{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T00:21:00Z","timestamp":1790468460159,"version":"4.1.0"},"reference-count":46,"publisher":"Springer Science and Business Media LLC","issue":"1","content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["BMC Neurosci"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n          <jats:sec>\n            <jats:title>Background<\/jats:title>\n            <jats:p>Alzheimer's Disease (AD) is the most common of the conformational neurodegenerative disorders characterized by the conversion of a normal biological protein into a \u03b2-sheet-rich pathological isoform. In AD the normal soluble A\u03b2 (sA\u03b2) forms oligomers and fibrils which assemble into neuritic plaques. The most toxic form of A\u03b2 is thought to be oligomeric. A recent study reveals the cellular prion protein, PrP<jats:sup>C<\/jats:sup>, to be a receptor for A\u03b2 oligomers. A\u03b2 oligomers suppress LTP signal in murine hippocampal slices but activity remains when pretreated with the PrP monoclonal anti-PrP antibody, 6D11. We hypothesized that targeting of PrP<jats:sup>C<\/jats:sup> to prevent A\u03b2 oligomer-related cognitive deficits is a potentially novel therapeutic approach. APP\/PS1 transgenic mice aged 8 months were intraperitoneally (i.p.) injected with 1 mg 6D11 for 5 days\/week for 2 weeks. Two wild-type control groups were given either the same 6D11 injections or vehicle solution. Additional groups of APP\/PS1 transgenic mice were given either i.p. injections of vehicle solution or the same dose of mouse IgG over the same period. The mice were then subjected to cognitive behavioral testing using a radial arm maze, over a period of 10 days. At the conclusion of behavioral testing, animals were sacrificed and brain tissue was analyzed biochemically or immunohistochemically for the levels of amyloid plaques, PrP<jats:sup>C<\/jats:sup>, synaptophysin, A\u03b240\/42 and A\u03b2 oligomers.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Behavioral testing showed a marked decrease in errors in 6D11 treated APP\/PS1 Tg mice compared with the non-6D11 treated Tg groups (p &lt; 0.0001). 6D11 treated APP\/PS1 Tg mice behaved the same as wild-type controls indicating a recovery in cognitive learning, even after this short term 6D11 treatment. Brain tissue analysis from both treated and vehicle treated APP\/PS1 groups indicate no significant differences in amyloid plaque burden, A\u03b240\/42, PrP<jats:sup>C<\/jats:sup> or A\u03b2 oligomer levels. 6D11 treated APP\/PS1 Tg mice had significantly greater synaptophysin immunoreactivity in the dentate gyrus molecular layer of the hippocampus compared to vehicle treated APP\/PS1 Tg mice (p &lt; 0.05).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>Even short term treatment with monoclonal antibodies such as 6D11 or other compounds which block the binding of A\u03b2 oligomers to PrP<jats:sup>C<\/jats:sup> can be used to treat cognitive deficits in aged AD transgenic mice.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1471-2202-11-130","type":"journal-article","created":{"date-parts":[[2010,10,15]],"date-time":"2010-10-15T18:15:41Z","timestamp":1287166541000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":152,"title":["Anti-PrPC monoclonal antibody infusion as a novel treatment for cognitive deficits in an alzheimer's disease model mouse"],"prefix":"10.1186","volume":"11","author":[{"given":"Erika","family":"Chung","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yong","family":"Ji","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanjie","family":"Sun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard J","family":"Kascsak","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Regina B","family":"Kascsak","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pankaj D","family":"Mehta","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen M","family":"Strittmatter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Wisniewski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2010,10,14]]},"reference":[{"key":"1907_CR1","volume-title":"World Alzheimer Report 2010: the global economic impact of dementia","author":"A Wimo","year":"2010","unstructured":"Wimo A, Prince M: World Alzheimer Report 2010: the global economic impact of dementia. 2010, Alzheimer's Disease International"},{"key":"1907_CR2","doi-asserted-by":"publisher","first-page":"186","DOI":"10.1016\/j.jalz.2007.04.381","volume":"3","author":"R Brookmeyer","year":"2007","unstructured":"Brookmeyer R, Johnson E, Ziegler-Graham K, Arrighi HM: Forecasting the global burden of Alzheimer's disease. 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