In a preclinical study, researchers from the Univerity of South Florida have found that a vaccine that targets neurotoxic forms of amyloid-beta (oligomeric Aβ), a key biomarker for Alzheimer'sAlzheimer's, could halt the progression of the disease.
For this study, the researchers tested a vaccine, known as E22W42, that is formulated from modified Aβ-sensitized dendritic cells derived from mouse bone marrow. Dendritic cells work with other immune cells such as T-cells and B-cells to regulate the immune system and suppress harmful responses that threaten healthy tissues.
To test the vaccine, the researchers included three groups of genetically engineered mice to develop high levels of Aβ and behavioral and cognitive abnormalities that mimic those from Alzheimer's disease. While one group was vaccinated with the experimental vaccine, another group received an endogenous amyloid-beta peptide to stimulate dendritic cells. Meanwhile, the third group was injected with dendritic cells without Aβ peptide. The researchers also observed a fourth group comprising of healthy, older mice who had not been genetically engineered.
In the end, the researchers found that the vaccine significantly slowed memory impairment in the mice with Alzheimer's. In fact, they found that mice treated with the vaccines performed similarly to the mice in the non-engineered group in memory tests. These mice also showed significantly fewer errors in working memory than the mice injected with dendritic cells.
Meanwhile, the researchers noticed that there were no significant differences in the quantities of inflammatory cytokines in the blood of the vaccinated mice as opposed to those in the control group. As such, they say that the vaccine has ''little potential for overpriming the immune system''.
"Though the E22W42-sensitized DC vaccine is being developed for patients with Alzheimer's disease, it can potentially help strengthen the immune system of elderly patients (with other age-related disorders) as well," say the study's authors.
Sources: Medical Xpress, IOS Press
