Funding has been secured for the development of an innovative vaccine to combat dementia.

The latest generation of drugs for treating Alzheimer's disease targets the accumulation of beta-amyloid protein through specially designed antibodies. However, the results of their use have not been particularly impressive, and they come with a range of side effects, not to mention that the use of such antibodies can be prohibitively expensive.

Researchers from Washington University in St. Louis are employing a new approach, aiming to develop vaccines that will teach the human immune system to eliminate these clusters of beta-amyloid and tau protein.

Having received a grant of $2.9 million from the National Institute on Aging, part of the National Institutes of Health (NIH), researchers Jai Rudra, Ph.D., an associate professor in the Department of Biomedical Engineering at the McKelvey School of Engineering, and Meredith Jackrel, Ph.D., an associate professor in the Department of Chemistry in the College of Arts and Sciences, will develop vaccines that generate antibodies against beta-amyloid and tau protein using Rudra's peptide nanofiber platform for vaccines.

A key factor in the success of this project is the development of vaccines that do not provoke inflammation, as combating chronic inflammation that arises with age is a persistent challenge in this field.

According to Rudra, previous trials used strong vaccine adjuvants to ensure an attack on beta-amyloid, but some patients experienced side effects. Adjuvants can ensure that the immune system perceives misfolded proteins as "foreign material," but the resulting inflammation can cause more harm than good. Instead, Rudra is utilizing the nanofiber platform he developed during previous vaccine research.

Nanofibers possess unique properties that make them attractive for generating antibodies against tau and beta-amyloid proteins, and they do not induce inflammation like other adjuvants.

The anti-inflammatory nature of these fibers is a very good strategy.

Nanofibers work better because beta-amyloid and tau protein are presented on the surface of the nanofibers in such a way that the immune system does not generate inflammation in response to their presence.

Jackrel and Rudra will collaborate with researchers from Washington University to test their vaccines. They will trial the vaccines on transgenic mice that develop disorders mimicking various types of dementia in the brain.

The vaccine trials will be conducted both as a preventive measure and for treatment after symptoms appear, although Rudra expects the preventive application to be more effective. The challenge of dismantling clusters of amyloid and tau protein after dementia symptoms have emerged is that it may already be too late.

"Dismantling them will be a very complex task," says Rudra, noting that it will likely be much easier to try to prevent the onset of dementia symptoms by addressing neuroinflammation at the outset, possibly as people enter middle age.

This also aligns with other initiatives at Washington University aimed at developing blood tests for the early detection of various neurodegenerative diseases. Other projects, unrelated to biomedical engineering, focus on applying a variety of treatments and lifestyle changes, not just those targeting the immune system.