A new Alzheimer’s vaccine developed by scientists at the University of Texas Southwestern could conceivably cut the number of dementia cases in half.

Unlike a previous attempt that caused swelling in the brain when DNA was injected into the test mice’s muscles, the new vaccine was administered by injecting it superficially into the skin.

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. The new vaccine, injected into the skin, triggers the skin cells to produce a three-molecule chain of beta-amyloid. The immune system is then catalyzed to produce antibodies to fight beta-amyloid; the antibodies also fight tau proteins. This means the body anticipates the Alzheimer’s plaques and tangles before they happen.

As the Daily Mail reports, 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 explained:

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.

The study concluded, “It is expected that DNA Aβ42 trimer immunotherapy in a clinical trial will reduce both plaques and tangles in patients with AD.”

Dr. Roger Rosenberg, founding director of the Alzheimer’s Disease Center at University of Texas Southwestern, said the new vaccine “is the culmination of a decade of research that has repeatedly demonstrated that this vaccine can effectively and safely target in animal models what we think may cause Alzheimer’s disease.” He added, “I believe we’re getting close to testing this therapy in people.”

Study senior author Dr. Doris Lambracht-Washington said: “If the onset of the disease could be delayed by even five years, that would be enormous for the patients and their families. The number of dementia cases could drop by half.”

The study was published in the journal Alzheimer’s Research and Therapy.