Cellular Protection Mechanism To Halt Parkinson’s. A novel therapy for Parkinson's disease seeks to make use of the way the mitochondria is protected from common viruses. The research at the University of Cambridge, published this week in the Journal of Experimental Medicine, involved molecular virologists working in collaboration with neuroscientists to share their expertise across disciplines. Current treatments for Parkinson's centre on symptomatic drugs which help treat some of the motor features of the disease, but they are not able to stop it from progressing. Indeed, over time these drugs can produce their own side-effects. The novel methodology developed by the Cambridge researchers stemmed from the work of Professor John Sinclair and colleagues at the Department of Medicine in studying the ways in which common viruses - such as herpes - seek to survive and replicate in cells in the body.
The researchers emphasise that much work remains to be done in taking the therapy to the point at which clinical trials can be undertaken. Scientists identify a novel therapy with potential for treating Parkinson's disease. Scientists at the University of Cambridge have made a significant step in the development of a novel therapy that could one day help to slow down, or even halt, the damage caused by Parkinson’s disease (PD), one of the most common neurodegenerative disorders.
The therapy, which has been shown to be effective in rat models of the condition, involves exploiting the natural process by which common viruses protect mitochondria (the energy-producing power house of cells) in order to keep cells alive while they replicate. The research, published this week in the Journal of Experimental Medicine, involved molecular virologists working in collaboration with neuroscientists to share their expertise across disciplines.
Building on an earlier study published in 2007, the researchers have now shown proof of principle for their methodology which offers a potential novel disease -modifying approach to treating PD. Innovative new strategy to treat Parkinson's disease. Public release date: 19-Dec-2011 [ Print | E-mail Share ] [ Close Window ] Contact: Rita Sullivannews@rupress.org 212-327-8603Rockefeller University Press Stabilizing the cell's power-generating center protects against Parkinson's disease (PD) in a rat model, according to a report published online this week in the Journal of Experimental Medicine (www.jem.org). Mitochondria—the energy production center of cells—are damaged in PD, leading to loss of dopaminergic neurons and degeneration of brain function.
Rats injected with this beta2.7 before or after the formation of PD-like brain lesions performed better on tests of behavior and motor function. About The Journal of Experimental Medicine The Journal of Experimental Medicine (JEM) is published by The Rockefeller University Press. Kuan, W. [ Print | E-mail AAAS and EurekAlert! Genetic factors can predict the progression of Parkinson's disease. Parkinson's disease is marked by the abnormal accumulation of α-synuclein and the early loss of dopamine neurons in the substantia nigra region of the brain. A polymorphism in the promotor of α-synuclein gene known as NACP-Rep1 has been implicated as a risk factor for the disease.
Now, researchers have found that different variants of NACP-Rep1 and its interaction with the microtubule-associated protein tau (MAPT) H1 haplotype can influence the speed of clinical deterioration in patients with Parkinson's disease. "Our data are the first to show that polymorphisms of NACP and MAPT interact to influence the rate of progression of Parkinson's disease, a finding with clinical utility," says lead author Yue Huang of Neuroscience Research Australia and the University of New South Wales, Sydney, Australia. 123 patients with Parkinson's disease underwent genetic testing to determine NACP-Rep 1 and MAPT H1 allele or genotype.
Three common variations, or alleles, of NACP-Rep1 were detected. Increased arm swing asymmetry is early sign of Parkinson's disease. People with Parkinson's disease swing their arms asymmetrically -- one arm swings less than the other -- when walking. This unusual movement is easily detected early when drugs and other interventions may help slow the disease, according to Penn State researchers who used inexpensive accelerometers on the arms of Parkinson's disease patients to measure arm swing.
"Scientists have known for some time that people with Parkinson's disease exhibit reduced arm swing during the later stages of the disease, but no one had come up with an easy way to measure this," said Stephen Piazza, associate professor of kinesiology. "We found that not only do people with the disease exhibit reduced arm swing, but they also exhibit asymmetric arm swing, and this asymmetric arm swing can easily be detected early in the disease's progression. " "In other words, if I measure the location of your right arm, it is difficult to use that measurement to predict the location of your left arm," he said.
Reprogramming Brain Cells Important First Step for New Parkinson's Therapy, Penn Study Finds. PHILADELPHIA - In efforts to find new treatments for Parkinson’s Disease (PD), researchers from the Perelman School of Medicine at the University of Pennsylvania have directly reprogrammed astrocytes, the most plentiful cell type in the central nervous system, into dopamine-producing neurons.
PD is marked by the degeneration of dopaminergic neurons in the midbrain. Dopamine is a brain chemical important in behavior and cognition, voluntary movement, sleep, mood, attention, and memory and learning. “These cells are potentially useful in cell-replacement therapies for Parkinson’s or in modeling the disease in the lab,” says senior author John Gearhart, PhD, director of the Institute for Regenerative Medicine (IRM) at Penn.
The team reports their findings in PLoS One. “Our study is the first to demonstrate conversion of astrocytes to midbrain dopaminergic neurons, opening the door for novel reprogramming strategies to treat Parkinson’s disease,” says first author Russell C. First Steps. More Widespread Brain Atrophy Detected in Parkinson's Disease with Newly Developed Structural Pattern. PHILADELPHIA – Atrophy in the hippocampus, the region of the brain known for memory formation and storage, is evident in Parkinson’s disease (PD) patients with cognitive impairment, including early decline known as mild cognitive impairment (MCI), according to a study by researchers in the Perelman School of Medicine at the University of Pennsylvania.
The study is published in the December issue of the Archives of Neurology, one of the JAMA/Archives journals. First, using traditional imaging analyses, researchers found that Parkinson’s patients with MCI had more atrophy in the hippocampus, basal ganglia, amygdala, and insula compared with Parkinson’s patients with normal cognition, whereas Parkinson’s patients with normal cognition showed no significant loss of brain volume compared with healthy controls. Parkinson’s patients with normal cognition showed no atrophy and had similar brain volumes to healthy controls without Parkinson’s or cognitive impairment. Unexpected signaling role for foul-smelling hydrogen sulfide in cell response to protein misfolding. Cold Spring Harbor, NY -- Something rotten never smelled so sweet. This is what members of a team of scientists at Cold Spring Harbor Laboratory (CSHL) are telling one another as they discuss a new finding they did not expect to make. They have discovered that hydrogen sulfide (H2S) – the flammable, highly toxic gas that we usually associate with the smell of rotten eggs in landfills and sewers – plays an important role in the regulation of a signaling pathway implicated in biological malfunctions linked to Alzheimer’s and Parkinson’s diseases, among others.
“H2S comes under the category of things that people think of as toxic and nasty, but which can actually be harnessed to serve a useful purpose,” says CSHL Professor Nicholas K. Tonks, FRS, who led the research team. Tonks and colleagues were intrigued by reports in the scientific literature suggesting that H2S was produced as part of the cell’s response to what is called ER stress. About Cold Spring Harbor Laboratory. New technology aids early Parkinson's diagnosis. To diagnose Parkinson's disease, physicians for decades have had to rely largely on a keen eye and experience. Now the pairing of a new drug and a high-tech nuclear brain scan is offering long-awaited help in recognizing the progressive movement disorder, which has neither a specific test nor a cure. Researchers hope that by finding Parkinson's earlier, it may be possible someday to halt the disease's progress. The telltale signs of Parkinson's — among them trembling of the head, hands, legs or face, rigid posture, lack of facial expression — can range from severe to very subtle, especially at the early stages.
Adding to the difficulty, other neurological conditions can be mistaken for Parkinson's, but require different treatments. Research has shown that about 10 percent of patients suspected of having Parkinson's do not have it. End result: The proper diagnosis and treatment can be delayed for years. The scan confirmed the diagnosis. Using Eyebrain Tracker In Parkinson's Therapy Clinical Trial.
Test for Alzheimer's disease predicts cognitive decline in Parkinson's disease. Public release date: 12-Dec-2011 [ Print | E-mail Share ] [ Close Window ] Contact: Kim Menardkim.menard@uphs.upenn.edu 215-662-6183University of Pennsylvania School of Medicine PHILADELPHIA – A method of classifying brain atrophy patterns in Alzheimer's disease patients using MRIs can also detect cognitive decline in Parkinson's disease, according to a new study by researchers from the Perelman School of Medicine at the University of Pennsylvania.
Researchers also found that higher baseline Alzheimer's patterns of atrophy predicted long-term cognitive decline in cognitively normal Parkinson's patients. "On the basis of a simple neuroimaging study, we can now predict which patients with Parkinson's disease will experience long-term cognitive decline or develop dementia in the future," said the study's lead author, Daniel Weintraub, MD, associate professor of Geriatric Psychiatry with Penn's Perelman School of Medicine and the Philadelphia Veterans Affairs Medical Center. . [ Print | E-mail. Exercise/memory research for Parkinson's. Researchers from the University of Maryland School of Medicine and the Baltimore VA Medical Center have launched a study of exercise and computerized memory training to see if those activities may help people with Parkinson's disease prevent memory changes.
The type of memory that will be examined is known as "executive function;" it allows people to take in information and use it in a new way. Many Parkinson's patients develop problems with executive function, which can prevent them from working and may eventually require a caregiver to take over more of the complex cognitive tasks of daily living. "Studies of normal aging show that memory and executive function can be improved with exercise, such as walking several days a week," explains Karen Anderson, M.D., principal investigator and an assistant professor of neurology and psychiatry at the University of Maryland School of Medicine. Dr.