Taurine Directly Binds to Oligomeric Amyloid-β and Recovers Cognitive Deficits in Alzheimer Model Mice

Adv Exp Med Biol. 2017;975 Pt 1:233-241. doi: 10.1007/978-94-024-1079-2_21.


Alzheimer's disease (AD) is the most common cause of dementia leading to severe cognitive decline. During the progression of AD, amyloid-β (Aβ) monomers aggregate into neurotoxic soluble oligomeric Aβ that causes cognitive impairments. Our previous study indicates that oral supplementation of taurine at 1000 mg/kg/day significantly ameliorates hippocampal-dependent cognitive deficits in APP/PS1 transgenic AD mouse model. However, Aβ plaques and oligomeric Aβ levels are not affected after administration of taurine and the oral dosage of taurine was relatively high. Thus, in this study, we focused on direct correlation between taurine and oligomeric Aβ, causing memory deficits in a lower oral dosage of taurine, 250 mg/kg/day. We induced AD-like cognitive impairments to adult normal mice and orally administered taurine via drinking water for 10 days. We confirmed that taurine administration improved cognitive deficits in oligomeric Aβ-infusion mice in Y-maze and passive avoidance tests without activity alteration of mice. In addition, we found that taurine directly bound to oligomeric Aβ in surface plasmon resonance analyses. Our results propose that taurine can ameliorate cognitive impairment by directly binding to oligomeric Aβ in oral administration of 250 mg/kg/day for 10 days.

Keywords: Alzheimer’s disease; Amyloid-β; Dementia; Taurine.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease
  • Amyloid beta-Peptides / drug effects*
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Cognition / drug effects*
  • Disease Models, Animal
  • Maze Learning / drug effects
  • Mice
  • Mice, Inbred C57BL
  • Taurine / pharmacology*


  • Amyloid beta-Peptides
  • Taurine