{"id":4541,"date":"2020-06-22T14:32:31","date_gmt":"2020-06-22T18:32:31","guid":{"rendered":"https:\/\/ccna-ccnv.ca\/ccna_publication\/perturbed-mitochondria-er-contacts-in-live-neurons-that-model-the-amyloid-pathology-of-alzheimers-disease-2\/"},"modified":"2024-12-03T14:56:58","modified_gmt":"2024-12-03T19:56:58","slug":"perturbed-mitochondria-er-contacts-in-live-neurons-that-model-the-amyloid-pathology-of-alzheimers-disease-2","status":"publish","type":"ccna_publication","link":"https:\/\/ccna-ccnv.ca\/fr\/ccna_publication\/perturbed-mitochondria-er-contacts-in-live-neurons-that-model-the-amyloid-pathology-of-alzheimers-disease-2\/","title":{"rendered":"Perturbed mitochondria-ER contacts in live neurons that model the amyloid pathology of Alzheimer&rsquo;s disease"},"content":{"rendered":"<h2 class=\"\">ABSTRACT<\/h2>\n<p id=\"p-1\">The use of fixed fibroblasts from familial and sporadic Alzheimer&rsquo;s disease patients has previously indicated an upregulation of mitochondria\u2013ER contacts (MERCs) as a hallmark of Alzheimer&rsquo;s disease. Despite its potential significance, the relevance of these results is limited because they were not extended to live neurons. Here we performed a dynamic\u00a0<em>in vivo<\/em>\u00a0analysis of MERCs in hippocampal neurons from McGill-R-Thy1-APP transgenic rats, a model of Alzheimer&rsquo;s disease-like amyloid pathology. Live FRET imaging of neurons from transgenic rats revealed perturbed \u2018lipid-MERCs\u2019 (gap width &lt;10\u2005nm), while \u2018Ca<sup>2+<\/sup>-MERCs\u2019 (10\u201320\u2005nm gap width) were unchanged.\u00a0<em>In situ<\/em>\u00a0TEM showed no significant differences in the lipid-MERCs:total MERCs or lipid-MERCs:mitochondria ratios; however, the average length of lipid-MERCs was significantly decreased in neurons from transgenic rats as compared to controls. In accordance with FRET results, untargeted lipidomics showed significant decreases in levels of 12 lipids and bioenergetic analysis revealed respiratory dysfunction of mitochondria from transgenic rats. Thus, our results reveal changes in MERC structures coupled with impaired mitochondrial functions in Alzheimer&rsquo;s disease-related neurons.<\/p>\n","protected":false},"author":19,"featured_media":0,"template":"","meta":{"_acf_changed":false},"studies-relation":[],"class_list":["post-4541","ccna_publication","type-ccna_publication","status-publish","hentry"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v28.2 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Perturbed mitochondria-ER contacts in live neurons that model the amyloid pathology of Alzheimer&#039;s disease - CCNA - CCNV<\/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:\/\/ccna-ccnv.ca\/fr\/ccna_publication\/perturbed-mitochondria-er-contacts-in-live-neurons-that-model-the-amyloid-pathology-of-alzheimers-disease-2\/\" \/>\n<meta property=\"og:locale\" content=\"fr_CA\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Perturbed mitochondria-ER contacts in live neurons that model the amyloid pathology of Alzheimer&#039;s disease - 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