Contrary to decades of research suggesting Parkinson’s disease behaves one way, a new study from Columbia University proposes an alternate disease profile that moves the affliction away from being entirely a neurological disorder and toward that of an autoimmune disease.

The idea, while controversial, suggests that when neurons die, they’re doing it specifically because the antigens (or bacteria) on the surface of the neurons are being displayed. This allows the body’s T cells, which mediate immunity, to attack the antigen, thereby mistakenly killing the neuron. Up until this research, neurons weren’t thought to display any antigens, meaning the immune system wouldn’t respond. But new data presents a contrary view to this deep-seated belief.

For a long time, scientists believed T cell attacks were no match for the brain’s neurons. “That idea made sense because, except in rare circumstances, our brains cannot make new neurons to replenish ones killed by the immune system," explained Dr. David Sulzer, the study’s senior author and Columbia professor of neurobiology, in a statement. It wouldn’t make sense, in other words, for the brain to allow its own cells to die, essentially by surrendering. "But, unexpectedly, we found that some types of neurons can display antigens."

Most cells, when they’re infected by a virus or invading bacteria, reveal pieces of it on their surface. Parkinson’s is an interesting case because scientists still don’t understand the cause of neuronal death — the why. What the present study offers is insight into the how. Sulzer and his team believe the body’s immune system mistakes neurons as foreign invaders, similar to other cells in the case of type I diabetes, celiac disease, and multiple sclerosis, before killing the cells in hopes of eradicating the “virus.”

The problem, of course, is that there is no virus. To understand why the immune system may behave like this, the research team used healthy postmortem brain tissue to analyze the nature of the T cell attacks. They specifically looked at a set of cell surface molecules called major histocompatibility complex (MHC) molecules, which are present when the antigen is displayed. They found, to their surprise, MHC proteins in two types of neurons. Both of these neurons degenerate during Parkinson’s disease.

"Right now, we've showed that certain neurons display antigens and that T cells can recognize these antigens and kill neurons," Dr. Sulzer said, "but we still need to determine whether this is actually happening in people. We need to show that there are certain T cells in Parkinson's patients that can attack their neurons."

Parkinson’s is currently the 14th leading cause of death in the U.S., according to the Centers for Disease Control and Prevention (CDC). The disease may also be on the rise, as the CDC reports a 4.6 percent increase in prevalence in 2010, the most recent year for which the data is available. It’s characterized by tremors, difficulty walking and moving, and impairment with general coordination. The present research has made leaps, researchers assert, but they aren’t at their destination.

What’s left to uncover is decidedly fundamental. Just because a response takes place in the presence of another response, in this case antigens being displayed in neurons typically involved with Parkinson’s, doesn’t mean one causes the other. Follow-up tests need to show whether other functions are at play. Alternatively, it may be the case that neuronal death is mediated by the immune system, but only as the last step in a long string of malfunctions.

"This idea may explain the final step," Sulzer said. "We don't know if preventing the death of neurons at this point will leave people with sick cells and no change in their symptoms, or not."

Source: Cebrián C, Zucca F, Mauri P, et al. MHC-I expression renders catecholaminergic neurons susceptible to T-cell-mediated degeneration. Nature Communications. 2014.