{"id":4724,"date":"2021-03-11T19:30:23","date_gmt":"2021-03-12T00:30:23","guid":{"rendered":"https:\/\/ccna-ccnv.ca\/ccna_publication\/multimodal-imaging-in-rat-model-recapitulates-alzheimers-disease-biomarkers-abnormalities-2\/"},"modified":"2024-12-03T14:57:29","modified_gmt":"2024-12-03T19:57:29","slug":"multimodal-imaging-in-rat-model-recapitulates-alzheimers-disease-biomarkers-abnormalities-2","status":"publish","type":"ccna_publication","link":"https:\/\/ccna-ccnv.ca\/fr\/ccna_publication\/multimodal-imaging-in-rat-model-recapitulates-alzheimers-disease-biomarkers-abnormalities-2\/","title":{"rendered":"Multimodal Imaging in Rat Model Recapitulates Alzheimer&rsquo;s Disease Biomarkers Abnormalities"},"content":{"rendered":"<h2 id=\"idm139981394009792title\" class=\"head no_bottom_margin ui-helper-clearfix\">Abstract<\/h2>\n<div>\n<p id=\"__p2\" class=\"p p-first\">Imaging biomarkers are frequently proposed as endpoints for clinical trials targeting brain amyloidosis in Alzheimer&rsquo;s disease (AD); however, the specific impact of amyloid-\u03b2 (A\u03b2) aggregation on biomarker abnormalities remains elusive in AD. Using the McGill-R-Thy1-APP transgenic rat as a model of selective A\u03b2 pathology, we characterized the longitudinal progression of abnormalities in biomarkers commonly used in AD research. Middle-aged (9\u201311 months) transgenic animals (both male and female) displayed mild spatial memory impairments and disrupted cingulate network connectivity measured by resting-state fMRI, even in the absence of hypometabolism (measured with PET [<sup>18<\/sup>F]FDG) or detectable fibrillary amyloidosis (measured with PET [<sup>18<\/sup>F]NAV4694). At more advanced ages (16\u201319 months), cognitive deficits progressed in conjunction with resting connectivity abnormalities; furthermore, hypometabolism, A\u03b2 plaque accumulation, reduction of CSF A\u03b2<sub>1-42<\/sub>\u00a0concentrations, and hippocampal atrophy (structural MRI) were detectable at this stage. The present results emphasize the early impact of A\u03b2 on brain connectivity and support a framework in which persistent A\u03b2 aggregation itself is sufficient to impose memory circuits dysfunction, which propagates to adjacent brain networks at later stages.<\/p>\n<p id=\"__p3\" class=\"p p-last\"><strong>SIGNIFICANCE STATEMENT<\/strong>\u00a0The present study proposes a \u201cback translation\u201d of the Alzheimer pathological cascade concept from human to animals. We used the same set of Alzheimer imaging biomarkers typically used in large human cohorts and assessed their progression over time in a transgenic rat model, which allows for a finer spatial resolution not attainable with mice. Using this translational platform, we demonstrated that amyloid-\u03b2 pathology recapitulates an Alzheimer-like profile of biomarker abnormalities even in the absence of other hallmarks of the disease such as neurofibrillary tangles and widespread neuronal losses.<\/p>\n<\/div>\n","protected":false},"author":19,"featured_media":0,"template":"","meta":{"_acf_changed":false},"studies-relation":[],"class_list":["post-4724","ccna_publication","type-ccna_publication","status-publish","hentry"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v25.8 - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>Multimodal Imaging in Rat Model Recapitulates Alzheimer&#039;s Disease Biomarkers Abnormalities - 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\/multimodal-imaging-in-rat-model-recapitulates-alzheimers-disease-biomarkers-abnormalities-2\/\" \/>\n<meta property=\"og:locale\" content=\"fr_CA\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Multimodal Imaging in Rat Model Recapitulates Alzheimer&#039;s Disease Biomarkers Abnormalities - 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