Researchers Seek to Create Vaccine Against Alzheimer’s

October 08, 2003

William Bowers, Ph.D., research associate professor in the Center for Aging and Developmental Biology at the University of Rochester Medical Center

            Researchers are embarking on a five-year study to develop a vaccine that exploits the herpes virus in the fight against Alzheimer’s disease.

            The work aims not at developing a vaccine in the traditional sense, which would prevent the disease in someone who does not have the disease. Rather, the vaccine would spur the body’s immune system to fight the disease in someone who is in the earliest stages of Alzheimer’s disease.

            The project, funded with $1.25 million from the National Institutes of Health, is led by William Bowers, Ph.D., research associate professor in the Center for Aging and Developmental Biology at the University of Rochester Medical Center, and Howard Federoff, M.D., Ph.D., the center director.

            The pair is taking an unusually sophisticated approach to making a vaccine. Normally the body’s immune system has at its disposal an assortment of cells with fancy names – macrophages, cytotoxic T-cells, monocytes, neutrophils, leukocytes, B-lymphocytes, natural killer cells, basophils, eosinophils, and so on – all designed to somehow protect the body and give the boot to invaders. Bowers and Federoff are actively trying to shape the immune system’s response, seeking to pinpoint and then create a cohort of molecules working in concert to produce exactly the type of immune response they desire to fight the disease.

            The work builds on another study where researchers tested a vaccine designed to prod the body to dissolve a protein known as amyloid beta peptide, which accumulates in the brains of people with Alzheimer’s disease. That study was halted because the vaccine caused inflammation in the brains of several participants – but nestled within the data were some promising results showing less plaque in the brains of several participants.

            The Rochester team is working on a way to duplicate the positive effects of such a vaccine without the harmful side effects.

            “In Alzheimer’s disease amyloid beta comes together in the brain to create a large aggregated structure, basically a collection of extracellular junk, that disrupts normal transmission of nerve signals,” says Bowers. “We’re trying to elicit an immune response specifically against just the disease-related aggregated form. This, we hypothesize, will be less likely to cause harmful brain inflammation.”

            To do this the pair will turn to the herpes virus, which Federoff is also using in other experiments to treat or prevent AIDS, cancer, and the harmful effects of stroke. The team strips herpes of its ability to harm, then packs the virus with a payload of genetic material customized to spur the body to fight the damaging form of amyloid beta.

            Included in the package are instructions for making an assortment of compounds specially chosen to customize the body’s immune response. The team will try to boost the body’s ability to recognize amyloid beta so that immune cells can spot the disease form of the protein more readily and remove it from the body. Altogether, dozens of different vaccine combinations will be tested.

            “Our understanding of the modulation of the immune system in the treatment of an inflammatory process such as Alzheimer’s disease is in its infancy,” says Federoff. “Efforts to create and characterize protective responses may lead to new ways to treat Alzheimer’s disease.”

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