New research looks to brain lipids to identify a new therapeutic target for Parkinson’s disease.
Parkinson’s disease is a neurodegenerative condition that affects about half a million people in the United States, according to the National Institutes of Health.
One of the main characteristics of this condition is the buildup of alpha-synuclein, a type of protein that forms into toxic plaques, in the brain.
Earlier this year, a study that featured in the journal Neurobiology of Aging suggested that there may be a link between the levels of certain brain lipids, or fat molecules, and the development of Parkinson’s disease.
ALMOST HALF OF WOMEN and more than one-third of men will develop Parkinson’s disease, dementia or suffer a stroke after age 45.
A new study published Tuesday in the Journal of Neurology, Neurosurgery & Psychiatry examined 12,102 people aged 45 and older from 1990 through 2016 to observe their lifetime risk of these diseases. Researchers found that 1,489 people were diagnosed with dementia, 1,285 had a stroke and 263 were diagnosed with Parkinson’s disease.
Women are more likely than men to experience any of these conditions. A woman’s lifetime risk for any one of the three is 48.2 percent, compared to 36.3 percent for men. Among the participants, 438 of them, 14.6 percent developed multiple conditions, with women more likely to suffer from disease co-occurrence. Women were nearly twice as likely as men to suffer both a stroke and to be diagnosed with dementia – 2.9 percent of women compared to 1.9 percent of men.
The eyes may be a window to the brain for people with early Parkinson’s disease. People with the disease gradually lose brain cells that produce dopamine, a substance that helps control movement. Now a new study has found that the thinning of the retina, the lining of nerve cells in the back of the eye, is linked to the loss of such brain cells. The study is published in the August 15, 2018, online issue of Neurology®, the medical journal of the American Academy of Neurology.
“Our study is the first to show a link between the thinning of the retina and a known sign of the progression of the disease — the loss of brain cells that produce dopamine,” said study author Jee-Young Lee, MD, PhD, of the Seoul Metropolitan Government — Seoul National University Boramae Medical Center in South Korea. “We also found the thinner the retina, the greater the severity of disease. These discoveries may mean that neurologists may eventually be able to use a simple eye scan to detect Parkinson’s disease in its earliest stages, before problems with movement begin.”
The study involved 49 people with an average age of 69 who were diagnosed with Parkinson’s disease an average of two years earlier but who had not yet started medication. They were compared to 54 people without the disease who were matched for age.
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.