{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T18:58:18Z","timestamp":1790621898267,"version":"4.1.0"},"reference-count":4,"publisher":"S. Karger AG","issue":"1-3","license":[{"start":{"date-parts":[[2010,1,1]],"date-time":"2010-01-01T00:00:00Z","timestamp":1262304000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2010,1,1]],"date-time":"2010-01-01T00:00:00Z","timestamp":1262304000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neurodegener Dis"],"published-print":{"date-parts":[[2010]]},"abstract":"<jats:p>&lt;i&gt;Background:&lt;\/i&gt; Intracellular accumulation of \u03b2-amyloid (A\u03b2) is one of the early features in the neuropathology of Alzheimer\u2019s disease (AD) and Down\u2019s syndrome. This can be reproduced in cell and transgenic animal models of the AD-like amyloid pathology. In a transgenic rat model, our lab has previously shown that the intracellular accumulation of A\u03b2 is sufficient to provoke cognitive impairments and biochemical alterations in the cerebral cortex and hippocampus in the absence of amyloid plaques. &lt;i&gt;Objective:&lt;\/i&gt; To investigate an early, pre-plaque inflammatory process in AD-like transgenic models and establish whether the neurotoxic effects of A\u03b2 oligomers and proinflammatory responses can be arrested with minocycline. &lt;i&gt;Methods:&lt;\/i&gt; For these studies, we used na\u00efve mice and transgenic animal models of the AD-like amyloid pathology and applied neurochemical, immunohistochemical and behavioral experimental approaches. &lt;i&gt;Results:&lt;\/i&gt; In the early stages of the AD-like amyloid pathology, intracellular A\u03b2 oligomers accumulate within neurons of the cerebral cortex and hippocampus. Coincidental with this, behavioral impairments occur prior to the appearance of amyloid plaques, together with an upregulation of MHC-II, i-NOS and COX-2, well-known proinflammatory markers. Treatment with minocycline corrected behavioral impairments, lowered inflammatory markers and levels of A\u03b2 trimers. &lt;i&gt;Conclusion:&lt;\/i&gt; A pharmacological approach targeting the early neuroinflammatory effects of A\u03b2 might be a promising strategy to prevent or delay the onset of AD.<\/jats:p>","DOI":"10.1159\/000285514","type":"journal-article","created":{"date-parts":[[2010,2,18]],"date-time":"2010-02-18T11:28:13Z","timestamp":1266492493000},"page":"96-98","source":"Crossref","is-referenced-by-count":45,"title":["Early-Stage Inflammation and Experimental Therapy in Transgenic Models of the Alzheimer-Like Amyloid Pathology"],"prefix":"10.1159","volume":"7","author":[{"given":"A.C.","family":"Cuello","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.T.","family":"Ferretti","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W.C.","family":"Leon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.F.","family":"Iulita","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"Melis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Ducatenzeiler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.A.","family":"Bruno","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F.","family":"Canneva","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"127","published-online":{"date-parts":[[2010,2,18]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1016%2FS1474-4422%2804%2900937-8"},{"key":"ref2","doi-asserted-by":"publisher","DOI":"10.1097%2FNEN.0b013e3181aed9e6"},{"key":"ref3","doi-asserted-by":"publisher","DOI":"10.1016%2Fj.neuroscience.2004.07.036"},{"key":"ref4","doi-asserted-by":"publisher","DOI":"10.1016%2Fj.neuroscience.2005.06.057"}],"container-title":["Neurodegenerative Diseases"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/285514","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/285514","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T20:25:28Z","timestamp":1745439928000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000285514"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2010]]},"references-count":4,"journal-issue":{"issue":"1-3","published-online":{"date-parts":[[2010,4,1]]}},"URL":"https:\/\/doi.org\/10.1159\/000285514","archive":["Portico"],"relation":{},"ISSN":["1660-2854","1660-2862"],"issn-type":[{"value":"1660-2854","type":"print"},{"value":"1660-2862","type":"electronic"}],"subject":[],"published":{"date-parts":[[2010]]}}}