According to the University of New Mexico Health Sciences Department, researchers at the university have created a vaccine that could prevent the development of Alzheimer’s disease.
The department’s newsroom website stated that the vaccine uses virus-like particles (VLPs) to eliminate the tangling of the tau protein, which when accumulated in the brain can interrupt neurons in the brain from communicating. Alzheimer’s, which is expected to strike triple the number of people by 2050, cripples the brain as human beings age, as beta-amyloid proteins in the brain get stuck together and tau proteins start to tangle, both of which inhibit neural connections.
Nicole Maphis, a PhD candidate who was working in the lab of Kiran Bhaskar, PhD, an associate professor in UNM’s Department of Molecular Genetics & Microbiology, stated, “We’re excited by these findings, because they seem to suggest that we can use the body’s own immune system to make antibodies against these tangles, and that these antibodies actually bind and clear these tau tangles.”
Maphis tested the vaccine in mice and they showed a marked improvement in their capacity to deal with mazes. The UNM Health Department site stated, “MRI scans showed that the vaccinated animals had less brain shrinkage, suggesting that the vaccine prevented neurons from dying. Maphis also found significantly fewer tangles in both the cortex and the hippocampus – areas in the brain that are important for learning and memory, and which are destroyed in Alzheimer’s.”
UNM scientists David Peabody and Bryce Chackerian also aided in the process; they were instrumental in starting to use VLPs to create vaccines targeting dengue virus, hepatitis B, human papillomavirus and amyloid beta protein.
In November 2018, a study published in Alzheimer’s Research & Therapy touted a new Alzheimer’s vaccine developed by scientists at the University of Texas Southwestern that could conceivably cut the number of dementia cases in half. The research team tested four groups of mice; the vaccinated mice experienced as much as 40% of their beta-amyloid plaques reduced and as much as 50% of their tau tangles diminished. No adverse immune response was observed.
The study stated:
We report, for the first time in an AD mouse model, that active DNA Aβ42immunization into the skin targets two pathologies: amyloid-containing plaques and tau. DNA vaccination, in which not the antigen (peptide or protein) but the DNA encoding this peptide is administered, is an alternative route of vaccination. Genes encoded by the DNA are expressed within the skin, and the peptides are taken up by dendritic cells traveling to the regional lymph nodes and presenting the antigen to B and T cells. Immune responses to DNA or peptide immunization differ qualitatively.
We have shown previously that full-length DNA Aβ42 trimer immunization is noninflammatory and induces a regulatory immune response. DNA Aβ42 trimer immunization has been shown to be effective in removing amyloid from the brain in immunized double-transgenic mice. In the present study, we used a triple-transgenic AD mouse model that exhibits Aβ and tau pathologies characteristic of human AD. We found that immunotherapy with DNA Aβ42 trimer leads to reduction of Aβ40/Aβ42 peptides and amyloid plaques, and we show for the first time that DNA Aβ42 trimer immunization leads also to significant reduction of tau from the mouse brain.