{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,30]],"date-time":"2026-05-30T01:50:00Z","timestamp":1780105800311,"version":"3.54.0"},"reference-count":0,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2015,4,13]],"date-time":"2015-04-13T00:00:00Z","timestamp":1428883200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2015,4,13]]},"abstract":"<jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Synaptic deficits and neuronal loss are the major pathological manifestations of Alzheimer\u2019s disease. However, the link between the early synaptic loss and subsequent neurodegeneration is not entirely clear. Cell culture studies have shown that amyloid-\u03b2 (A\u03b2) applied to axonal terminals can cause retrograde degeneration leading to the neuronal loss, but this process has not been demonstrated in live animals.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>To test if A\u03b2 applied to retinal ganglion cell axonal terminals can induce axonal damage in the optic nerve and optic tract in mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>A\u03b2 was injected into the terminal field of the optic tract, in the left lateral geniculate nucleus of wildtype C57BL\/6 mice. Following the injection, monthly diffusion tensor imaging was performed. Three months after the injection, mice underwent visual evoked potential recordings, and then sacrificed for immunohistochemical examination.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>There were no significant changes seen with diffusion tensor imaging in the optic nerve and optic tract 3 months after the A\u03b2 injection. The myelin and axons in these regions remained intact according to immunohistochemistry. The only significant changes observed in this study were delayed transduction and reduced amplitude of visual evoked potentials, although both A\u03b2 and its reversed form caused similar changes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec specific-use=\"heading-level-1\">\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>Despite the published in vitro studies, there was no significant axonal damage in the optic nerve and optic tract after injecting A\u03b2 onto retinal ganglion cell axonal terminals of wildtype C57BL\/6 mice.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3233\/jad-142154","type":"journal-article","created":{"date-parts":[[2018,6,4]],"date-time":"2018-06-04T06:55:18Z","timestamp":1528095318000},"page":"1139-1148","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":7,"title":["Axonal Terminals Exposed to Amyloid-\u03b2 May Not Lead to Pre-Synaptic Axonal Damage"],"prefix":"10.1177","volume":"45","author":[{"given":"Shu-Wei","family":"Sun","sequence":"first","affiliation":[{"name":"Basic Sciences, Schools of Medicine, Loma Linda University, Loma Linda, CA, USA"},{"name":"Radiation Medicine, Schools of Medicine, Loma Linda University, Loma Linda, CA, USA"},{"name":"Pharmaceutical Science, School of Pharmacy, Loma Linda University, Loma Linda, CA, USA"},{"name":"Neuroscience, University of California in Riverside, Riverside, CA, USA"},{"name":"Bioengineering, University of California in Riverside, Riverside, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher","family":"Nishioka","sequence":"additional","affiliation":[{"name":"Neuroscience, University of California in Riverside, Riverside, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wessam","family":"Labib","sequence":"additional","affiliation":[{"name":"Family Medicine, Loma Linda University Medical Center, Loma Linda, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hsiao-Fang","family":"Liang","sequence":"additional","affiliation":[{"name":"Basic Sciences, Schools of Medicine, Loma Linda University, Loma Linda, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2015,4,13]]},"container-title":["Journal of Alzheimer\u2019s Disease"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.3233\/JAD-142154","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.3233\/JAD-142154","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T10:02:01Z","timestamp":1777370521000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/10.3233\/JAD-142154"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2015,4,13]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2015,4,13]]}},"alternative-id":["10.3233\/JAD-142154"],"URL":"https:\/\/doi.org\/10.3233\/jad-142154","relation":{"is-cited-by":[{"id-type":"doi","id":"10.3389\/fneur.2016.00053","asserted-by":"object"}]},"ISSN":["1387-2877","1875-8908"],"issn-type":[{"value":"1387-2877","type":"print"},{"value":"1875-8908","type":"electronic"}],"subject":[],"published":{"date-parts":[[2015,4,13]]}}}