Researchers develop vaccine that stops Alzheimers in mice

Researchers from University of Rochester Medical Centre have developed a new vaccine, which triggers an immune response that may protect against Alzheimers without causing inflammation or significant side effects.

Washington, May 20 : Researchers from University of Rochester Medical Centre have developed a new vaccine, which triggers an immune response that may protect against Alzheimer's without causing inflammation or significant side effects.

The team conducted their study using a mouse model with Alzheimer's-like pathology and found that the vaccinated mice generated an immune response to the protein known as amyloid-beta peptide, which accumulates in what are called "amyloid plaques" in brains of people with Alzheimer's.

The vaccinated mice demonstrated normal learning skills and functioning memory in spite of being genetically designed to develop an aggressive form of the disease.

"Our study demonstrates that we can create a potent but safe version of a vaccine that utilizes the strategy of immune response shaping to prevent Alzheimer's-related pathologies and memory deficits," said William Bowers lead author and Associate professor of neurology and of microbiology and immunology at the Medical Centre.

"The vaccinated mice not only performed better, we found no evidence of signature amyloid plaque in their brains," he added.

For the vaccine, Bowers' team used a herpes virus that is stripped of the viral genes that can cause disease or harm. They then load the virus container with the genetic code for amyloid beta and interleukin-4, a protein that stimulates immune responses involving type 2 T helper cells, which are lymphocytes that play an important role in the immune system.

Key features of the disease included accumulation of amyloid plaques in the brains of patients and the loss of normal functioning tau, a protein that stabilizes the transport networks in neurons.

Prior to vaccine study, the mice were trained to navigate a maze using spatial clues.

They were then tested periodically during the 10-month study on the amount of time and distance travelled to an escape pod and the number of errors made along the way.

"What we found exciting was that by targeting one pathology of Alzheimer's - amyloid beta - we were able to also prevent the transition of tau from its normal form to a form found in the disease state," said Bowers.

"We have learned a great deal from this ongoing project.

"Importantly, it has demonstrated the combined strengths of the gene delivery platform and the immune shaping concept for the creation of customized vaccines for Alzheimer's disease, as well as a number of other diseases.

"We are currently working on strategies we believe can make the vaccine even safer," he added.

The study appears in May issue of Molecular Therapy, the journal of The American Society of Gene Therapy.

ANI