{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T23:14:00Z","timestamp":1781046840950,"version":"3.54.1"},"reference-count":14,"publisher":"S. Karger AG","issue":"1-4","license":[{"start":{"date-parts":[[2012,1,1]],"date-time":"2012-01-01T00:00:00Z","timestamp":1325376000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2012,1,1]],"date-time":"2012-01-01T00:00:00Z","timestamp":1325376000000},"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":[[2012]]},"abstract":"<i>Background:<\/i> Soluble amyloid-F peptide oligomers (AFOs), which are centrally involved in the pathogenesis of Alzheimer&#8217;s disease, trigger Ca<sup>2+<\/sup> influx through N-methyl-<i>D<\/i>-aspartate receptors and stimulate reactive oxygen species generation in primary hippocampal neurons. We have previously reported that AFOs promote Ca<sup>2+<\/sup> release mediated by ryanodine receptors (RyR), which in turn triggers mitochondrial fragmentation. We have also reported that the antioxidant N-acetylcysteine (NAC) prevents AFOs-induced Ca<sup>2+<\/sup> signal generation. <i>Objectives:<\/i> To determine if RyR-mediated Ca<sup>2+<\/sup> release activated by the specific agonist 4-chloro-m-cresol (4-CMC) induces fragmentation of the mitochondrial network, and to ascertain if NAC prevents the mitochondrial fragmentation induced by AFOs and\/or 4-CMC. <i>Methods:<\/i> Mature primary rat hippocampal neurons were incubated for 24 h with sublethal concentrations of AFOs (500 n<i>M<\/i>) or for 1&#8211;3 h with 4-CMC (0.5&#8211;1 m<i>M<\/i>), w10 m<i>M<\/i> NAC. Mitochondrial morphology was assessed by confocal microscopy of fixed neurons stained with anti-mHsp70. Intracellular Ca<sup>2+<\/sup> levels were determined by time series microscopy of neurons preloaded with Fluo-4 AM. <i>Results:<\/i> Preincubation of neurons for 30 min with NAC prevented the mitochondrial fragmentation induced by AFOs or 4-CMC. In addition, we confirmed that preincubation with NAC abolished the stimulation of RyR-mediated Ca<sup>2+<\/sup> release induced by AFOs or 4-CMC. <i>Conclusion:<\/i> The present results strongly suggest that the general antioxidant NAC prevents AFO-induced mitochondrial fragmentation by preventing RyR-mediated Ca<sup>2+<\/sup>-induced Ca<sup>2+<\/sup> release. Copyright i 2012 S. Karger AG, Basel<\/jats:p>","DOI":"10.1159\/000334901","type":"journal-article","created":{"date-parts":[[2012,1,24]],"date-time":"2012-01-24T08:45:08Z","timestamp":1327394708000},"page":"34-37","source":"Crossref","is-referenced-by-count":34,"title":["The Antioxidant N-Acetylcysteine Prevents the Mitochondrial Fragmentation Induced by Soluble Amyloid-F Peptide Oligomers"],"prefix":"10.1159","volume":"10","author":[{"given":"C.D.","family":"SanMartin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"Adasme","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.","family":"Hidalgo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.C.","family":"Paula-Lima","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"127","published-online":{"date-parts":[[2012,1,24]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1016%2Fj.nlm.2011.08.003"},{"key":"ref2","doi-asserted-by":"publisher","DOI":"10.1074%2Fjbc.M607483200"},{"key":"ref3","doi-asserted-by":"publisher","DOI":"10.1089%2Fars.2010.3287"},{"key":"ref4","doi-asserted-by":"publisher","DOI":"10.1007%2Fs11064-010-0371-4"},{"key":"ref5","doi-asserted-by":"publisher","DOI":"10.1101%2Flm.929008"},{"key":"ref6","doi-asserted-by":"publisher","DOI":"10.1073%2Fpnas.1013580108"},{"key":"ref7","doi-asserted-by":"publisher","DOI":"10.1089%2Fars.2007.1886"},{"key":"ref8","doi-asserted-by":"publisher","DOI":"10.1016%2FS0306-4522%2899%2900042-1"},{"key":"ref9","doi-asserted-by":"publisher","DOI":"10.4161%2Fchan.5.1.14124"},{"key":"ref10","doi-asserted-by":"publisher","DOI":"10.1016%2Fj.ceca.2009.12.014"},{"key":"ref11","doi-asserted-by":"publisher","DOI":"10.1038%2Fcr.2011.87"},{"key":"ref12","doi-asserted-by":"publisher","DOI":"10.1523%2FJNEUROSCI.1357-09.2009"},{"key":"ref13","doi-asserted-by":"publisher","DOI":"10.1016%2Fj.molcel.2010.06.029"},{"key":"ref14","doi-asserted-by":"publisher","DOI":"10.1016%2Fj.ceca.2006.08.013"}],"container-title":["Neurodegenerative Diseases"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/334901","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/334901","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T18:52:02Z","timestamp":1745434322000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000334901"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2012]]},"references-count":14,"journal-issue":{"issue":"1-4","published-online":{"date-parts":[[2012,4,1]]},"published-print":{"date-parts":[[2012,4,19]]}},"URL":"https:\/\/doi.org\/10.1159\/000334901","archive":["Portico"],"relation":{"is-supplemented-by":[{"id-type":"doi","id":"10.6084\/m9.figshare.5241376","asserted-by":"subject"}]},"ISSN":["1660-2854","1660-2862"],"issn-type":[{"value":"1660-2854","type":"print"},{"value":"1660-2862","type":"electronic"}],"subject":[],"published":{"date-parts":[[2012]]}}}