Researchers at the University of Basel have discovered a factor that could support the early detection of neurodegenerative diseases such as Alzheimer’s or Parkinson’s. This cytokine is induced by cellular stress reactions after disturbances of the mitochondria, the “cell’s power plants,” as neuropathologists write in the journal Cell Reports.
The normal functioning of human cells is based on the coordinated interaction of different cellular organelles. In many cases, an impaired communication between these organelles will lead to the activation of a stress response to ensure the survival of affected cells. A research group was able to demonstrate this in detail for brain neurons. The group is headed by Prof. Dr. Stephan Frank from the Institute of Medical Genetics and Pathology at the University of Basel and University Hospital of Basel; the universities of Cambridge (UK) and Padua (Italy) were also involved.
The neuropathologists were able to show that impairments on the level of mitochondria, commonly known as the “cell’s powerhouses,” also affect neighboring organelles, such as the so-called endoplasmic reticulum. A consecutively activated stress reaction leads to the release of fibroblast growth factor-21 (FGF21) by nerve cells with disturbed mitochondria. The Basel researchers further observed that the same substance is also induced in various models of neurodegenerative disorders, where it can be detected prior to neuronal cell death.
Mutations in the gene LRRK2 have been linked to about three percent of Parkinson’s disease cases. Researchers have now found evidence that the activity of LRRK2 protein might be affected in many more patients with Parkinson’s disease, even when the LRRK2 gene itself is not mutated. The study was published in Science Translational Medicineand was supported in part by the National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health (NIH).
“This is a striking finding that shows how normal LRRK2 may contribute to the development of Parkinson’s disease,” said Beth-Anne Sieber, Ph.D., program director at NINDS. “This study also identifies LRRK2 as an integral protein in the neurobiological pathways affected by the disease.”
More than 10 years ago, researchers linked mutations in the LRRK2 gene with an increased risk for developing Parkinson’s disease. Those mutations produce a version of LRRK2 protein that behaves abnormally and is much more active than it would be normally.
Analysis of data from a clinical trial conducted at Vanderbilt suggests that deep brain stimulation (DBS) administered to patients with very early-stage Parkinson’s disease slowed the progression of rest tremor.
The study, published June 29 in Neurology, is significant because it is the first evidence of a treatment that may possibly delay the progression of one of the cardinal features of Parkinson’s disease. However, the study’s authors strongly caution that a larger-scale clinical trial across multiple investigational centers is needed to validate the finding.
“The finding around tremor is truly exceptional,” said David Charles, MD, professor and vice-chair of Neurology and senior author. “What it suggests is that DBS applied in early stage Parkinson’s disease may slow the progression of tremor. Why it is so remarkable is because there are no treatments for Parkinson’s that have been proven to slow the progression of any element of the disease.”
Doctors may be able to modify or slow down the progress of the neurological condition Parkinson’s disease in the future by spotting signs of it in patients with inflammatory bowel disease (IBD), suggest a study published in the journal Gut.
Danish researchers found patients with IBD appeared to have a 22% greater risk of developing Parkinson’s disease in a study that monitored participants for almost 40 years.
IBD, Crohn’s disease and ulcerative colitis are chronic conditions with onset in young adulthood.
It has already been suggested in previous studies that inflammation plays a role in the development of Parkinson’s disease and multiple system atrophy.
The mechanism our immune cells use to clear bacterial infections like tuberculosis (TB) might also be implicated in Parkinson’s disease, according to a new collaborative study led by the Francis Crick Institute, Newcastle University and GSK.
The findings, which will be published in The EMBO Journal, provide a possible explanation of the cause of Parkinson’s disease and suggest that drugs designed to treat Parkinson’s might work for TB too.
The most common genetic mutation in Parkinson’s disease patients is in a gene called LRRK2, which makes the LRRK2 protein overactive.
A Norwegian study shows that the taking of diabetes medicine reduces the risk of getting Parkinson´s disease.
Researchers at the Department of Clinical Medicine at the University of Bergen (UiB) have discovered that medical treatment against diabetes reduces the risk of getting Parkinson´s disease by 35 per cent.
“We have made an important discovery, which takes us a step further towards solving the Parkinson´s riddle,” says researcher Charalampos Tzoulis. He has lead the study together with researcher Kristoffer Haugarvoll at the same department.
Researchers in Australia asked volunteers to draw a spiral on a sheet of paper. By analyzing how long it took them to draw the spiral and how hard they pressed on the paper with the pen, the team could not only tell which volunteers had Parkinson’s disease, they could also tell how severe it was.
Parkinson’s disease is a neurodegenerative disorder that causes shaking, muscle rigidity and difficulty with walking. Many treatment options for Parkinson’s are only effective when doctors diagnose the disease early, and when symptoms are very noticeable it may be too late. It’s also important for doctors to be able to tell how severe the disease is, to make the right treatment decisions, and to follow-up the progression of symptoms.
Elizabeth Stegemöller arranged a circle of metal folding chairs around a piano as clients started arriving for a weekly music therapy class for people with Parkinson’s disease.
For the next hour, Stegemöller, an assistant professor of kinesiology at Iowa State University, will lead the class through a series of vocal exercises and songs. Singing uses the same muscles associated with swallowing and respiratory control — two functions complicated by Parkinson’s disease, which can lead to death — and Stegemöller’s research has shown singing significantly improves this muscle activity. The results are published in the journals Disability and Rehabilitation and Complementary Therapies in Medicine.
“We’re not trying to make them better singers, but to help them strengthen the muscles that control swallowing and respiratory function,” Stegemöller said. “We work on proper breath support, posture and how we use the muscles involved with the vocal cords, which requires them to intricately coordinate good, strong muscle activity.”
Researchers at Binghamton University have developed a new drug that may limit the progression of Parkinson’s disease while providing better symptom relief to potentially hundreds of thousands of people with the disease.
Symptoms of Parkinson’s disease are commonly managed using a selective dopamine receptor agonists. While these drugs are useful in early-stage Parkinson’s, they tend to lose efficacy in later disease stages. As important, currently marketed drugs do not appear to modify disease progression. A research team including Binghamton University psychology professor Chris Bishop and former graduate student David Lindenbach recently employed a preclinical model of Parkinson’s disease to compare the effects of the dopamine agonist ropinirole to their new drug, known as D-512. Results demonstrated that D-512 was more efficacious than ropinirole in treating the symptoms of Parkinson’s disease while also prolonging the time window in which the animals showed benefits. These findings followed on the heels of prior work by this collaborative group which demonstrated that D-512 may also protect again the progression of Parkinson’s disease.
Scientists at the University of Florida have discovered a new method of observing the brain changes caused by Parkinson’s disease, which destroys neurons important for movement. The development suggests that fluid changes in a specific brain area could provide a way to track that damage. The study, published in the journal Brain, was supported by the NIH’s National Institute of Neurological Disorders and Stroke (NINDS).
“By finding a new way to detect and track how Parkinson’s affects the brain, this study provides an important tool for assessing whether a drug might slow or stop those changes and keep symptoms from getting worse,” said NINDS Program Director Daofen Chen, Ph.D.