Approximately 50% of familial Alzheimer's disease (AD) cases are linked to
the presenilin (PS) gene. This suggests that an altered function of mutated
PSs accounts for a fundamental process leading to AD. Here we identify a n
ew PS binding protein, PBP, which is highly expressed in cerebral cortex an
d hippocampus. Immunohistochemical studies and cell fractionation analysis
show that PBP redistributes from cytoplasm to membranes in the presence of
PS. In addition, PBP is deficient in the soluble fraction of sporadic AD br
ains.