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Chen, Y. et al.

Yuzhi Chen, Angela M. Bodles, Donna L. McPhie, Rachael L. Neve, Robert E. Mrak, W. Sue T. Griffin,

APP-BP1 inhibits Abeta42 levels by interacting with Presenilin-1.

BACKGROUND: The beta-amyloid precursor protein (APP) is sequentially cleaved by the beta- and then gamma-secretase to generate the amyloid beta-peptides Abeta40 and Abeta42. Increased Abeta42/Abeta40 ratios trigger amyloid plaque formations in Alzheimer's disease (AD). APP binds to APP-BP1, but the biological consequence is not well understood. RESULTS: We report that when the endogenous APP-BP1 was suppressed by small interfering RNAs (siRNAs), cell-associated Abeta42 was dramatically increased in APP695 expressing primary neurons. The accumulation of Abeta42 was accompanied by significant increases in APP and APP-CTF in APP-BP1 siRNA expressing neurons. In contrast, APP-BP1 overexpression in primary neurons significantly decreased the levels of Abeta and endogenous APP but not APLPs. We also investigated the potential mechanism of APP-BP1-mediated APP processing. APP-BP1 co-precipitated with Presenilin-1 (PS1) in native rat brain extracts, co-migrated with the gamma-secretase components in brain membrane extracts in glycerol gradient centrifugation, and colocalized in primary neurons. Further, the endogenous PS1-CTF was significantly downregulated by APP-BP1 expression. CONCLUSION: Our data suggest that APP-BP1 may inhibit Abeta42 production by interacting with PS1 under physiological conditions.[1]

References

APP-BP1 inhibits Abeta42 levels by interacting with Presenilin-1. Chen, Y., Bodles, A.M., McPhie, D.L., Neve, R.L., Mrak, R.E., Griffin, W.S. Mol. Neurodegener (2007) [Pubmed]

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