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. 2010 Jun 15;5(6):e11102. doi: 10.1371/journal.pone.0011102

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This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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In healthy individuals, APP is transcribed in the endoplasmatic reticulum (ER, grey), modified in the golgi network (Golgi, grey) and then shuttled to the cell surface through the secretory pathway (SecP, grey). The cell takes up APP through endocytosis (End, light blue). From here, APP can either be degraded via autophagy (Aut, yellow) and the lysosomes (Lys, dark blue) or APP can be recycled via the recycling endosomes (R-End, light blue) and enter the cycle again. In AD brains and Becn1 deficient cells BECN1 deficiency impairs both induction of autophagy (through the complex with PIK3C3) and autophagosomal degradation (potentially through a complex with an unknown binding partner). APP containing vesicles (endosomes, autophagosomes, and others) build up inside the cell. APP is increasingly cleaved by secretases and large amounts of APP-CTF and Aβ are being released, causing neurotoxic events. The disruption of autophagosomal degradation includes an increasing accumulation of autophagosomes. This accumulation can further inhibit autophagy and BECN1 expression (red arrow), worsening the reduction in APP turnover and degradation.