The Experimental Alzheimer's Disease Drug Posiphen [(+)-Phenserine] Lowers Amyloid-β Peptide Levels in Cell Culture and Mice

@article{Lahiri2007TheEA,
  title={The Experimental Alzheimer's Disease Drug Posiphen [(+)-Phenserine] Lowers Amyloid-$\beta$ Peptide Levels in Cell Culture and Mice},
  author={Debomoy K. Lahiri and Demao Chen and Bryan Maloney and Harold W. Holloway and Qian-sheng Yu and Tadanobu Utsuki and Tony Giordano and K. Sambamurti and Nigel H. Greig},
  journal={Journal of Pharmacology and Experimental Therapeutics},
  year={2007},
  volume={320},
  pages={386 - 396}
}
  • D. LahiriDemao Chen N. Greig
  • Published 1 January 2007
  • Biology, Chemistry
  • Journal of Pharmacology and Experimental Therapeutics
Major characteristics of Alzheimer's disease (AD) are synaptic loss, cholinergic dysfunction, and abnormal protein depositions in the brain. The amyloid β-peptide (Aβ), a proteolytic fragment of amyloid β precursor protein (APP), aggregates to form neuritic plaques and has a causative role in AD. A present focus of AD research is to develop safe Aβ-lowering drugs. A selective acetylcholinesterase inhibitor, phenserine, in current human trials lowers both APP and Aβ. Phenserine is dose-limited… 

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  • K. ShawT. Utsuki N. Greig
  • Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 2001
It is suggested that phenserine reduces Aβ levels by regulating βAPP translation via the recently described iron regulatory element in the 5′-untranslated region of βAPP mRNA, which has been shown previously to be up-regulated in the presence of interleukin-1.
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