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Funding received for the development of an innovative dementia vaccine
Alzheimer’s disease and frontal temporal dementia are devastating diseases that occur after the accumulation of misshapen proteins in the brain.
The latest generation of Alzheimer’s disease drugs targets the accumulation of amyloid beta protein with specially designed antibodies, but the results have been less than impressive, and they have a number of side effects, not to mention that the use of such antibodies can be prohibitively expensive.
Alzheimer’s disease is characterized by the accumulation of amyloid plaques and neurofibrillary tangles in brain tissue. The plaques are constructed of beta-amyloid peptide, which is coiled in the form of beta folds. In turn, neurofibrillary tangles are composed of a special tau protein. In contrast to normal proteins, amyloid plaques and neurofibrillary tangles are in a sticky and irregularly coiled form.
Researchers at Washington University in St. Louis are taking a novel approach in an effort to develop vaccines that will teach a person’s own immune system to destroy these clusters of amyloid beta and tau protein.
With a $2.9 million grant from the National Institute on Aging, part of the National Institutes of Health (NIH), researchers Jai Rudra, Ph.D., associate professor of biomedical engineering at the McKelvey School of Engineering, Inc, and Meredith Jackrel, PhD, associate professor of chemistry in the Faculty of Arts and Sciences, will develop vaccines that produce antibodies against amyloid beta and tau protein using Jai Rudra’s peptide nanofiber vaccine platform.
Key to the success of this project is the development of vaccines that do not provoke inflammation, as combating chronic inflammation that occurs with age is an ongoing challenge in the field.
According to Rudra, previous trials have used strong vaccine adjuvants to ensure that amyloid beta is attacked, but this has caused side effects in some patients. Adjuvants can ensure that the immune system sees misfolded proteins as “foreign material,” but the resulting inflammation can do more harm than good. Instead, Rudra is using a nanofiber platform that he developed during previous vaccine research.
Nanofibers have unique properties that make them attractive for making antibodies to tau proteins and amyloid beta, and they don’t cause inflammation like other adjuvants.
The non-inflammatory nature of these fibers is a very good strategy.
Nanofibers work better because amyloid beta and tau protein are presented on the surface of nanofibers in such a way that the immune system will not generate inflammation in response to their exposure.
Jackrel and Rudra will collaborate with researchers at the University of Washington to test their vaccines. They will test the vaccines on transgenic mice that develop disorders that mimic different types of dementia in the brain.
The vaccine trials will be conducted both as a preventative and as a treatment after symptoms appear, although Rudra expects the preventative application to be more effective. The problem with breaking down amyloid and tau protein accumulations after symptoms of dementia appear is that it may be too late.
“Breaking them down is going to be very challenging,” Rudra says, noting that it will likely be much easier to try to prevent the buildup of dementia symptoms by nipping neuroinflammation in the bud, perhaps as early as people enter middle age.
This is also consistent with other initiatives at the University of Washington to develop blood tests for early detection of various neurodegenerative diseases. Other non-biomedical engineering projects are targeting all sorts of treatments and lifestyles, not just the immune system.
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