Exercise is Regenerative Medicine: Impact on Parkinson’s Disease

The May NeuroScience Cafe is right around the corner and this month’s topic is Exercise is Regenerative Medicine: Impact on Parkinson’s Disease. Brought to you by UAB’s Comprehensive Neuroscience Center (CNC), the May cafe will be held at the Hoover Public Library (200 Municipal Drive, Hoover, AL 35216) Monday, May 21 at 6:30 PM and lead by Dr. Marcas Bamman from the Department of Neurology at UAB.

The overall goal of these cafés is to help educate the public on the latest clinical care and neuroscience-related research taking place at UAB. Our audience is typically made up of older adults as well as individuals and family members who have been affected by the topic. The program runs for about an hour and is very casual and relaxed!

We would love for anyone involved in the Parkinson Association of Alabama to come and learn about the insights from neuroscience research.

Brian Grant Won’t Back Down From Parkinson’s Disease

by Chris Ballard

He could hear the roar from the back hallway of the Rose Garden, the clatter of 20,000 fans.

For years, Brian Grant had fed off that roar, back when Blazers fans wore T-shirts that read “Rasta Monsta” and embraced him as they had few others. Never the fastest, biggest or most skilled, Grant got by on hustle and desire. What was it Tim Duncan once said? “Hardest-working guy in the league. You’ve got to respect that cat.” And Grant took pride in that. On playing an entire season with a torn labrum. On never backing down, whether it was guarding Karl Malone or levering his 6’9″ frame into Shaquille O’Neal. On trying harder than anyone else. He got out of Georgetown, Ohio, by not trying; survived 12 years in the league by trying; tore up both knees by trying.

But now, standing in that concrete corridor on a November night in 2008, two years after his final NBA game, Grant felt only fear and anxiety. He was there to honor an old friend, former Blazer Kevin Duckworth, who’d died of heart failure at 44. All Grant needed to do was be present. Wave, bow his head, pay his respects. And yet he’d already sweated through his white undershirt, the perspiration breaching his blue button-down and threatening his navy blazer. He thought about ducking into the bathroom to towel off, maybe even bolting the arena. Read more at Sports Illustrated…

Source: Sports Illustrated

 

Cell Study Provides Hope for Treatment of Parkinson’s Disease

By Alice Melão

Deregulation of calcium levels in nerve cells has been linked to early symptoms of Parkinson’s disease. Now, researchers at Aarhus University have found that inhibition of a protein called SERCA can prevent calcium variations and protect nerve cells from degeneration.

This finding may open new therapeutic avenues to treat Parkinson’s motor symptoms, but also non-motor symptoms such as sleep disorders, gastrointestinal problems, anxiety, and depression.

The study, “Alpha‐synuclein aggregates activate calcium pump SERCA leading to calcium dysregulation,” was published in the journal EMBO Reports.

The team showed that in nerve cells with the same type of stress involved in Parkinson’s disease, there is a significant loss of calcium, a basic element in the body without which cells cannot function and eventually die.

The reason behind this observation seems to be the fact that in these cells, α-synuclein aggregates — protein aggregates thought to be behind Parkinson’s development — interact and activate a calcium pump known as the SERCA protein. Interestingly, this process is specific to α-synuclein clumps, as isolated molecules did not interact or activate SERCA.

To further confirm the relevance of these findings, the team analyzed samples of human brain collected from patients affected by dementia with Lewy bodies, characterized by α-synuclein aggregates. They again found the same pattern in which α-synuclein clumps interacted with SERCA and promoted calcium transport outside of the cell.

“The study indicates that the treatment of calcium disturbances is meaningful because the nerve cells are protected. This may help to prevent the disease from developing into such a disabling disease as would otherwise be the case,” Cristine Betzer, PhD, investigator at the brain research centre DANDRITE at Aarhus University and lead author of the study, said in a press release.

By inhibiting SERCA activity with a chemical compound that specifically blocks SERCA in a worm model of Parkinson’s, calcium levels became more stable and cell survival improved. Importantly, inhibition of SERCA protected nerve cells from α-synuclein aggregates’ neurotoxic stress.

“Experiments in the United States with similar models have shown that once the worms with the Parkinson’s protein have lived for eight days, their nerve cells begin to die. In our study, we treated the worms with an inhibitor against the calcium pump and then counted the nerve cells in the worms. And there were many cells left. Which is a sensational and encouraging result,” Betzer said.

Although these findings cannot be directly translated to the human disease they can open new study opportunities that may be useful for the development of new, more efficient therapies.

“Our study points towards the usefulness of treating patients throughout the whole course of the disease, as the calcium pump will otherwise continue to pump and thus contribute to the patient’s symptoms,” Betzer added. “Perhaps the protection of nerve cells can also mean that the damage caused by Parkinson’s disease in the brain does not develop as severely as it otherwise would.”

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Source:: Parkinson’s Today