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

ABSTRACT

Alzheimer's disease (AD) is the most common cause of dementia leading to severe cognitive decline. During the progression of AD, amyloid-ß (Aß) monomers aggregate into neurotoxic soluble oligomeric Aß 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, Aß plaques and oligomeric Aß 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 Aß, 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 Aß-infusion mice in Y-maze and passive avoidance tests without activity alteration of mice. In addition, we found that taurine directly bound to oligomeric Aß in surface plasmon resonance analyses. Our results propose that taurine can ameliorate cognitive impairment by directly binding to oligomeric Aß in oral administration of 250 mg/kg/day for 10 days.