PerspectiveFeatureRejecting the Alzheimer's disease vaccine development for the wrong reasons

- Tested Alzheimer vaccines were more suited for transgenic mouse models than humans.
- Immunogen must have the conformational epitope found in toxic oligomeric β-amyloid.
- Selected adjuvant should induce a sole Th2 anti-inflammatory immunity.
- Alzheimer vaccines must mimic natural protective immunity rather than replacing it.

The development of amyloid β (Aβ) vaccines for Alzheimer's disease (AD) has consistently failed clinically, an outcome that is assumed to result from flaws in the proposed role of Aβ as the crucial causative agent of this disease. This opinion resulted in this research approach being disregarded, yet, review of the development of these vaccines indicates that they are more suited to transgenic mice, which is unsurprising given that these animal models were used to determine the efficacy of these vaccines, and that the approach overlooked research findings relevant to AD vaccines. Hence, new strategies using new immunogens and anti-inflammatory adjuvants mimicking the natural protective immunity against AD should be implemented to develop effective preventive vaccines.