l-Theanine, an Amino Acid in Green Tea, Attenuates Beta-Amyloid-Induced Cognitive Dysfunction and Neurotoxicity: Reduction in Oxidative Damage and Inactivation of ERK/p38 Kinase and NF-kappaB Pathways

Free Radic Biol Med. 2009 Dec 1;47(11):1601-10. doi: 10.1016/j.freeradbiomed.2009.09.008. Epub 2009 Sep 16.

Abstract

Amyloid beta (Abeta)-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 Abeta(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 Abeta(1-42) (2 microg/mouse, icv), significantly attenuated Abeta(1-42)-induced memory impairment. Furthermore, l-theanine reduced Abeta(1-42) levels and the accompanying Abeta(1-42)-induced neuronal cell death in the cortex and hippocampus of the brain. Moreover, l-theanine inhibited Abeta(1-42)-induced extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase as well as the activity of nuclear factor kappaB (NF-kappaB). 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-kappaB as well as the reduction of macromolecular oxidative damage. Thus, l-theanine may be useful in the prevention and treatment of AD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / physiopathology
  • Amyloid beta-Peptides / chemistry
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Apoptosis / drug effects
  • Camellia sinensis
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Glutamates / chemistry
  • Glutamates / metabolism*
  • Glutamates / pharmacology*
  • Glutathione / biosynthesis
  • Lipid Peroxidation
  • Male
  • Memory Disorders / drug therapy
  • Mice
  • Mice, Inbred ICR
  • NF-kappa B / metabolism
  • Neurons / drug effects*
  • Neurons / metabolism
  • Neurons / pathology
  • Oxidative Stress / drug effects
  • Peptide Fragments / metabolism
  • Peptide Fragments / pharmacology
  • Signal Transduction / drug effects
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Amyloid beta-Peptides
  • Glutamates
  • NF-kappa B
  • Peptide Fragments
  • theanine
  • Extracellular Signal-Regulated MAP Kinases
  • p38 Mitogen-Activated Protein Kinases
  • Glutathione