l-Theanine, an amino acid in green tea, attenuates β-amyloid-induced cognitive dysfunction and neurotoxicity: Reduction in oxidative damage and inactivation of ERK/p38 kinase and NF-κB pathways

Abstract Amyloid β (Aβ)-induced neurotoxicity is a major pathological mechanism of Alzheimer disease (AD). In this study, we investigated the inhibitory effect of l -theanine, a component of green tea ( Camellia sinensis ), on Aβ 1-42 -induced neuronal cell death and memory impairment. Oral treatment of l -theanine (2 and 4 mg/kg) for 5 weeks in the drinking water of mice, followed by injection of Aβ 1-42 (2 μg/mouse, icv), significantly attenuated Aβ 1-42 -induced memory impairment. Furthermore, l -theanine reduced Aβ 1-42 levels and the accompanying Aβ 1-42 -induced neuronal cell death in the cortex and hippocampus of the brain. Moreover, l -theanine inhibited Aβ 1-42 -induced extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase as well as the activity of nuclear factor κB (NF-κB). l -Theanine also significantly reduced oxidative protein and lipid damage and the elevation of glutathione levels in the brain. These data suggest that the positive effects of l -theanine on memory may be mediated by suppression of ERK/p38 and NF-κB as well as the reduction of macromolecular oxidative damage. Thus, l -theanine may be useful in the prevention and treatment of AD.