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Tu, H. et al.

Presenilins Form ER Ca(2+) Leak Channels, a Function Disrupted by Familial Alzheimer's Disease-Linked Mutations.

Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative disorder. Mutations in presenilins 1 and 2 ( PS1 and PS2) account for approximately 40% of familial AD ( FAD) cases. FAD mutations and genetic deletions of presenilins have been associated with calcium (Ca(2+)) signaling abnormalities. We demonstrate that wild-type presenilins, but not PS1-M146V and PS2-N141I FAD mutants, can form low-conductance divalent-cation-permeable ion channels in planar lipid bilayers. In experiments with PS1/2 double knockout (DKO) mouse embryonic fibroblasts (MEFs), we find that presenilins account for approximately 80% of passive Ca(2+) leak from the endoplasmic reticulum. Deficient Ca(2+) signaling in DKO MEFs can be rescued by expression of wild-type PS1 or PS2 but not by expression of PS1-M146V or PS2-N141I mutants. The ER Ca(2+) leak function of presenilins is independent of their gamma-secretase activity. Our data suggest a Ca(2+) signaling function for presenilins and provide support for the "Ca(2+) hypothesis of AD."[1]

References

Presenilins Form ER Ca(2+) Leak Channels, a Function Disrupted by Familial Alzheimer's Disease-Linked Mutations. Tu, H., Nelson, O., Bezprozvanny, A., Wang, Z., Lee, S.F., Hao, Y.H., Serneels, L., De Strooper, B., Yu, G., Bezprozvanny, I. Cell (2006) [Pubmed]

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