{"id":30885094,"date":"2025-02-06T05:41:29","date_gmt":"2025-02-06T04:41:29","guid":{"rendered":"https:\/\/www.upo.es\/diario\/?p=30885094"},"modified":"2025-02-07T17:40:16","modified_gmt":"2025-02-07T16:40:16","slug":"the-two-proteins-involved-in-alzheimers-disease-affect-brain-circuits-differently","status":"publish","type":"post","link":"https:\/\/www.upo.es\/diario\/english\/2025\/02\/the-two-proteins-involved-in-alzheimers-disease-affect-brain-circuits-differently\/","title":{"rendered":"The two proteins involved in Alzheimer\u2019s disease affect brain circuits differently"},"content":{"rendered":"
\"El<\/a>
\u00c1ngel Deprada, Arnaldo Parra-Damas, Paula Sotillo, Carles Saura y Maria Dolores Capilla-L\u00f3pez | UAB<\/figcaption><\/figure>\n

Published in Molecular Psychiatry<\/em> (Nature<\/em> group), the findings reveal that tau accumulation in the hippocampus leads to memory deficits, while beta-amyloid buildup in the amygdala triggers emotional disturbances such as anxiety and fear\u2014both early symptoms of the disease. Moreover, the combination of these two pathologies intensifies brain inflammation and dysfunction, amplifying their overall impact.<\/p>\n

For decades, research into Alzheimer\u2019s disease has been shaped by two theories: one suggesting that the disease originates from tau buildup inside neurons, and another pointing to beta-amyloid accumulation as the primary trigger. These perspectives have largely dictated current therapeutic approaches, with treatments aiming to prevent the buildup of either tau or beta-amyloid in hopes of slowing disease progression. However, the research team led by researchers Carles Saura and Arnaldo Parra-Damas, from the UAB Department of Biochemistry and Molecular Biology and the INc-UAB, argues that a dual-targeted therapeutic strategy may be necessary to effectively combat this disease.<\/p>\n

This breakthrough was made possible by the development of a novel transgenic mouse model that replicates both tau and beta-amyloid pathologies. \u201cAlthough both proteins accumulate in the brains of Alzheimer\u2019s patients, most animal models used for studying the disease typically focus on only one of these factors\u201d, explains researcher Maria Dolores Capilla, lead author of the study. \u201cIn our research, we generated a transgenic mouse model exhibiting both tau and beta-amyloid accumulation, allowing us to analyze their individual and combined effects\u201d, adds the INc-UAB researcher.<\/p>\n

These findings could reshape current treatment strategies, which often target only one of these toxic proteins. \u201cExisting therapies have not achieved clear clinical benefits. Our study suggests that a therapeutic approach addressing multiple disease mechanisms\u2014such as phosphorylated tau and beta-amyloid\u2014could be more effective\u201d, concludes Carles Saura.<\/p>\n

While further research is needed to confirm its applicability to humans, this study represents a significant step toward new investigative pathways for Alzheimer\u2019s treatment, the research team concludes.<\/p>\n

Article:<\/strong> Capilla-L\u00f3pez MD., Deprada A., Andrade-Talavera Y., Mart\u00ednez-Gallego I., Coatl-Cuaya H., Sotillo P., Rodr\u00edguez-Alvarez J., Rodr\u00edguez-Moreno A., Parra-Damas A., Saura C.A. Synaptic vulnerability to amyloid-<\/strong>\u03b2<\/strong> and tau pathologies differentially disrupts emotional and memory neural circuits<\/strong> Mol Psychiatry<\/em> (2025). https:\/\/www.nature.com\/articles\/s41380-025-02901-9<\/a><\/p>\n","protected":false},"excerpt":{"rendered":"

A study using a new animal model of Alzheimer\u2019s disease suggests a potential breakthrough in treatment strategies. Current therapies mainly focus on blocking just one of the toxic proteins associated with the disease, but this discovery could pave the way for more comprehensive approaches.<\/p>\n","protected":false},"author":6,"featured_media":30885063,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0,"footnotes":""},"categories":[3258],"tags":[272],"class_list":["post-30885094","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-english","tag-alzheimer"],"_links":{"self":[{"href":"https:\/\/www.upo.es\/diario\/wp-json\/wp\/v2\/posts\/30885094","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.upo.es\/diario\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.upo.es\/diario\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.upo.es\/diario\/wp-json\/wp\/v2\/users\/6"}],"replies":[{"embeddable":true,"href":"https:\/\/www.upo.es\/diario\/wp-json\/wp\/v2\/comments?post=30885094"}],"version-history":[{"count":2,"href":"https:\/\/www.upo.es\/diario\/wp-json\/wp\/v2\/posts\/30885094\/revisions"}],"predecessor-version":[{"id":30885127,"href":"https:\/\/www.upo.es\/diario\/wp-json\/wp\/v2\/posts\/30885094\/revisions\/30885127"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.upo.es\/diario\/wp-json\/wp\/v2\/media\/30885063"}],"wp:attachment":[{"href":"https:\/\/www.upo.es\/diario\/wp-json\/wp\/v2\/media?parent=30885094"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.upo.es\/diario\/wp-json\/wp\/v2\/categories?post=30885094"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.upo.es\/diario\/wp-json\/wp\/v2\/tags?post=30885094"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}