2003
DOI: 10.1074/jbc.m300503200
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The Neuronal Adaptor Protein X11α Reduces Aβ Levels in the Brains of Alzheimer's APPswe Tg2576 Transgenic Mice

Abstract: Increased production and deposition of the 40 -42-amino acid ␤-amyloid peptide (A␤) is believed to be central to the pathogenesis of Alzheimer's disease. A␤ is derived from the amyloid precursor protein (APP), but the mechanisms that regulate APP processing to produce A␤ are not fully understood. X11␣ (also known as munc-18-interacting protein-1 (Mint1)) is a neuronal adaptor protein that binds APP and modulates APP processing in transfected non-neuronal cells. To investigate the in vivo effect of X11␣ on A␤ p… Show more

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Cited by 77 publications
(57 citation statements)
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“…After overexpression of the adapter protein X11α in APPswe Tg2576 transgenic mice, amyloid plaque formation was reduced, although Aβ42 levels were unchanged and Aβ40 levels were decreased by only about 24% (43). Overexpression of a mutant copper transporter in transgenic APP mice (TgCRND8) clearly decreased the amyloid plaque burden in the cortex and hippocampus, although the brain levels of Aβ40 and Aβ42 were only slightly and not significantly reduced (44).…”
Section: Discussionmentioning
confidence: 99%
“…After overexpression of the adapter protein X11α in APPswe Tg2576 transgenic mice, amyloid plaque formation was reduced, although Aβ42 levels were unchanged and Aβ40 levels were decreased by only about 24% (43). Overexpression of a mutant copper transporter in transgenic APP mice (TgCRND8) clearly decreased the amyloid plaque burden in the cortex and hippocampus, although the brain levels of Aβ40 and Aβ42 were only slightly and not significantly reduced (44).…”
Section: Discussionmentioning
confidence: 99%
“…The amount of A40 and the number of amyloid plaques were deceased in double-transgenic mice expressing X11 and APPswe compared to control [70]. There were also low levels of A peptides and plaque formation in the cerebrum of double-transgenic mice expressing X11L and APPswe [71].…”
Section: X11/mint Family Of Proteinsmentioning
confidence: 82%
“…Transgenic mice that overexpress Swedish mutant APP and X11 or X11L show lower levels of A␤ in their brains as compared with transgenic mice overexpressing Swedish mutant APP alone (20,21). Moreover, X11L-deficient mice show enhanced amyloidogenic metabolism of endogenous brain APP (22).…”
Section: Discussionmentioning
confidence: 99%
“…Transgenic mice expressing the APP Swedish mutation and also overexpressing X11 or X11L show a decreased level of cerebral A␤ and a reduction of A␤ plaques in the cerebral cortex and hippocampus in comparison with the mice expressing Swedish mutant APP alone (20,21). Conversely, the amyloidogenic metabolism of endogenous APP and the generation of A␤ are facilitated in the brains of X11L-deficient mice (22).…”
Section: Gyenptymentioning
confidence: 99%