L-theanine attenuates AlCl3-induced cognitive dysfunction and neurotoxicity in rats: a behavioral and biochemical study.

BACKGROUND/AIM: The effects of L-theanine (LTN), a natural compound found in tea leaves, on biochemical parameters and cognitive functions were investigated in an aluminum chloride (AlCl3)-induced Alzheimer's disease-like experimental model.

MATERIALS AND

METHODS

A total of 32 male Wistar rats were allocated into four groups: control, AlCl3-induced AD-like group, LTN-treated AD-like group, and donepezil-treated AD-like group. Donepezil was used as a reference drug. For the induction of AlCl3-induced neurotoxicity, AlCl3 was administered by gavage at a dose of 25 mg/kg/day during the 1st week and 150 mg/kg/day for the subsequent 3 weeks. LTN was administered orally at a dose of 100 mg/kg. Spatial memory was assessed using the Morris water maze and the novel object recognition test. Brain tissues were collected to analyze acetylcholinesterase, catalase, and myeloperoxidase activities, as well as amyloid beta (Aβ), lipid peroxidation, glutathione, and nitric oxide levels.

RESULTS

LTN reversed AlCl3-induced cognitive deficits. Moreover, the elevations in acetylcholinesterase and myeloperoxidase activities, as well as increased Aβ levels in the brain tissues of AlCl3-treated rats, were significantly reduced following LTN treatment. The increases in lipid peroxidation and nitric oxide observed in the AlCl3 group were suppressed by LTN treatment, while decreased antioxidant defenses, namely reduced glutathione levels and catalase activity, were restored.

CONCLUSION

The findings demonstrate that AlCl3 exposure impairs cholinergic function, induces oxidative damage, and leads to cognitive dysfunction, whereas LTN treatment effectively mitigates these effects, suggesting potential neuroprotective benefits against aluminum-induced neurotoxicity.