Nasal mucosal inhalation of AD vaccine attenuates Aβ1-42-induced cytotoxicity

Cholinergic inhibitors and N-methyl-D-aspartate receptor antagonists can alleviate the symptoms of Alzheimer's disease, but fail to affect irreversible cognitive dysfunction and effectively scavenge amyloid beta peptide in the brain. Amyloid beta peptide (Aβ) vaccines reduced and eliminated Aβ deposition in an Alzheimer's disease (AD) transgenic mouse model, and significantly improved behavioral and cognitive impairment.

Dr. Yunpeng Cao and his team, First Affiliated Hospital of China Medical University, China immunized AD transgenic mouse models with Plp-Adeno-X-CMV-(Aβ3-10)10-CpG via nasal mucosal inhalation. They found that Plp-Adeno-X-CMV-(Aβ3-10)10-CpG vaccine can produce strong T helper 2 humoral immune responses, and avoid Aβ1-42-caused T helper 1 immune responses and Aβ1-42-induced cytotoxicity. Therefore, Plp-Adeno-X-CMV-(Aβ3-10)10-CpG vaccine can be used as a novel type of AD vaccine.

These findings were published in Neural Regeneration Research (Vol. 9, No. 8, 2014).

More information:
Jiang TZ, Guo WS, Sha S, Xing XN, Guo R, Cao YP. Nasal mucosal inhalation of amyloid-beta peptide 3-10 defective adenovirus attenuates cytotoxicity induced by beta-amyloid (1–42). Neural Regen Res. 2014;9(8):872-877.

Provided by Neural Regeneration Research