{"id":3248,"date":"2024-06-27T10:54:00","date_gmt":"2024-06-27T08:54:00","guid":{"rendered":"https:\/\/www.sfb274.de\/?p=3248"},"modified":"2024-10-23T12:07:37","modified_gmt":"2024-10-23T10:07:37","slug":"amyloidosis-triggers-age-related-oligodendrocyte-and-myelin-damage","status":"publish","type":"post","link":"https:\/\/www.sfb274.de\/en\/amyloidosis-triggers-age-related-oligodendrocyte-and-myelin-damage\/","title":{"rendered":"Amyloidosis triggers age-related oligodendrocyte and myelin damage"},"content":{"rendered":"\n<p><strong>Age-related myelin damage leads to white matter inflammation, but its impact on chronic neurodegenerative diseases remains unclear. A recent study reveals that amyloidosis alone can cause age-related oligodendrocyte and myelin damage in mouse models of Alzheimer&#8217;s disease. The research team discovered that CD8 T cells contribute to neurodegenerative diseases associated with amyloidosis by abnormally activating microglia, resulting in myelin damage.<\/strong><\/p>\n\n\n\n<p>Our results show that antibody mediated CD8+ T cell depletion rescued oligodendrocyte and myelin damage in 5xFAD mice. Additionally, CD8+ T cell depletion improved spatial learning and memory. To mechanistically understand how CD8+ T cells drive the pathology, we performed single cell RNA sequencing and identified a decrease in a specific microglia cluster enriched in major histocompatibility complex class II (MHCII) genes in CD8+ T cell depleted mice. We observed an upregulation in MHCII+ microglia populations in the vicinity of T cells in both mouse and human autopsy tissue. We further provide evidence that these abnormally activated microglia display myelin damaging activity.<\/p>\n\n\n\n<p>Read the full press release <a href=\"https:\/\/www.synergy-munich.de\/news-events\/news\/amyloidosis-triggers-age-related-oligodendrocyte-and-myelin-damage\/24b43a307e39155f\" target=\"_blank\" rel=\"noreferrer noopener\">here<\/a>.<\/p>\n\n\n\n<p>Read the full article <a href=\"https:\/\/doi.org\/10.1038\/s41593-024-01682-8\" target=\"_blank\" rel=\"noreferrer noopener\">here<\/a>.<br><em>Shreeya Kedia,\u00a0Hao Ji,\u00a0Ruoqing Feng,\u00a0Peter Androvic,\u00a0Lena Spieth,\u00a0Lu Liu,\u00a0Jonas Franz,\u00a0Hanna Zdiarstek,\u00a0Katrin Perez Anderson,\u00a0Cem Kaboglu,\u00a0Qian Liu,\u00a0Nicola Mattugini,\u00a0Fatma Cherif,\u00a0Danilo Prtvar,\u00a0<mark style=\"background-color:rgba(0, 0, 0, 0)\" class=\"has-inline-color has-theme-palette-1-color\">Ludovico Cantuti-Castelvetri,\u00a0Arthur Liesz,\u00a0Martina Schifferer,\u00a0Christine Stadelmann,<\/mark>\u00a0Sabina Tahirovic,\u00a0Ozgun Gokce\u00a0&amp;\u00a0<mark style=\"background-color:rgba(0, 0, 0, 0)\" class=\"has-inline-color has-theme-palette-1-color\"><strong>Mikael Simons,<\/strong><\/mark> T cell-mediated microglial activation triggers myelin pathology in a mouse model of amyloidosis. publishes in Nature Neuroscience (2024).\u00a0https:\/\/doi.org\/10.1038\/s41593-024-01682-8<\/em><\/p>\n\n\n\n<p><strong><mark style=\"background-color:rgba(0, 0, 0, 0)\" class=\"has-inline-color has-theme-palette-1-color\">Mikael Simons<\/mark><\/strong> is the project leader of projects <a href=\"https:\/\/www.sfb274.de\/en\/project\/linking-lipid-metabolism-to-inflammation-in-models-of-demyelinating-injury\/\" target=\"_blank\" rel=\"noreferrer noopener\">A06 <\/a>and <a href=\"https:\/\/www.sfb274.de\/en\/project\/function-of-satellite-oligodendrocytes-in-remyelination\/\" target=\"_blank\" rel=\"noreferrer noopener\">B01<\/a>, as well as service project <a href=\"https:\/\/www.sfb274.de\/en\/project\/genomics-and-bioinformatics-platform\/\" target=\"_blank\" rel=\"noreferrer noopener\">Z02<\/a>.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Age-related myelin damage leads to white matter inflammation, but its impact on chronic neurodegenerative diseases remains unclear. A recent study reveals that amyloidosis alone can cause age-related oligodendrocyte and myelin damage in mouse models of Alzheimer&#8217;s disease. The research team discovered that CD8 T cells contribute to neurodegenerative diseases associated with amyloidosis by abnormally activating&#8230;<\/p>\n","protected":false},"author":4,"featured_media":3258,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_kad_blocks_custom_css":"","_kad_blocks_head_custom_js":"","_kad_blocks_body_custom_js":"","_kad_blocks_footer_custom_js":"","_kad_post_transparent":"","_kad_post_title":"","_kad_post_layout":"","_kad_post_sidebar_id":"","_kad_post_content_style":"","_kad_post_vertical_padding":"","_kad_post_feature":"","_kad_post_feature_position":"","_kad_post_header":false,"_kad_post_footer":false,"footnotes":""},"categories":[33],"class_list":["post-3248","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-other"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v25.7 - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>Amyloidosis triggers age-related oligodendrocyte and myelin damage - 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