Alzheimer’s Vaccine Candidate Produced Positive Data in a Mice Study

DNA vaccine reduces both harmful proteins associated with Alzheimer’s disease

older woman

An experimental Alzheimer's disease vaccine candidate may be able to reduce dementia cases in half and delay effects of the degenerative brain disease by 5 years. 

Researchers at the University of Texas Southwestern Medical Center in Dallas said in a press release that ‘this experimental vaccine delivered to the skin prompts an immune response that reduces the buildup of harmful tau and beta-amyloid proteins – without triggering severe brain swelling. 

This non-human study consisted of four cohorts between 15 and 24 mice each and showed the vaccine prompted a 40 percent reduction in beta-amyloid, and up to a 50 percent reduction in tau, with no adverse immune response. 

“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,” said Dr. Roger Rosenberg, founding Director of the Alzheimer’s Disease Center at UT Southwestern. 

This vaccine strategy is on a shortlist of promising antibody treatments aimed at protecting against both types of proteins that kill brain cells as they spread in deadly plaques and tangles on the brains of Alzheimer’s disease patients. 

“I believe we’re getting close to testing this therapy in people,” said Dr. Rosenberg. 

Dr. Rosenberg’s lab has shown similar immune responses in rabbit and monkey studies. 

Dr. Rosenberg’s team predicts that if amyloid and tau are indeed the cause of Alzheimer’s disease, achieving these reductions in humans could have major therapeutic value. 

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 more than double by 2050, according to the Centers for Disease Control and Prevention.     

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No effective treatment currently exists, though several antibody and other therapies are being researched and tested in clinical trials to target amyloid plaques and tau tangles – both hallmarks of the disease. 

This study is the latest contribution to decades of research focusing on clearing toxic proteins in hopes of preventing or slowing the progression of Alzheimer’s disease. 

The healthy human brain contains tens of billions of neurons—specialized cells that process and transmits information via 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 disrupts this communication among neurons, resulting in loss of function and cell death. 

Dr. Rosenberg is a Professor of Physiology and Neurology & Neurotherapeutics. He holds the Abe (Brunky), Morris and William Zale Distinguished Chair in Neurology. 

The research was supported by the National Institutes of Health; the Zale Foundation; the Rudman Foundation; the Presbyterian Village North Foundation; Freiberger, Losinger, and Denker Family Funds; Triumph Over Alzheimer’s; and AWARE. 

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

The Center for Alzheimer’s and Neurodegenerative Diseases was created in 2014 to find therapies to cure or halt the progression of dementia and related disorders. Alzheimer’s disease (AD) is the single largest health threat to our aging population and demands a research effort commensurate with this problem.