Amyloid-beta (Aβ) active immunization in Alzheimer's disease can increase the rate of Aβ clearance, and delay cognitive dysfunction, but it is easy to induce meningoencephalitis, which may be related to activation of Th1 lymphocytes. To enhance anti-Aβ antibody generation and induce a Th2 immune response, Prof. Yunpeng Cao and team from the First Affiliated Hospital of China Medical University, China constructed a new DNA vaccine p(Aβ3–10)10-C3d-p28.3 encoding ten repeats of Aβ3–10 and three copies of C3d-p28 as a molecular adjuvant. The researchers administered this adjuvant intramuscularly to female C57BL/6J mice at 8–10 weeks of age, and found that the p(Aβ3–10)10-C3d-p28.3 vaccine induced high titers of anti-amyloid-β antibodies, which bound to Aβ plaques in APP/PS1 transgenic mouse brain tissue, demonstrating that the vaccine is effective against plaques in a mouse model of Alzheimer's disease. Moreover, the vaccine elicited a predominantly IgG1 humoral response and low levels of interferon-γ in ex vivo cultured splenocytes, indicating that the vaccine could shift the cellular immune response towards a Th2 phenotype. This indicated that the vaccine did not elicit a detrimental immune response and had a favorable safety profile. These findings were published in the Neural Regeneration Research (Vol. 8, No. 27, 2013).
Source: Neural Regeneration Research