Despite significant advances in the development of Alzheimer's disease (AD) vaccines effective in animal models, these prototypes have been clinically unsuccessful; apparently the result of using immunogens modified to prevent inflammation. Hence, a new paradigm is needed that uses entire AD-associated immunogens, a notion supported by recent successful passive immunotherapy results, with adjuvants that induce Th2-only while inhibiting without abrogating Th1 immunity. Here, we discuss the obstacles to AD vaccine development and Th2-adjuvants that by acting on dendritic and T cells, would elicit regardless of the antigen a safe and effective antibody response, while preventing damaging neuroinflammation and ameliorating immunosenescence.