{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T20:02:48Z","timestamp":1791489768543,"version":"4.3.4"},"reference-count":48,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2001,11,2]],"date-time":"2001-11-02T00:00:00Z","timestamp":1004659200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2001,11,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The main objective of the present study was to develop an alternative singly\u2010transgenic (tg) hAPP model where amyloid deposition will occur at an earlier age. For this purpose, we generated lines of tg mice expressing hAPP751 cDNA containing the London (V717I) and Swedish (K670M\/N671L) mutations under the regulatory control of the murine (m)Thy\u20101 gene (mThy1\u2010hAPP751). In the brains of the highest (line 41) and intermediate (lines 16 and 11) expressers, high levels of hAPP expression were found in neurons in layers 4\u20135 of the neocortex, hippocampal CA1 and olfactory bulb. As early as 3\u20134 months of age, line 41 mice developed mature plaques in the frontal cortex, whereas at 5\u20137 months plaque formation extended to the hippocampus, thalamus and olfactory region. Ultrastructural and double\u2010immunolabeling analysis confirmed that most plaques were mature and contained dystrophic neurites immunoreactive with antibodies against APP, synaptophysin, neurofilament and tau. In addition, a decrease in the number of synaptophysin\u2010immunoreactive terminals was most prominent in the frontal cortex of mice from line 41. Mice from line 11 developed diffuse amyloid deposits at 11 months of age, whereas mice from line 16 did not show evidence of amyloid deposition. Analysis of A\u03b2 by ELISA showed that levels of A\u03b2<jats:sub>1\u201340<\/jats:sub> were higher in mice that did not show any amyloid deposits (line 16), whereas A\u03b2<jats:sub>1\u201342<\/jats:sub> was the predominant species in tg animals from the lines showing plaque formation (lines 41 and 11). Taken together this study indicates that early onset plaque formation depends on levels of A\u03b2<jats:sub>1\u201342<\/jats:sub>. J. Neurosci. Res. 66:573\u2013582, 2001. \u00a9 2001 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.1247","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T21:18:31Z","timestamp":1030310311000},"page":"573-582","source":"Crossref","is-referenced-by-count":187,"title":["Early formation of mature amyloid\u2010\u03b2 protein deposits in a mutant APP transgenic model depends on levels of 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