1 b-Amyloid peptide (Ab), a 39 ± 43 amino acid peptide, is believed to induce oxidative stress and in¯ammation in the brain, which are postulated to play important roles in the pathogenesis of Alzheimer's disease. Ferulic acid is an antioxidant and anti-in¯ammatory agent derived from plants; therefore, the potential protective activity of ferulic acid against Ab toxicity in vivo was examined. 2 Mice were allowed free access to drinking water (control) or water containing ferulic acid (0.006%). After 4 weeks, Ab1-42 (410 pmol) was administered via intracerebroventricular injection. 3 Injection of control mice with Ab1-42 impaired performance on the passive avoidance test (35% decrease in step-through latency), the Y-maze test (19% decrease in alternation behaviour), and the water maze test (32% decrease in percentage time in platform-quadrant). In contrast, mice treated with ferulic acid prior to Ab1-42 administration were protected from these changes (9% decrease in step-through latency; no decrease in alternation behaviour; 14% decrease in percentage time in platform-quadrant). Ab1-42 induced 31% decrease in acetylcholine level in the cortex, which was tended to be ameliorated by ferulic acid. 4 In addition, Ab1-42 increased immunoreactivities of the astrocyte marker glial ®brillary acidic protein (GFAP) and interleukin-1b (IL-1b) in the hippocampus, eects also suppressed by pretreatment with ferulic acid. 5 Administration of ferulic acid per se unexpectedly induced a transient and slight increase in GFAP and IL-1b immunoreactivity in the hippocampus on day 14, which returned to basal levels on day 28. A slight (8%) decrease in alternation behaviour was observed on day 14. 6 These results demonstrate that long-term administration of ferulic acid induces resistance to Ab1-42 toxicity in the brain, and suggest that ferulic acid may be a useful chemopreventive agent against Alzheimer's disease.

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