In a recently published study in Alzheimer’s Research and Therapy, a research team from UT Southwestern’s Medical Center (TX, USA), have demonstrated that a vaccine delivered to the skin stimulates an immune response that reduces build-up of beta-amyloid and tau protein in the brains of mice.
“This study 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,” explained Roger Rosenberg, UT Southwestern’s Medical Center. “I believe we’re getting close to testing this therapy in people.”
Earlier research found that antibodies greatly reduce amyloid accumulation in the brain; however, when a vaccine developed in a different study was tested in humans it caused side effects such as brain swelling.
Rosenberg’s team induced a different kind of immune response by injecting the DNA vaccine into the skin of the mice rather than the muscle. The injected skin cells produced a three-molecule chain of beta-amyloid (Aβ42), and the body responded by producing antibodies that inhibited the accumulation of amyloid and tau. The vaccine showed a 40% reduction in beta-amyloid and up to a 50% reduction in tau, with no adverse reactions.
The team suggests that if amyloid and tau are truly the cause of AD, accomplishing these reductions in humans could have major therapeutic value.
“If the onset of the disease could be delayed by even 5 years , that would be enormous for the patients and their families,” explained senior author Doris Lambracht-Washington. “The number of dementia cases could drop by half.”
The scientists at UT Southwestern have also discovered the precise point at which a healthy tau molecule has not yet formed tangles in the brain, but becomes detrimental. These scientists are currently working on a spinal fluid test that can detect abnormal tau proteins before symptoms occur.
Looking forward Rosenberg believes that this test could be important in identifying people for vaccine treatment where symptoms of AD have not yet arisen but, have high levels of amyloid and tau in their brain.
“The longer you wait, the less effect it will probably have,” Rosenberg explained. “Once those plaques and tangles have formed, it may be too late.”