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Melatonin deficiency in cerebrospinal fluid has been postulated to be critical for the development of Alzheimer Disease (AD). As a potent free radical scavengers and antioxidant, melatonin has been proposed to delay or inhibit progression of neurodegenertion in AD. Since the effect of melatonin on Aβ peptide toxicity in the rat oxidative stress model of AD is not fully understood, we observed the effect of melatonin on Aβ protein and APP mRNA in the hippocampus and frontal cortex of AD rats model established by Bennett and found melatonin inhibited the Aβ and APP mRNA. The effect of melatonin could be partly attenuated by pretreatment with the GABA antagonist bicuculline. The results suggest melatonin reduced the Aβ production probably by inhibiting overexpression of APP in the CNS of AD model rats. Maybe these effects of melatonin were influenced by GABA. [ABSTRACT FROM AUTHOR]