{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T17:06:55Z","timestamp":1777396015561,"version":"3.51.4"},"reference-count":26,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2019,12,9]],"date-time":"2019-12-09T00:00:00Z","timestamp":1575849600000},"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":[[2020,1,21]]},"abstract":"<jats:p>\n                    Alzheimer\u2019s disease (AD) is the most common form of dementia, characterized by amyloid-\u03b2 peptide (A\u03b2) aggregates, phosphorylated tau protein ( p-tau), and progressive neurodegeneration. Amyloid-\u03b2 peptide 42 (A\u03b2\n                    <jats:sub>42<\/jats:sub>\n                    ) is considered an early trigger of AD pathogenesis. We have previously reported that A\u03b2 N-terminus monoclonal antibody (mAb) A8 alleviated cognitive dysfunction and reduced the abundance of soluble A\u03b2 in the brains of the senescence-accelerated mouse prone 8 (SAMP8) mouse model. To confirm the efficacy of mAb A8 in the double-transgenic APPswe\/PS1 \u0394E9 (APP\/PS1) mice, here we reported the related findings. The Morris water maze (MWM) data showed that the A8 treatment group had a shorter escape latency than the control groups in the place navigation test and the probe trial ( p\u200a&lt;\u200a0.05). Moreover, immunohistochemistry showed decreased levels of both A\u03b2 and p-tau in the brains of APP\/PS1 mice. Regarding A\u03b2 levels, western blot results showed that A\u03b2\n                    <jats:sub>42<\/jats:sub>\n                    oligomer ( p\u200a&lt;\u200a0.01) but not A\u03b2\n                    <jats:sub>40<\/jats:sub>\n                    levels were diminished in brains of A8-treated APP\/PS1 mice. Western blot results showed that phospho-tau (pSer\n                    <jats:sup>231<\/jats:sup>\n                    ) ( p\u200a&lt;\u200a0.01) but not tau levels were reduced in A8-treated mouse brains. Furthermore, transmission electron microscopy images indicated ultrastructural improvements, including an increased ( p\u200a&lt;\u200a0.01) density of synapses and a reduction of abnormally enlarged mitochondria ( p\u200a&lt;\u200a0.01), in the brains of A8-treated mice. Taken together, our data showed that mAb A8 is highly efficacious in APP\/PS1 mice as a treatment for AD, and the underlying mechanism may target synaptic pathology by inhibiting the amyloid cascade.\n                  <\/jats:p>","DOI":"10.3233\/jad-190874","type":"journal-article","created":{"date-parts":[[2019,12,13]],"date-time":"2019-12-13T13:18:39Z","timestamp":1576243119000},"page":"657-670","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":9,"title":["Intraperitoneal Administration of Monoclonal Antibody Against Pathologic A\u03b2\n                    <sub>42<\/sub>\n                    Aggregates Alleviated Cognitive Deficits and Synaptic Lesions in APP\/PS1 Mice"],"prefix":"10.1177","volume":"73","author":[{"given":"Shuo","family":"Xiao","sequence":"first","affiliation":[{"name":"College of Life Sciences and Bioengineering, Beijing Jiaotong University, Beijing, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lin-Lin","family":"Song","sequence":"additional","affiliation":[{"name":"College of Life Sciences and Bioengineering, Beijing Jiaotong University, Beijing, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jiang-Tao","family":"Li","sequence":"additional","affiliation":[{"name":"College of Life Sciences and Bioengineering, Beijing Jiaotong University, Beijing, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"He","family":"Wang","sequence":"additional","affiliation":[{"name":"College of Life Sciences and Bioengineering, Beijing Jiaotong University, Beijing, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Na","family":"Yu","sequence":"additional","affiliation":[{"name":"College of Life Sciences and Bioengineering, Beijing Jiaotong University, Beijing, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zi-Qi","family":"Wang","sequence":"additional","affiliation":[{"name":"College of Life Sciences and Bioengineering, Beijing Jiaotong University, Beijing, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ying","family":"Zhang","sequence":"additional","affiliation":[{"name":"College of Life Sciences and Bioengineering, Beijing Jiaotong University, Beijing, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jin-Sheng","family":"He","sequence":"additional","affiliation":[{"name":"College of Life Sciences and Bioengineering, Beijing Jiaotong University, Beijing, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tao","family":"Hung","sequence":"additional","affiliation":[{"name":"College of Life Sciences and Bioengineering, Beijing Jiaotong University, Beijing, China"},{"name":"Institute for Viral Disease Control and Prevention, China CDC, Beijing, China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2019,12,9]]},"reference":[{"key":"ref001","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2010.08.018"},{"key":"ref002","doi-asserted-by":"publisher","DOI":"10.1186\/s12883-017-0850-1"},{"key":"ref003","doi-asserted-by":"publisher","DOI":"10.1016\/j.dadm.2016.02.004"},{"key":"ref004","doi-asserted-by":"publisher","DOI":"10.1080\/14712598.2018.1389885"},{"key":"ref005","first-page":"264","volume":"4","author":"Doody R","year":"2017","journal-title":"J Prev Alzheimers Dis"},{"key":"ref006","first-page":"255","volume":"4","author":"Budd Haeberlein S","year":"2017","journal-title":"J Prev Alzheimers 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