17 April 2012

Study Suggest Trigger Protein Starts and Spreads Parkinson's Disease

Parkinson's disease is a brain disorder that causes shaking(tremors) and negatively affects movement, muscle control, and balance.

It usually affects people over the age of 50. Patients with Parkinson's also experience escalating symptoms of tiredness, pain, depression, and constipation as the disease progresses. The disease worsens over time.

Parkinson's disease happens when brain cells that produce dopamine are destroyed in certain parts of the brain stem, particularly the crescent-shaped cell mass known as the substantia nigra. Nerve cells in this area send out fibers to tissue located in both sides of the brain. There the cells release essential neurotransmitters that help control movement and coordination.

Dopamine is used by the brain to help control muscle movement. Without this chemical, the nerve cells in the brain cannot properly send and receive signals. This leads to the loss of muscle function.

How Parkinson's disease starts and spreads

Injection of a small amount of clumped protein triggers a cascade of events leading to a Parkinson's-like disease in mice, according to an article published online this week in the Journal of Experimental Medicine.

Progressive accumulation of clumps of the protein alpha-synuclein in the brains of patients with Parkinson's disease coincides with the onset of motor dysfunction. However, whether these clumps are sufficient to trigger neurodegeneration, and how these clumps spread throughout the brain, remained unclear.

Video: Parkinson's Disease and Stem Cell Research

To answer these questions, a team led by Virginia M.Y. Lee at the University of Pennsylvania School of Medicine studied mice expressing a mutated form of alpha-synuclein found in patients with Parkinson's disease. These mice show symptoms of disease around one year of age but not earlier.

Lee and colleagues found that injecting preformed clumps of human alpha-synuclein into the brains of young mice accelerated disease onset and severity. These clumps seemed to act as "seeds" that recruited even the mouse version of alpha-synuclein into new clumps, which then spread throughout the brain. The pattern of spreading from neuron to neuron suggests that the clumps may hijack the highway traveled by normal brain signals.

These findings suggest that Parkinson's disease, like other neurodegenerative diseases including Alzheimer's, may start and progress due to abnormal aggregation and accumulation of proteins within the brain. What gets these clumps going in the first place remains unclear.


Rockefeller University Press
Journal of Experimental Medicine
Perelman School of Medicine, University of Pennsylvania
Eating Flavonoids Can Help Protect Against Parkinson's Disease
Power of the Mind: Therapy for Parkinson's Disease
Stem Cell Breakthrough for Parkinson's Disease Treatment
US$10 Million Contest to Sequence Centenarian Genome
Healthy Diet Leads to Better Mental Performance and Minimizes Brain Shrinkage
New Stem Cell Line Offers Safe and Prolific Source for Disease and Transplant Studies