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Published on: May 22, 2018

Selective amyloid-beta lowering agents.

Michael S Wolfe1

  • 1Center for Neurologic Diseases, Brigham & Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. mwolfe@rics.bwh.harvard.edu

BMC Neuroscience
|December 19, 2008
PubMed
Summary
This summary is machine-generated.

Targeting amyloid-beta (Abeta) production is key for Alzheimer's disease (AD) therapeutics. Novel agents lower Abeta without impacting Notch signaling, potentially revealing new therapeutic targets.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Alzheimer's disease (AD) pathogenesis involves amyloid-beta peptide (Abeta) accumulation.
  • Abeta is produced by beta- and gamma-secretase enzymatic activity on amyloid precursor protein (APP).
  • Targeting these proteases offers a therapeutic strategy for AD.

Purpose of the Study:

  • To review strategies for inhibiting Abeta production.
  • To discuss challenges and alternative approaches in developing AD therapeutics.
  • To explore novel Abeta-lowering agents and their mechanisms.

Main Methods:

  • Review of existing literature on beta- and gamma-secretase inhibitors.
  • Discussion of structure-based design for beta-secretase.
  • Analysis of cell-based screening for novel Abeta-lowering agents.

Main Results:

  • Gamma-secretase inhibitors faced toxicity issues due to Notch receptor interference.
  • Beta-secretase inhibitors showed less favorable pharmacological properties initially.
  • Novel cell-based screening identified Abeta-lowering agents sparing Notch signaling.

Conclusions:

  • Targeting gamma-secretase requires strategies to avoid Notch pathway disruption.
  • Novel therapeutic agents may offer new targets for Alzheimer's disease.
  • Further research is needed to elucidate the mechanisms of these novel agents.