Oxidative stress and excessive redox metals have been implicated in the pathogenesis of Alzheimer's disease (AD), which leads to the tentative employment of radical scavengers and metal chelators in clinical therapy of AD. The preliminary successes of both therapy strategies inspire us to propose that better clinical effects can be expected for a compound combining radical-scavenging potential with metal-protein-attenuating ability. Based on theoretical investigation, we indicate that two novel metal chelators (1-(benzimidazole-2-ylmethyl)-1,4,7-triazacyclononane and 1,4-bis(benzimidazole-2-ylmethyl)-1,4,7-triazacyclonone), especially the latter, are promising to fulfill this new strategy.