Our team found out at the latest meeting of the Society for Neuroscience (SfN) meeting in Washington, DC, which took place in November.
At the meeting, PDF’s James Beck, Ph.D., VP for Scientific Affairs, and Beth Vernaleo, Ph.D., Senior Manager, Research Programs, were joined by PDF Research Advocates Todd Hebb and Paul Zimmet, D.D.S., both of whom live with PD. (Drs. Zimmet and Vernaleo are pictured inset).
In this blog, first see a video update from Todd and Paul, discussing their experience as patient advocates at SfN, then browse the top scientific highlights observed by our research team.
Video from Todd and Paul:
Top Three Science Stories from SfN:
- New Brain Area Implicated in PD: Perhaps it is time for PD researchers to take a harder look at an area of the brain called the insula. This region of the brain, nestled deep within the cortex, seems to be more important in PD than originally thought, according to a poster by graduate student Marion Criaud, from the laboratory of former PDF-funded researcher Antonio Strafella, M.D., Ph.D., at the University of Toronto. Despite being a hub that processes information related to cognition, mood and bodily awareness, the insula has been largely overlooked in PD research. The new analysis combined a large body of brain imaging studies, finding that abnormalities in specific parts of the insula may contribute to the motor and non-motor symptoms of PD.
- Going After Glutamate: When it comes to PD, we all blame dopamine neurons. Could another type of neuron also be involved? For the first time, research presented by Arun Singh, Ph.D., from the laboratory of Stella Papa, M.D. at Emory University, measured the activity of medium spiny neurons in people with PD as they underwent deep brain stimulation surgery. Dr. Singh observed that the spiny neurons in people with PD were hyperactive, which has also been hypothesized by other researchers. Even more interesting is that medium spiny neurons can be controlled by glutamate. The findings suggest that reducing glutamate signaling might provide additional symptom relief for those with advanced PD who take levodopa. Another study from the same lab discussed how increased glutamate plays a role in levodopa-induced dyskinesia. When the researchers blocked glutamate in monkeys with PD-like symptoms, the activity of their medium spiny neurons decreased. When the monkeys received levodopa (after glutamate) the neurons maintained a normal activity level, preventing the onset of dyskinesia. And, blocking glutamate also reduced the dyskinesia in monkeys that were already treated with levodopa. Along with the results of the human study, this suggests that glutamate plays an important role in PD, and that reducing its signal could be beneficial to those with PD.
- Stem Cell Transplant Success in Mice: Clinical trials of dopamine neuron transplantations have seen some success in both animal studies, and to a lesser degree, in humans. New research presented by graduate student Natalie Goldberg and Mathew Blurton-Jones, Ph.D., and their colleagues from the University of California, Irvine looks at factors that may influence the success of transplantation. They transplanted neural stem cells into the brains of mice whose symptoms mimic PD. Depending on the surrounding environment, neural stem cells can be coaxed to become nearly any neuron in the brain, including those that produce dopamine. The researchers found that one month after transplantation of the stem cells into the striatum, the mice had enhanced dopamine and glutamate signaling, as well as increased neural growth factors, leading to improved cognitive and motor functioning. They also found that without these growth factors, animals with transplanted neural stem cells failed to show a similar motor and cognitive improvement. If these preliminary results in mice hold true in humans, this knowledge may help refine future stem cell treatments for PD.
Do you have questions about any of these stories or Parkinson’s disease in general? Find answers by contacting PDF’s HelpLine at (800) 457-6676 or email@example.com.