New Vaccine Approach to Parkinson’s


by Brenda Patoine

November, 2006

Immunotherapy for neurodegenerative diseases is alive and well despite the setback in 2002 when several patients died from treatment complications in the first clinical trial of an Alzheimer’s vaccine. At SfN dozens of investigators reported on new immune-based strategies to treat Alzheimer’s, prion diseases, and—perhaps most promising—Parkinson’s.

One approach, outlined by R. Lee Mosley, an immunologist at the University of Nebraska, may have broad application because it targets microglia, a type of immune cell unique to the brain. Activated microglia are thought to be a primary source of brain inflammation, a common thread that links all neurodegenerative diseases, as well as stroke and certain autoimmune disorders.

Mosley presented results from an animal model of Parkinson’s, a disease that progressively kills dopamine neurons and has a strong neuroinflammatory component. Previous work has shown that reducing this inflammation spares up to 90 percent of neurons that would otherwise die as the disease progresses. In humans, epidemiologic studies have linked daily use of over-the-counter anti-inflammatory drugs with a reduced incidence of Parkinson’s.

The latest research from Mosley’s laboratory uses a specialized subset of immune cells called regulatory T cells, which are known to suppress inflammatory responses in the brain and appear to be neuroprotective. Researchers harvested regulatory T cells from mice that had been treated with glatiramer acetate (Copaxone), a drug used in multiple sclerosis, which itself suppresses both microglia and pro-inflammatory cytokines, and then injected the donated T cells into mice with Parkinson’s-like symptoms.

Using this strategy, Mosley said, “we can ameliorate nearly all of the Parkinson-associated neuronal loss in the substantia nigra and striatum,” two brain areas where the loss of dopamine neurons is most profound. Microglia activation was reduced as well, supporting the hypothesis that tamping down these inflammatory mediators can spare dopamine neurons.