{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T16:27:13Z","timestamp":1761236833035},"reference-count":29,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2001,12,25]],"date-time":"2001-12-25T00:00:00Z","timestamp":1009238400000},"content-version":"vor","delay-in-days":999,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[1999,4]]},"abstract":"<jats:p> <jats:bold>Abstract:<\/jats:bold> Hippocampal neurons from the trisomy 16 (Ts16) mouse, a potential animal model of Down\u2019s syndrome (trisomy 21) and neurodegenerative disorders such as Alzheimer\u2019s disease (AD), die at an accelerated rate in vitro. Here, we present evidence that the accelerated neuronal death in Ts16 occurs by apoptosis, as has been reported for neurons in AD. First, the nuclei of dying Ts16 neurons are pyknotic and undergo DNA fragmentation, as revealed by terminal transferase\u2010mediated dUTP nick end\u2010labeling. Second, the accelerated death of Ts16 neurons is prevented by inhibitors of the caspase family of proteases, which are thought to act at a late, obligatory step in the apoptosis pathway. In the presence of maximally effective concentrations of caspase inhibitors, Ts16 neuron survival was indistinguishable from that of control neurons. These results suggest that overexpression of one or more genes on mouse chromosome 16 leads to caspase\u2010mediated apoptosis in Ts16 neurons.<\/jats:p>","DOI":"10.1046\/j.1471-4159.1999.721769.x","type":"journal-article","created":{"date-parts":[[2003,3,12]],"date-time":"2003-03-12T06:38:23Z","timestamp":1047451103000},"page":"1769-1772","source":"Crossref","is-referenced-by-count":26,"title":["Neuronal Apoptosis in Mouse Trisomy 16"],"prefix":"10.1111","volume":"72","author":[{"given":"Linda L.","family":"Bambrick","sequence":"first","affiliation":[]},{"given":"Bruce K.","family":"Krueger","sequence":"additional","affiliation":[]}],"member":"311","published-online":{"date-parts":[[2001,12,25]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.21.9692"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-1136(199704)19:4<352::AID-GLIA8>3.0.CO;2-Z"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/378776a0"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.7901908"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0166-2236(88)90075-6"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.135.5.1341"},{"key":"e_1_2_6_8_2","first-page":"121","article-title":"The calcium hypothesis for Alzheimer\u2019s disease: insights from animal and human studies.","volume":"17","author":"Disterhoft J.F.","year":"1995","journal-title":"Neurosci. 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