Elsevier

Neuroscience Letters

Volume 368, Issue 2, 23 September 2004, Pages 144-147
Neuroscience Letters

Apolipoprotein E receptor 2 is involved in neuritic plaque formation in APP sw mice

https://doi.org/10.1016/j.neulet.2004.06.081Get rights and content

Abstract

Apolipoprotein E receptor 2 (apoER2) is a receptor for apolipoprotein E containing lipoprotein and also for Reelin. Apolipoprotein E-associated risk of developing Alzheimer’s disease (AD) may be related to its binding to and clearance by cell surface receptors, including members of the low-density lipoprotein receptor family. Otherwise there is circumstantial evidence that the Reelin signaling pathway may contribute to neurodegeneration in AD. To investigate the role of apoER2 on amyloid deposition and neurodegeneration in vivo, we examined the presence of apoER2 in the brains of APP sw transgenic mice (Tg2576) using three apoER2 monoclonal antibodies. Our immunohistochemical study revealed that apoER2 was localized in fine granular structure and reactive astrocytes surrounding amyloid plaques. The double labeling immunohistochemistry revealed that this granular structure overlaps synaptophysin-positive dystrophic neurites. These findings indicate that neuronal apoER2 may play a role for amyloid deposition and neuronal degeneration in AD.

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    First, Reelin competes with apolipoprotein E (ApoE) for binding to the ApoE receptors, ApoER2 and VLDLR (D'Arcangelo et al., 1999; Hiesberger et al., 1999), and ApoE ɛ4, the major known genetic risk factor for AD, is one of the strongest competitors (D'Arcangelo et al., 1999). A direct role for ApoER2 on amyloid deposition and neurodegeneration in AD has also been suggested (Motoi et al., 2004). In addition, Reelin receptors convey intracellular signals through the adaptor Dab1 (Bar and Goffinet, 1999;Cooper and Howell, 1999; Trommsdorff et al., 1999), thereby leading to a signaling cascade that ultimately controls glycogen synthase kinase-3β (GSK-3β) (Beffert et al., 2002), an enzyme that regulates phosphorylation of the microtubule binding protein tau.

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    To the best of our knowledge, no data are available on the existence of Reelin-positive accumulations in the hippocampal formation of wild-type mice, rats, non-human primates or humans. Three studies described Reelin- and ApoER2-IR, respectively, in neuritic compartments of Aβ plaques in transgenic AD mice (Miettinen et al., 2005; Motoi et al., 2004; Wirths et al., 2001). It is unclear, however, whether they were associated with non-fibrillary or fibrillary plaques.

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