DNA Immunotherapy Targets Two Alzheimer's Diseases – Precautions Vaccinations



A New Animal Study by UT Southwestern Peter Oddonell Jr. The brain institute shows that a vaccine delivered to the skin prompts an immune response that reduces the installation of harmful Tau and beta-aminoid proteins without tearing severe brain swelling.

The study consisting of fourteen and twenty-four cats between each and every one showed that the vaccine had a 40 percent reduction in beta-amoioid and up to 50 percent reduction in Tau, with no adverse response.

The vaccine strategy is on a brief list of promising antibody treatments aimed at protecting both types of proteins that kill brain cells as they spread in deadly plaques and tangles on the intelligence of Alzheimer's disease patients.

"This study is the culmination of a decade of research that has repeatedly demonstrated that this vaccine can effectively and safely aim at animal models that we think may cause Alzheimer's disease," said Dr. Roger Rosenberg, founding Director of the Alzheimer's Disease Center at UT Southwestern, in a press release.

"I believe we get close to testing this therapy in people."

The research is published Alzheimer's Research and Therapy Demonstrates how a vaccine with DNA coding for a beta-amoiloid segment also reduces Tau in mice to have Alzheimer's disease.

In addition, the vaccine elisits a different immune response that may be safe for humans.

Two previous studies of Dr. Rosenberg's Lab showed similar immune responses in rabbits and monkeys.

Dr. Rosenberg's team predicts that if the aminoid and Tau are the cause of Alzheimer's disease, the reductions in humans can have a major therapeutic value.

"If the onset of Alzheimer's disease can be delayed by 5 years, it would be huge for patients and their families," said Dr. Doris Lambracht-Washington, the senior author of the study.

"The number of dementia cases may fall by half."

Alzheimer's disease is characterized by progressive deterioration of the brain as neurons are destroyed.

About 5.7 million Americans have the fatal disease, with the number expected to double by 2050, according to the Disease Control and Prevention Centers.

No effective treatment exits, although some antibodies and other therapies were researched and tested in clinical trials to target amiboid plaques and Tau tangles – both hormars of the disease.

This study is the recent contribution to decades of research focusing on chlorinated toxic proteins in hopes of preventing or slowing the progression of Alzheimer's disease.

Scientists have also been trying to develop a method of diagnosing the condition in its earliest stage so that a future breakthrough therapy can be given before the brain enters.

The field advanced significantly earlier this year when UT Southwestern scientists found a "Big Bang" of Alzheimer's disease – the precise point in which a good Tau molecule becomes harmful, but has not yet produced tangles in the brain.

The healthy human brain contains tens of billions of neurons-specialized cells that process and transmits information by electrical and chemical signals. They send messages between different parts of the brain, and from the brain to the muscles and organs of the body, says the Nih.

Alzheimer's disease disorders the communication between neurons, resulting in loss of function and cell death.

Dr. Rosenberg is a professor of Physiology and Neurology & Neurotherapeutics. He holds the Abe (Brunky), Maurice and William Zale Discharged Chair in Neurology.

Dr. Lambracht-Washington is an Assistant Professor of Neurology & Neurotherapeutics.

The research is also supported by the National Institutes of Health; The zale Wikipedia; The Rudman Foundation; The Presbyterian Village North Foundation; Freiber, Loser, and Denker Family Funds; Triumph over Alzheimer's; And avare.

UT Southwestern, one of the first academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education.


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