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neuromorphogenesis:

Is Parkinson’s an Autoimmune Disease?

This is a new, and likely controversial, idea in Parkinson’s disease; but if true, it could lead to new ways to prevent neuronal death in Parkinson’s that resemble treatments for autoimmune diseases,” said the study’s senior author, David Sulzer, PhD, professor of neurobiology in the departments of psychiatry, neurology, and pharmacology at Columbia University College of Physicians & Surgeons.

The new hypothesis about Parkinson’s emerges from other findings in the study that overturn a deep-seated assumption about neurons and the immune system.

For decades, neurobiologists have thought that neurons are protected from attacks from the immune system, in part, because they do not display antigens on their cell surfaces. Most cells, if infected by virus or bacteria, will display bits of the microbe (antigens) on their outer surface. When the immune system recognizes the foreign antigens, T cells attack and kill the cells. Because scientists thought that neurons did not display antigens, they also thought that the neurons were exempt from T-cell attacks.

“That idea made sense because, except in rare circumstances, our brains cannot make new neurons to replenish ones killed by the immune system,” Dr. Sulzer says. “But, unexpectedly, we found that some types of neurons can display antigens.”

Cells display antigens with special proteins called MHCs. Using postmortem brain tissue donated to the Columbia Brain Bank by healthy donors, Dr. Sulzer and his postdoc Carolina Cebrián, PhD, first noticed—to their surprise—that MHC-1 proteins were present in two types of neurons. These two types of neurons—one of which is dopamine neurons in a brain region called the substantia nigra—degenerate during Parkinson’s disease.

To see if living neurons use MHC-1 to display antigens (and not for some other purpose), Drs. Sulzer and Cebrián conducted in vitro experiments with mouse neurons and human neurons created from embryonic stem cells. The studies showed that under certain circumstances—including conditions known to occur in Parkinson’s—the neurons use MHC-1 to display antigens. Among the different types of neurons tested, the two types affected in Parkinson’s were far more responsive than other neurons to signals that triggered antigen display.

The researchers then confirmed that T cells recognized and attacked neurons displaying specific antigens.

The results raise the possibility that Parkinson’s is partly an autoimmune disease, Dr. Sulzer says, but more research is needed to confirm the idea.

“Right now, we’ve showed that certain neurons display antigens and that T cells can recognize these antigens and kill neurons,” Dr. Sulzer says, “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.”

If the immune system does kill neurons in Parkinson’s disease, Dr. Sulzer cautions that it is not the only thing going awry in the disease. “This idea may explain the final step,” he says. “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.”

neurosciencestuff:

Head injuries can make children loners

New research has found that a child’s relationships may be a hidden casualty long after a head injury.

Neuroscientists at Brigham Young University studied a group of children three years after each had suffered a traumatic brain injury – most commonly from car accidents. The researchers found that lingering injury in a specific region of the brain predicted the health of the children’s social lives.

“The thing that’s hardest about brain injury is that someone can have significant difficulties but they still look okay,” said Shawn Gale, a neuropsychologist at BYU. “But they have a harder time remembering things and focusing on things as well and that affects the way they interact with other people. Since they look fine, people don’t cut them as much slack as they ought to.”

Gale and Ph.D. student Ashley Levan authored a study to be published April 10 by the Journal of Head Trauma Rehabilitation, the leading publication in the field of rehabilitation. The study compared the children’s social lives and thinking skills with the thickness of the brain’s outer layer in the frontal lobe. The brain measurements came from MRI scans and the social information was gathered from parents on a variety of dimensions, such as their children’s participation in groups, number of friends and amount of time spent with friends.

A second finding from the new study suggests one potential way to help. The BYU scholars found that physical injury and social withdrawal are connected through something called “cognitive proficiency.” Cognitive proficiency is the combination of short-term memory and the brain’s processing speed.

“In social interactions we need to process the content of what a person is saying in addition to simultaneously processing nonverbal cues,” Levan said. “We then have to hold that information in our working memory to be able to respond appropriately. If you disrupt working memory or processing speed it can result in difficulty with social interactions.”

Separate studies on children with ADHD, which also affects the frontal lobes, show that therapy can improve working memory. Gale would like to explore in future research with BYU’s MRI facility if improvements in working memory could “treat” the social difficulties brought on by head injuries.

“This is a preliminary study but we want to go into more of the details about why working memory and processing speed are associated with social functioning and how specific brain structures might be related to improve outcome,” Gale said.

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