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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.

Cellular Protection Mechanism To Halt Parkinson’s

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. 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.

Scientists identify a novel therapy with potential for treating Parkinson's disease

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.

Innovative new strategy to treat Parkinson's disease

Genetic factors can predict the progression of Parkinson's disease. 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.

Increased arm swing asymmetry is early sign of Parkinson's disease

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. 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.

Reprogramming Brain Cells Important First Step for New Parkinson's Therapy, Penn Study Finds

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. 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.

More Widespread Brain Atrophy Detected in Parkinson's Disease with Newly Developed Structural Pattern

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.

Unexpected signaling role for foul-smelling hydrogen sulfide in cell response to protein misfolding

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. In fact, H2S, which is produced naturally in small quantities in various tissues, is a gasotransmitter, one of a family of gaseous signaling molecules that includes nitrous oxide (NO) and carbon monoxide (CO). 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. Some prescription medications have side effects that can cause Parkinson's-like symptoms, further complicating a 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.

Test for Alzheimer's disease predicts cognitive decline in Parkinson's disease

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.

Exercise/memory research for Parkinson's

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.

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