autom\u00e0tic conegut com a xarxes neuronals per a extreure l’energia que impulsa el proc\u00e9s d’agregaci\u00f3 patol\u00f2gica per a cadascuna d’elles.\u201d, detalla la Dra. Mireia Seuma<\/strong>, coautora de l’estudi, anteriorment en l’IBEC i en el CRG, i ara cient\u00edfica s\u00e8nior de ALLOX. Aquesta escala, que no s’havia aconseguit abans, ajuda a millorar la qualitat i precisi\u00f3 dels models desenvolupats en l’estudi. \u201cLes mutacions, i les interaccions entre elles, ens van permetre “dibuixar un retrat” de l’estat de transici\u00f3 de la reacci\u00f3 d’agregaci\u00f3 del A\u03b242. Aquesta \u00e9s la conformaci\u00f3 clau que impulsa la reacci\u00f3 d’agregaci\u00f3, i \u00e9s extremadament complex (si no impossible) d’estudiar amb m\u00e8todes biof\u00edsics cl\u00e0ssics”, afegeix Seuma.<\/p>\n\n\n\n

Els investigadors van descobrir que nom\u00e9s unes poques interaccions clau entre parts espec\u00edfiques de la prote\u00efna amiloide tenien una forta influ\u00e8ncia en la velocitat de formaci\u00f3 de les fibril\u00b7les. Van descobrir que la reacci\u00f3 d’agregaci\u00f3 del A\u03b242 comen\u00e7a al final de la prote\u00efna, coneguda com a regi\u00f3 C-terminal, un dels nuclis hidrof\u00f2bics de la prote\u00efna, la regi\u00f3 repel\u00b7lent a l’aigua del p\u00e8ptid. Com \u00e9s aqu\u00ed on el p\u00e8ptid comen\u00e7a a agregar-se en una fibril\u00b7la, els investigadors suggereixen que s\u00f3n precisament les interaccions a la regi\u00f3 C-terminal les que han de prevenir-se per a protegir-se i tractar la malaltia d’Alzheimer.<\/p>\n\n\n\n

Aquest \u00e9s el primer mapa a gran escala que mostra com les mutacions influeixen en el comportament d’una prote\u00efna en el seu estat de transici\u00f3, que \u00e9s molt dif\u00edcil d’estudiar. En identificar les interaccions que impulsen la formaci\u00f3 de fibril\u00b7les d’amiloide, l’equip creu que prevenir la formaci\u00f3 d’aquest estat de transici\u00f3 podria aplanar el cam\u00ed per a noves estrat\u00e8gies terap\u00e8utiques, oferint esperan\u00e7a per a futurs tractaments per a l’alzheimer. A m\u00e9s, els investigadors posen l’accent en l’\u00e0mplia usabilitat del seu m\u00e8tode, assenyalant que t\u00e9 potencial per a ser utilitzat en una \u00e0mplia gamma de prote\u00efnes i malalties en futurs estudis.<\/p>\n\n\n\n

\n\n\n\n

Article de refer\u00e8ncia<\/strong><\/p>\n\n\n\n

Anna Arutyunyan, Mireia Seuma, Andre J. Faure, Benedetta Bolognesi, Ben Lehner. Massively parallel genetic perturbation suggests the energetic structure of an amyloid-<\/strong>\u03b2<\/strong> transition state<\/strong>. Science Advances<\/em> (2025). DOI: 10.1126\/sciadv.adv1422<\/a><\/p>\n\n\n\n

\n\n\n\n

[1]<\/a> Organitzaci\u00f3 Mundial de la Salut. Dem\u00e8ncia. Disponible en: https:\/\/www.who.int\/es\/news-room\/fact-sheets\/detail\/dementia<\/a> [\u00daltim acc\u00e9s: juny de 2025]<\/p>\n\n\n\n

[2]<\/a> C. M. Dobson (2017) The Amyloid Phenomenon and Its Links with Human Disease. Cold Spring Harb. Perspect. Biol. 9<\/p>\n\n\n\n

[3]<\/a> La seq\u00fcenciaci\u00f3 massiva en paral\u00b7lel (MPS, per les seves sigles en angl\u00e8s), tamb\u00e9 coneguda com a seq\u00fcenciaci\u00f3 de pr\u00f2xima generaci\u00f3 (NGS, per les seves sigles en angl\u00e8s), \u00e9s un m\u00e8tode d’alt rendiment per a seq\u00fcenciar fragments d’ADN o ARN en paral\u00b7lel. Permet seq\u00fcenciar milions de fragments simult\u00e0niament.<\/p>\n\n\n\n

[4]<\/a> L’aprenentatge autom\u00e0tic consisteix a utilitzar algorismes per a analitzar grans quantitats de dades procedents de conjunts de dades de gran grand\u00e0ria amb la finalitat d’identificar patrons en com els canvis en els amino\u00e0cids afecten la formaci\u00f3 de fibril\u00b7les i predir el panorama energ\u00e8tic de l’agregaci\u00f3 de beta amiloide.<\/p>\n","protected":false},"excerpt":{"rendered":"

Es tracta d’una an\u00e0lisi a una escala sense precedents: van estudiar m\u00e9s de 140.000 versions del p\u00e8ptid A\u03b242, que forma plaques nocives en el cervell. \u00c9s el primer mapa que revela com les mutacions afecten una prote\u00efna en el seu estat de transici\u00f3, una fase ef\u00edmera i dif\u00edcil d’estudiar. La troballa obre noves vies per a prevenir l’alzheimer i suggereix un m\u00e8tode aplicable a l’estudi d’altres prote\u00efnes implicades en diferents patologies. L’estudi, publicat en la revista cient\u00edfica Science Advances, ha estat una col\u00b7laboraci\u00f3 entre l’Institut Wellcome Sanger, del Regne Unit, l’Institut de Bioenginyeria de Catalunya i el Centre de Regulaci\u00f3 Gen\u00f2mica, a Barcelona.<\/p>\n","protected":false},"author":37,"featured_media":126356,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[96],"tags":[1627,1107,538,1776],"post_formats":[],"class_list":["post-126366","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-noticies-de-recerca","tag-alzheimer-ca-2","tag-benedetta-bolognesi-ca","tag-malalties-neurodegeneratives","tag-protein-phase-transitions-in-health-and-disease-ca"],"yoast_head":"\nCreen un mapa del primer pas en l'agregaci\u00f3 de prote\u00efnes de l'alzheimer que dona pistes per a futures ter\u00e0pies - Institute for Bioengineering of Catalonia<\/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:\/\/ibecbarcelona.eu\/ca\/creen-un-mapa-del-primer-pas-en-l'agregacio-de-proteines-de-l'alzheimer-que-dona-pistes-per-a-futures-terapies\/\" \/>\n<meta property=\"og:locale\" content=\"ca_ES\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Creen un mapa del primer pas en l'agregaci\u00f3 de prote\u00efnes de l'alzheimer que dona pistes per a futures ter\u00e0pies - Institute for Bioengineering of Catalonia\" \/>\n<meta property=\"og:description\" content=\"Es tracta d'una an\u00e0lisi a una escala sense precedents: van estudiar m\u00e9s de 140.000 versions del p\u00e8ptid A\u03b242, que forma plaques nocives en el cervell. \u00c9s el primer mapa que revela com les mutacions afecten una prote\u00efna en el seu estat de transici\u00f3, una fase ef\u00edmera i dif\u00edcil d'estudiar. 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