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Regulation of amyloid-β production by the prion protein

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Pages 217-222 | Received 26 Oct 2011, Accepted 08 Dec 2011, Published online: 01 Jul 2012

Figures & data

Figure 1. Schematic diagram depicting PrPC regulation of BACE1 in relation to APPWT and APPSwe. PrPC interacts with the pro-domain of BACE1 in its immature form in the TGN, slowing its maturation and trafficking to endosomes (via the cell surface). In the TGN, BACE1 preferentially cleaves APPSwe ; in the endosomes, it preferentially cleaves APPWT. Our model shows that PrPC inhibits BACE1 cleavage of APPWT, but not APPSwe which leads to increased Aβ formation. PM, plasma membrane.

Figure 1. Schematic diagram depicting PrPC regulation of BACE1 in relation to APPWT and APPSwe. PrPC interacts with the pro-domain of BACE1 in its immature form in the TGN, slowing its maturation and trafficking to endosomes (via the cell surface). In the TGN, BACE1 preferentially cleaves APPSwe ; in the endosomes, it preferentially cleaves APPWT. Our model shows that PrPC inhibits BACE1 cleavage of APPWT, but not APPSwe which leads to increased Aβ formation. PM, plasma membrane.

Figure 2. Schematic diagram depicting PrPC regulation of BACE1 in sporadic AD brains. In the healthy brain, PrPC interacts with BACE1 inhibiting its cleavage of APP and thereby keeping the level of Aβ in check. In sporadic AD, PrPC levels are reduced, leading to impaired BACE1 inhibition and increased Aβ formation.

Figure 2. Schematic diagram depicting PrPC regulation of BACE1 in sporadic AD brains. In the healthy brain, PrPC interacts with BACE1 inhibiting its cleavage of APP and thereby keeping the level of Aβ in check. In sporadic AD, PrPC levels are reduced, leading to impaired BACE1 inhibition and increased Aβ formation.

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