Taurine directly binds to oligomeric amyloid-β and recovers cognitive deficits in Alzheimer model mice

Ho Chung Jang, Sejin Lee, Sujin Lea Choi, Hye Yun Kim, Seungyeop Baek, Young Soo Kim

Research output: Contribution to journalArticlepeer-review

31 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)233-241
Number of pages9
JournalAdvances in experimental medicine and biology
Publication statusPublished - 2017

Bibliographical note

Funding Information:
Acknowledgements This work was supported by KHIDI (HI14C0466).

Publisher Copyright:
© 2017, Springer Science+Business Media B.V.

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)


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