{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T19:51:17Z","timestamp":1790970677009,"version":"4.1.0"},"reference-count":30,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2005,4,4]],"date-time":"2005-04-04T00:00:00Z","timestamp":1112572800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Glia"],"published-print":{"date-parts":[[2005,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>S\u2010100B is an astrocyte\u2010derived protein that is increased in focal areas of the brain most severely affected by neuropathological changes in Alzheimer's disease (AD). Cell\u2010based and clinical studies have implicated S\u2010100B in progression of a pathologic, glial\u2010mediated pro\u2010inflammatory state in the CNS. However, the relationship between S\u2010100B levels and susceptibility to AD\u2010relevant neuroinflammation and neuronal dysfunction in vivo has not been determined. To test the hypothesis that overexpression of S\u2010100B increases vulnerability to \u03b2\u2010amyloid (A\u03b2)\u2010induced damage, we used S\u2010100B\u2010overexpressing transgenic (Tg) and S\u2010100B knockout (KO) mice in a mouse model that involves intracerebroventricular infusion of human oligomeric A\u03b21\u201042. This model mimics many features of AD, including robust neuroinflammation, A\u03b2 plaques, synaptic damage and neuronal loss in the hippocampus. S\u2010100B Tg, KO, and wild\u2010type (WT) mice were infused with A\u03b2 for 28 days, sacrificed at 60 days, and hippocampal endpoints analyzed. We found that Tg mice showed increased vulnerability to A\u03b2\u2010induced neuropathology relative to either WT or KO mice. Specifically, Tg mice exhibited enhanced glial activation and neuroinflammation, increased nitrotyrosine staining (a marker of glial\u2010induced neuronal damage), and more pronounced loss of synaptic markers. Interestingly, Tg mice showed no significant differences in A\u03b2 plaque burden compared with WT or KO mice, suggesting that, as in the human situation, the severity of neuronal dysfunction did not correlate with amyloid deposition. Our data are consistent with a model in which S\u2010100B overexpression in AD enhances glial activation and leads to an augmented neuroinflammatory process that increases the severity of neuropathologic sequelae. \u00a9 2005 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/glia.20194","type":"journal-article","created":{"date-parts":[[2005,4,4]],"date-time":"2005-04-04T20:16:48Z","timestamp":1112645808000},"page":"209-216","source":"Crossref","is-referenced-by-count":42,"title":["Enhanced susceptibility of S\u2010100B transgenic mice to neuroinflammation and neuronal dysfunction induced by intracerebroventricular infusion of human \u03b2\u2010amyloid"],"prefix":"10.1002","volume":"51","author":[{"given":"Jeffrey M.","family":"Craft","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D. Martin","family":"Watterson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander","family":"Marks","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda J.","family":"Van Eldik","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2005,4,4]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0197-4580(00)00124-X"},{"key":"e_1_2_6_3_1","doi-asserted-by":"crossref","first-page":"1283","DOI":"10.1016\/j.neurobiolaging.2004.01.006","article-title":"Aminopyridazines inhibit \u03b2\u2010amyloid induced glial activation and neuronal damage in vivo","volume":"25","author":"Craft JM","journal-title":"Neurobiol Aging"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M201750200"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1357-2725(01)00046-2"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0197-4580(01)00300-1"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/0197-4580(95)02073-X"},{"key":"e_1_2_6_8_1","doi-asserted-by":"crossref","first-page":"4337","DOI":"10.1523\/JNEUROSCI.12-11-04337.1992","article-title":"Cell\u2010specific expression of high levels of human S100\u03b2 in transgenic mouse brain is dependent on gene dosage","volume":"12","author":"Friend WC","year":"1992","journal-title":"J Neurosci"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1017\/S0958067000019746"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1212\/01.WNL.0000063311.58879.01"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1750-3639.1998.tb00136.x"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.1997.69062294.x"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-06-02246.2002"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0197-0186(01)00047-X"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0197-4580(01)00233-0"},{"key":"e_1_2_6_16_1","doi-asserted-by":"publisher","DOI":"10.1002\/jnr.20127"},{"key":"e_1_2_6_17_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1651-2227.2002.tb01630.x"},{"key":"e_1_2_6_18_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1471-4159.2000.0740143.x"},{"key":"e_1_2_6_19_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.20-15-05709.2000"},{"key":"e_1_2_6_20_1","doi-asserted-by":"publisher","DOI":"10.1016\/0306-4522(94)90201-1"},{"key":"e_1_2_6_21_1","doi-asserted-by":"publisher","DOI":"10.1021\/jm015573g"},{"key":"e_1_2_6_22_1","doi-asserted-by":"publisher","DOI":"10.1097\/00024382-200116030-00001"},{"key":"e_1_2_6_23_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0197-4580(01)00287-1"},{"key":"e_1_2_6_24_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0197-4580(01)00293-7"},{"key":"e_1_2_6_25_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature01320"},{"key":"e_1_2_6_26_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0301-0082(02)00127-2"},{"key":"e_1_2_6_27_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.21-12-04183.2001"},{"key":"e_1_2_6_28_1","doi-asserted-by":"publisher","DOI":"10.1002\/jemt.10303"},{"key":"e_1_2_6_29_1","first-page":"97","article-title":"The Janus face of glial\u2010derived S100B: beneficial and detrimental functions in the brain","volume":"21","author":"Van Eldik LJ","year":"2003","journal-title":"Rest Neurol Neurosci"},{"key":"e_1_2_6_30_1","doi-asserted-by":"publisher","DOI":"10.1002\/ana.20142"},{"key":"e_1_2_6_31_1","doi-asserted-by":"publisher","DOI":"10.1006\/excr.2000.4902"}],"container-title":["Glia"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1002%2Fglia.20194","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1002\/glia.20194","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,9]],"date-time":"2023-10-09T18:58:13Z","timestamp":1696877893000},"score":1,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1002\/glia.20194"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2005,4,4]]},"references-count":30,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2005,8,15]]}},"alternative-id":["10.1002\/glia.20194"],"URL":"https:\/\/doi.org\/10.1002\/glia.20194","archive":["Portico"],"relation":{},"ISSN":["0894-1491","1098-1136"],"issn-type":[{"value":"0894-1491","type":"print"},{"value":"1098-1136","type":"electronic"}],"subject":[],"published":{"date-parts":[[2005,4,4]]}}}