The University hosted its first Parkinson’s disease research symposium Thursday, which focused on creative ways to approach the disease’s treatment.
William Dauer, director of the Morris K. Udall Centers of Excellence for Parkinson’s Disease Research, a collaboration between several universities, said the center aims to study topics outside of mainstream Parkinson’s research.
“The key theme is to look beyond the traditional focus to other aspects of the disease, to other chemical transmitters that are affected to try to better understand how those play a role is the disease,” he said.
Etienne Hirsch, director at the Institute for Neurosciences at the French Alliance for Life and Health Science, delivered the conference’s keynote address in the Biomedical Science Research Building’s Kahn Auditorium.
Hirsch’s talk focused on the ways in which brain cell deterioration causes symptoms associated with Parkinson’s, touching on his own research. He emphasized the role of glial cells, inflammatory cytokines and apoptosis, the automatic response within cells to destruct when they sustain a certain level of damage. Glial cells help maintain homeostasis, or stability, in the brain. Inflammatory cytokines are proteins that signal cells to cause inflammation.
He said while those three elements are not always viewed as pivotal to understanding the disease, he hoped to convince the audience that looking at Parkinson’s disease in this way would provide a new way to think about treatment.
In talking about his experiments, Hirsch said he found that a certain heat shock protein, HSP60, was responsible for increasing the amount of cellular degeneration. Heat shock proteins are a type of protein within the body that are produced when a cell experiences stressful conditions.
“From this experiment, we have shown that HSP60 isn’t used, it is released, and that HSP60 killed the neurons,” Hirsch said. “You see that when you apply AraC on the treatment of HSP60 you reduce the degree of normal degeneration.”
AraC refers to a protein known to block cancer by stopping cell division.
Hirsch also touched on experiments focused on mitigating problems with gait and balance, which is associated with Parkinson’s disease.
Some research has held that the disorder might stem from the pedunculopontine nucleus or PPN, a part of the brain stem.
Hirsch said through research on monkeys, his team was able to conclude that a popular method of treatment, dopamine, may not always be effective if the gait and balance issues do in fact stem from the PPN.
“What can we learn from the animal involvements of gait disorders?” he said. “PPN cholinergic lesion can cause dopamine resistant gait deficits.”
Neurology Assistant Prof. Vikas Kotagal, who presented a shorter talk later in the event, said the innovations Hirsch spoke of about were important in finding new ways to treat the disease.
“I think that the work that he’s presenting is very fundamental to the hypotheses that led to the creation of this out of the box idea for the Udall Center,” Kotagal said. “It relates to leading to clinically significant outcomes for patients with Parkinson’s disease.”
Hirsch’s keynote address was followed by seven other shorter presentations on Parkinson’s disease presented by other professionals working in the field, which Dauer said was another focus of the event.
“One of our goals is to support younger investigators and to help foster their careers in Parkinson’s, which is one of the key reasons we structured the symposium the way we did,” he said.