Parkinson’s News Today keeps you up-to-date with research into Parkinson’s disease as it emerges. We brought you daily coverage of experiments into the basic biology of Parkinson’s, results of clinical and pre-clinical trials, and key findings from Parkinson’s research around the globe.
We look forward to bringing more such news to those with Parkinson’s, their family, friends and caregivers throughout 2020.
Here are our 10 most-read stories of 2019, with a short summary of what makes each one relevant to the Parkinson’s community.
A study found that an active form of the vitamin B12 called AdoCbl can ease the effects of dopamine loss that occurs in Parkinson’s disease. Using cell lines and several animal models, researchers showed that by reducing LRRK2 enzyme activity, AdoCbl limits the death of dopamine-producing nerve cells, thereby preventing the appearance of symptoms associated with neurodegeneration. Overactivity of LRRK2 is linked to the development of a hereditary form of Parkinson’s. AdoCbl is already an FDA-approved compound, and “could be used as a basis to develop new therapies to combat hereditary Parkinson’s associated with pathogenic variants of the LRRK2 enzyme,” according to Iban Ubarretxena, director of the Biofisika Institute and a study co-author.
Canadian Parkinson’s disease patients now have access to Onstryv (safinamide), also known as Xadago. Onstryv increases the amount of active dopamine in the brain by both preventing the enzyme that breaks dopamine down from doing so, and by blocking that enzyme from entering cells. Other available treatments cause debilitating fluctuations between normal motor function (called “on episodes”) and poorer motor function (“off periods”) as their effects ebb and flow. Four placebo-controlled Phase 3 trials showed that the combination of Onstryv and levodopa led to more “on” and fewer “off” periods, and improved motor function in patients. “The approval of [Onstryv] in Canada is a step forward for patients who need new treatment options for Parkinson’s disease,” said Roberto Tascione, CEO of Zambon, one of the companies involved in commercializing this medication.
Xadago was approved by the U.S. Food and Drug Administration in March 2017 to improve motor function in Parkinson’s patients who experience “off periods” while on treatment with levodopa and/or Lodosyn (carbidopa).
A pre-clinical study conducted in China showed that alpha-arbutin, an antioxidant found in plants such as the blueberry, might restore mitochondrial function in nerve cells and ease the motor disabilities associated with Parkinson’s disease. Treatment with alpha-arbutin partially restored mitochondrial function in nerve cells undergoing oxidative stress (mitochondria act as a cell’s power house). It also restored these cells’ ability to remove toxic waste products. Feeding alpha-arbutin to flies carrying a mutated gene known to trigger Parkinson’s significantly eased several Parkinson’s-like symptoms. “Naturally derived-antioxidants might serve as a new class of therapeutic options for [Parkinson’s disease],” the researchers wrote.
Replacing damaged cells in Parkinson’s disease with dopamine-producing stem cells could ease motor symptoms and reduce or eliminate the need for pharmaceutical medicines. As current disease therapies lose their efficacy over time, stem cell therapy might “revolutionize” Parkinson’s treatment, its researchers said. “A single surgery could potentially provide a transplant that would last throughout a patient’s lifespan, reducing or altogether avoiding the need for dopamine-based medications,” said Claire Henchcliffe MD, PhD, and Malin Parmar, PhD, co-authors of a study on the benefits of stem cell therapy. However, “there are several biological, practical, and commercial hurdles that need circumventing for this to become a routine therapy,” according to the editors of the Journal of Parkinson’s Disease.
A study found evidence of interaction between the brain and the gut in Parkinson’s, in which Gram-negative bacterial infections in the gut trigger an immune response that damages nerve cells. Gut microorganisms are known to communicate with the central nervous system, and studies suggest that harmful proteins related to Parkinson’s may spread to the brain from the gut. Scientists at the Université de Montréal showed that Gram-negative bacteria, particularly those related to gut infections, triggered an immune response in cells taken from mice. They then showed that mice bred without the PINK1 gene (making them resistant to Parkinson’s-like symptoms), when infected with these bacteria, displayed an immune response that led to such symptoms. Mutations in the PINK1 gene cause damage to the mitochondria in brain cells, and are linked to early onset hereditary Parkinson’s. The work provides evidence that intestinal infection acts as a triggering event in Parkinson’s, and highlighted the relevance of a gut-brain connection in this disease.
By reviewing the past 20 years of research into Parkinson’s disease, two scientists see a strong potential for breakthroughs in how this disease is approached over the next 20 years. The review cited developments in better animal models, greater understanding of molecular mechanisms and risk factors, and advances in available and potential therapies as reasons for hope. Among highlights of many advances listed are: 1) the adaptation of existing medicines used in other diseases to treat Parkinson’s (drug repurposing); 2) targeting non-motor features such as cognition, speech and balance difficulties that often precede motor symptoms; 3) the use of nanoparticles to block the formation of toxic alpha-synuclein clusters; and, 4) emerging evidence of a link between harmful gut bacteria and brain inflammation. The review also stressed the importance of future trials to test combination therapies.
Good news for lovers of sports, caffeine, and happy hours — all of these things, in moderation, may help slow the onset of symptoms of Parkinson’s disease. Although how exactly these lifestyle factors affect disease progression remains poorly understood, they correlate strongly with better patient outcomes. Conversely, smoking, heavy drinking and no consumption of alcohol at all were linked to considerably worse outcomes. The study, published in the journal Movement Disorders, needs to be replicated to strengthen the usefulness of its findings. Nonetheless, the work “suggests that multiple lifestyle factors potentially modify the rate of symptom progression,” its researchers wrote.
The antioxidant dietary supplement N-acetyl-cysteine (NAC) may improve dopamine function and ease Parkinson’s disease symptoms, according to one study. The body uses NAC to produce an antioxidant called glutathione (GSH), which it uses to prevent the oxidative stress that leads to cell death. Damage due to oxidative stress within dopamine-producing neurons is a key clinical feature of Parkinson’s. A trial (NCT02445651), conducted by researchers at Thomas Jefferson University in Philadelphia, showed that NAC supplementation significantly eased both motor and non-motor symptoms among 42 Parkinson’s patients (21 men and 21 women). These results need to be confirmed in larger and placebo-controlled studies, but offer an encouraging start to a potential low-cost therapy.
Low levels of vitamin D were associated with more falls, and greater problems with insomnia, anxiety, and depression in people with Parkinson’s disease, according to a study by Chinese researchers. Vitamin D deficiency has often been seen in people with Parkinson’s, but its relationship to the disease remains controversial. This study, by researchers at the Second Affiliated Hospital of Soochow University and Soochow University, is one of the few to measure both motor and non-motor outcomes. By conducting detailed clinical evaluations in 182 Parkinson’s patients, as well as 185 healthy controls, the group found that low levels of vitamin D were more common in Parkinson’s patients than in healthy people, and that vitamin D supplements may ease the disease’s non‐motor symptoms.
Our year’s most-read story was of an early stage study reporting that a type of oral magnesium could enter the brain and ease motor symptoms and nerve cell loss in a mouse model of Parkinson’s disease. Mice given magnesium-L-threonate, which can cross the blood-brain barrier (a semipermeable membrane that protects the brain from the outside environment) reduced the loss of dopamine-producing neurons, slowed the decline in motor function, and limited the oxidative stress that is associated with Parkinson’s. It is important to note that while magnesium-L-threonate provided therapeutic benefits, magnesium sulfate — the first choice as a clinical magnesium supplement — did not. “[T]he combination of [magnesium] with an agent that promotes its transportation to the brain is essential for the neuroprotection of this element,” the study’s scientists wrote.
At Parkinson’s News Today we hope these stories and our reporting throughout 2020 help to better inform and improve the lives of everyone affected by Parkinson’s.
We wish all our readers a happy 2020.
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