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Introduction Vaccination against amyloid β protein (Aβ42) induces high levels of antibody, making it a promising strategy for treating Alzheimer's disease (AD). One drawback in the past was that clinical trial was withheld because of speculation that the Aβ42 vaccine induced CD4+ T cell infiltrations into the central nervous system. To reduce T cell activation while concomitantly maintaining high anti-Aβ42 titers is a great challenge in immunology. Methods We aimed to demonstrate that co-immunization with Aβ42 protein and expression plasmid can be beneficial in a mouse AD model and prevent inflammation. We immunized the AD mice with the co-immunization vaccine and assessed behavior change and Aβ42 deposition. Furthermore, to determine the safety of the co-immunization vaccine, we used an induced Aβ42-EAE model to mimic the meningoencephalitis that happened in the AN-1792 vaccine clinical phase II trial, and tested if the co-immunization vaccine could ameliorate T-cellmediated brain inflammation. Results The co-immunization vaccination reduced Aβ plaques and significantly ameliorated cognitive deficit while at the same time inhibiting T cell-mediated brain inflammation and infiltration. These studies demonstrate that the co-immunization strategy can ameliorate AD pathology without notable adverse effects in mice. Conclusions A co-immunization strategy leading to the development of a safe immunotherapeutic/preventive protocol against AD in humans is warranted. [ABSTRACT FROM AUTHOR]