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.
A Norwegian study shows that impairment in mitochondria may actually protect the brain in Parkinson’s disease.
Mitochondria are microscopic power stations found inside our cells. They convert foodstuffs (nutrients) into fuel, providing our bodies with the energy they need.
In 1989, studies in brain tissue from individuals with Parkinson’s disease showed that an essential component of the mitochondrial energy generators, called respiratory complex-I, becomes impaired in an area of the brain called the “substantia nigra” (latin for “the black substance”). Since this area is particularly vulnerable to Parkinson’s disease, this observation led to the hypothesis that complex I deficiency is highly deleterious and contributes to neurodegeneration.
Testing the level of caffeine in the blood may provide a simple way to aid the diagnosis of Parkinson’s disease, according to a study published in the January 3, 2018, online issue of Neurology®, the medical journal of the American Academy of Neurology.
The study found that people with Parkinson’s disease had significantly lower levels of caffeine in their blood than people without the disease, even if they consumed the same amount of caffeine.
“Previous studies have shown a link between caffeine and a lower risk of developing Parkinson’s disease, but we haven’t known much about how caffeine metabolizes within the people with the disease,” said study author Shinji Saiki, MD, PhD, of Juntendo University School of Medicine in Tokyo, Japan.
Dementia with Lewy bodies has a unique genetic profile, distinct from those of Alzheimer’s disease or Parkinson’s disease, according to the first large-scale genetic study of this common type of dementia.
The genome-wide association study, conducted by a UCL-led collaboration of 65 academics in 11 countries and funded by Alzheimer’s Society and the Lewy Body Society, is published in The Lancet Neurology.
“Dementia with Lewy bodies accounts for 10-15% of dementia cases, yet our understanding of it lags beyond the more well-known Alzheimer’s disease, partly because it’s commonly misdiagnosed. Our findings clarify the disease’s distinctive genetic signature, which should, in the future, help improve clinical trials, and lead to more targeted treatments,” said the study’s lead author, Dr Jose Bras (UCL Institute of Neurology and Alzheimer’s Society senior research fellow).
High-intensity exercise three times a week is safe for individuals with early-stage Parkinson’s disease and decreases worsening of motor symptoms, according to a new phase 2, multi-site trial led by Northwestern Medicine and University of Denver scientists.
This is the first time scientists have tested the effects of high-intensity exercise on patients with Parkinson’s disease, the second most common neurodegenerative disorder and the most common movement disorder, affecting more than a million people in the United States.
It previously had been thought high-intensity exercise was too physically stressful for individuals with Parkinson’s disease.
Researchers from Aarhus University have discovered that patients with the RBD sleep behaviour disorder lack dopamine and have a form of inflammation of the brain. This means that they are at risk of developing Parkinson’s disease or dementia when they grow older.
Do you sleep restlessly and hit out and kick in your sleep? This could be a sign of a disorder associated with diseases of the brain. Researchers from Aarhus University have studied the condition of the dopamine producing nerve cells in the brain and cells that participate in the brain’s immune system in people suffering from the sleep disorder Rapid eye movement sleep behaviour disorder, RBD.
The study shows that patients suffering from RBD have a risk of developing Parkinson’s disease or dementia in the future, because they already suffer from a lack of dopamine in the brain. Parkinson’s disease occurs precisely because the group of nerve cells in the brain that produce dopamine stop working.
Researchers have found that disconnections of brain areas involved in attention and visual processing may contribute to visual hallucinations in individuals with Parkinson’s disease, according to a new study published online in the journal Radiology. The disconnected brain areas seen on functional MRI (fMRI) may be valuable in predicting the development of visual hallucinations in patients with Parkinson’s disease.
Hallucinations are sensations that seem real but are created in a person’s mind. A person having a hallucination may see, hear or feel something that is not actually there. According to the National Parkinson Foundation, visual hallucinations can be a complication of Parkinson’s disease.
Parkinson´s disease is a chronic disease with unknown causes. The disease destroys the brain cells that control body movements. Shivering, stiff arms and legs and poor coordination are typical symptoms of Parkinson´s. The symptoms may develop slowly, and it sometimes takes time to make a correct diagnosis.
Researchers at the Department of Global Public Health and Primary Care (IGS) at the University of Bergen (UiB) have completed a large study that included data from the Norwegian Prescription Database, in cooperation with researchers at Harvard University.
“Our analysis of data from the whole Norwegian population has been decisive for the conclusion in this study,” says Professor Trond Riise at IGS. He leads the registery study in Norway.
Changes in the visual systems of newly diagnosed Parkinson’s disease patients may provide important biomarkers for the early detection and monitoring of the disease, according to a new study published online in the journal Radiology.
“Just as the eye is a window into the body, the visual system is a window into brain disorders,” said lead researcher Alessandro Arrigo, M.D., a resident in ophthalmology at the University Vita-Salute San Raffaele of Milan, Italy.
Parkinson’s disease is a neurodegenerative condition caused by neuronal loss in several brain structures. Parkinson’s disease is characterized by tremors, rigidity or stiffness throughout the body, and impaired balance and coordination.
People with the movement disorder Parkinson’s disease have a much higher risk of the skin cancer melanoma, and vice versa, a Mayo Clinic study finds. While further research is needed into the connection, physicians treating one disease should be vigilant for signs of the other and counsel those patients about risk, the authors say. The findings are published in Mayo Clinic Proceedings.
Overall, patients with Parkinson’s were roughly four times likelier to have had a history of melanoma than those without Parkinson’s, and people with melanoma had a fourfold higher risk of developing Parkinson’s, the research found.
Medical experts have speculated about the relationship between Parkinson’s and melanoma for decades, with varying conclusions, the Mayo researchers note. Several studies have suggested levodopa, a drug for Parkinson’s, may be implicated in malignant melanoma, but others have found an association between the two diseases regardless of levodopa treatment, they add.