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
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.
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
by: ABC 33/40
ABC 33/40′ spoke with two people who live with the disease about new findings from Purdue University researchers.
Published in the scientific journal Molecular and Cellular Neuroscience, the researchers say they have pinpointed an important compound in the development of Parkinson’s disease in the brain.
Their work could be significant because it may impact how we treat the disease in several ways: like better therapies, new drugs and earlier diagnoses or preventative care.
Two men gave reporter Patrick Thomas a glimpse into what new treatments in their lives could do.
Whether he stands or sits, with shaky hands and trembling feet, Parkinson’s is life for Wayne Cook for the last ten years. “The things that you, used to take for granted,” Cook says as he tries to raise his left hand to his chest but can’t hold it still. “The fine motor skills are difficult.”
The same goes for Ken Cater over the last nearly 13 years of his life. “But you know it’s tough. Right now I’m dealing with a progressive disease,” says Cater.
Which Purdue University researchers say when they located the compound called Acrolein, it may lead to discoveries that alleviate symptoms of Parkinson’s. Cook tries to explain how it affects his speech. “You get something here (points to his brain) and then you know what you want to say, but it just stops right here. It won’t come out all the way.”
Cater explains what he thinks most fighting the disease want right now. Cater says, “The Holy Grail that we are looking for right now is something that can slow or stop the progression of the disease.”
Right now the research includes work that has been tested in animal models and cells, not humans.
Cook says he is even willing to be a part of any research that may eventually include human testing. “I’m anxious for it to happen. If they have got a study and they need volunteers I raise my hand,” says Cook.
But through the research, scientists say they lessened and reversed effects of Parkinson’s using the drug Hydralazine
Since it’s still only pre-clinical research Cater says he will wait and see. “I’m hopeful for a cure in the near future if not at least better treatments,” he says.
If you have questions about living with Parkinson’s as a patient or caretaker, the Parkinson Association of Alabama may be able to help.
Registration is now open for Adaptive Fitness at EW Motion therapy. Taught by Katie Cederberg (ACSM CPT) Adaptive Fitness is designed for Parkinson’s patients to increase overall fitness through evidence-based, safe, and effective full body workouts. The class seeks to improve participant balance, strength, flexibility, and mobility with adaptive exercises using exercise bands, medicine balls, weights, and Kettlebells. All exercises are adapted to fit each person’s strength and individual needs, including the option for chair, or wheel-chair based exercises.
The cost is $30 per class or $200 for 8 sessions. The class is taught each Saturday at 10:30 AM. CLICK THIS LINK TO SIGN-UP FOR THE CLASS ONLINE.
Katie Cederberg, ACSM CPT, is a doctoral student in the Rehabilitation Science Program at the University of Alabama at Birmingham, where she dedicates her time and effort to increasing physical activity and exercise for people with physical disabilities. She received her Bachelor’s degree from Linfield College in McMinnville, Oregon and her Master’s Degree in Exercise Science from Central Washington University. She previously worked as a fitness specialist at Oregon Health and Science University in Portland, Oregon where she developed individualized exercise programs for people with and without disabilities.
Tears may be used to diagnose Parkinson’s disease, according to preliminary findings of a study that will be presented at the 2018 American Academy of Neurology’s (AAN) Annual Meeting in Los Angeles, California, April 21-27.
“We believe our research is the first to show that tears may be a reliable, inexpensive and noninvasive biological marker of Parkinson’s,” Mark Lew, MD, the study’s author from the Keck School of Medicine of University of Southern California, said in a press release.
Parkinson’s disease is mainly characterized by selective loss of neurons that produce dopamine in a brain area called substantia nigra. Patients with Parkinson’s typically exhibit Lewy bodies – protein clumps mainly composed of aggregated alpha-synuclein – in the brain, leading to nerve damage and disease progression.
Besides pathological changes in the brain, the disease also affects nerve function in the periphery. As the secretory cells of the tear gland are stimulated by nerves, researchers hypothesized that nerve changes in Parkinson’s could result in altered protein levels in tears.
The scientists collected tear samples from 55 Parkinson’s patients and 27 healthy controls who were the same age and gender.
The tears were analyzed for the levels of four proteins. The results revealed that levels of normal, non-clumped alpha-synuclein were lower in Parkinson’s patients than in controls. However, levels of unhealthy, aggregated alpha-synuclein were increased in tears of Parkinson’s patients (1.45 nanograms per milligram of tear proteins versus 0.27 nanograms, respectively).
Researchers hypothesize that the secretory cells in the tear gland could themselves produce these different forms of alpha-synuclein, which would be secreted directly into tears.
“Knowing that something as simple as tears could help neurologists differentiate between people who have Parkinson’s disease and those who don’t in a noninvasive manner is exciting,” Lew said.
“And because the Parkinson’s disease process can begin years or decades before symptoms appear, a biological marker like this could be useful in diagnosing, or even treating, the disease earlier,” he added.
Nonetheless, larger studies need to be done to evaluate whether these changes in alpha-synuclein levels can be detected in tears from Parkinson’s patients before symptoms start.
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Source:: Parkinson’s Today