A new study shows that a vaccine delivered to the skin produces an immune response that reduces the formation of harmful tau and beta-amyloids without causing severe brain swelling that previously treated with antibodies in some patients.
Professor Roger Rosenberg, founder of the Center for Alzheimer's at the University of Texas Southwestern, said: "This study is the culmination of a decade of research that has repeatedly demonstrated that this vaccine can effectively and safely focus on animal models what we think can cause Alzheimer's disease.
"I believe we are approaching testing for this therapy in humans."
The findings, published in Alzheimer's Research and Therapy, show that a vaccine containing DNA encoding a beta-amyloid segment also reduces tau in mice modeled to have Alzheimer's disease.
The vaccine also carries out another immune response that can be safe for humans.
Two previous studies from the laboratory prof. Rosenberg showed a similar immune response in rabbits and monkeys.
The vaccine is on a short list of promising treatments for antibodies to protect against both types of proteins that kill brain cells because they spread in lethal plaques and tangle in the brains of patients with Alzheimer's disease.
Although earlier research has shown that antibodies significantly reduce amyloid formation in the brain, prof. Rosenberg needed to find a safe way of getting them into the body.
The vaccine developed elsewhere proved promising at the beginning of 2000, but in human testing it caused brain swelling in some patients.
The idea of prof. Rosenberga was supposed to start coding DNA for amyloid and injecting it into the skin rather than into the muscle to induce another type of immune response.
Injected skin cells form a three-chain beta-amyloid, and the body reacts by producing antibodies that inhibit amyloid formation and indirectly also tau.
The latest study – consisting of four groups of between 15 and 24 mice – shows that the vaccine caused a 40% decrease in beta-amyloid and up to 50% tau reduction without a negative immune response.
The team of prof. Rosenberg predicts that if amyloid and tau are actually the cause of Alzheimer's disease, achieving such a reduction in the number of people could be of considerable therapeutic value.
Dr. Doris Lambracht-Washington's study said, "If the onset of illness could be postponed for even five years, it would be enormous for patients and their families.
"The number of dementia cases could drop by half."
Alzheimer's disease is characterized by progressive brain deterioration because the neurons are destroyed.
There is no effective treatment, but in clinical studies, several antibodies and other therapies for amyloid plaques and tau spleen are both investigated and tested – both signs of the disease.
One strategy, which is still tested for clinical benefits, involves the production of antibodies in the laboratory and their application to the body – a method called passive immunization.
Prof Rosenberg said that allowing the body to produce its own antibodies through active immunization would be a more profitable strategy if it can be done safely.
Among these benefits he said the vaccine would be more accessible and cheaper. It also produces a broader range of antibody types than pre-generated antibodies containing only one specific antibody.
Scientists are also trying to develop a method of diagnosing Alzheimer's disease at the earliest stage so that future breakthrough therapies can be given before the brain worsens.
Prof Rosenberg added, "The longer you wait, the less likely it will be.
"Once these boards and meshes are created, it may be too late."