RESUMEN
Abnormal amyloid-ß (Aß) aggregates are a striking feature of Alzheimer's disease (AD), and Aß oligomers have been proven to be crucial in the pathology of AD. Any intervention targeting the generation or aggregation of Aß can be expected to be useful in AD treatment. Oxidative stress and inflammation are common pathological changes in AD that are involved in the generation and aggregation of Aß. In the present study, 6-month-old PS1V97L transgenic (Tg) mice were treated with sulforaphane, an antioxidant, for 4 months, and this treatment significantly inhibited the generation and aggregation of Aß. Sulforaphane also alleviated several downstream pathological changes that including tau hyperphosphorylation, oxidative stress, and neuroinflammation. Most importantly, the cognition of the sulforaphane-treated PS1V97L Tg mice remained normal compared to that of wild-type mice at 10 months of age, when dementia typically emerges in PS1V97L Tg mice. Pretreating cultured cortical neurons with sulforaphane also protected against neuronal injury caused by Aß oligomers in vitro. These findings suggest that sulforaphane may be a potential compound that can inhibit Aß oligomer production in AD.
