Increased in vivo amyloid-β42 production, exchange, and loss in presenilin mutation carriers.

@article{Potter2013IncreasedIV,
  title={Increased in vivo amyloid-β42 production, exchange, and loss in presenilin mutation carriers.},
  author={Rachel Church Potter and Bruce W. Patterson and Donald L. Elbert and Vitaliy Ovod and Tom P Kasten and Wendy C. Sigurdson and Kwasi G. Mawuenyega and Tyler M. Blazey and Alison M. Goate and Robert Chott and Kevin E Yarasheski and David M Holtzman and John C. Morris and Tammie L. Benzinger and Randall J. Bateman},
  journal={Science translational medicine},
  year={2013},
  volume={5 189},
  pages={189ra77}
}
Alzheimer's disease (AD) is hypothesized to be caused by an overproduction or reduced clearance of amyloid-β (Aβ) peptide. Autosomal dominant AD (ADAD) caused by mutations in the presenilin (PSEN) gene have been postulated to result from increased production of Aβ42 compared to Aβ40 in the central nervous system (CNS). This has been demonstrated in rodent models of ADAD but not in human mutation carriers. We used compartmental modeling of stable isotope labeling kinetic (SILK) studies in human… CONTINUE READING