Nov 11, 2010 10:35 GMT  ·  By
Stress has a major role in Parkinson's disease, because it seems that exhausted neurons die prematurely and trigger the symptoms of the disease.
   Stress has a major role in Parkinson's disease, because it seems that exhausted neurons die prematurely and trigger the symptoms of the disease.

Stress has a major role in Parkinson's disease, because it seems that exhausted neurons die prematurely and trigger the symptoms of the disease, according to Northwestern Medicine study.

Stress is what makes us age faster and become more sensible to viruses and bacteria around us, and it looks like it is doing the exact same thing to our neurons.

The team of researchers carried out some tests that showed that dopamine-releasing neurons in an area of the brain called the substantia nigra, in stressed-out people, have a lifestyle that needs lots of energy.

Unfortunately this creates stress that can lead the neurons to premature death, and it is this death that causes Parkinson's disease.

However, the good news is that this stress can be controlled by a drug that has already been approved for human use, called isradipine.

Isradipine prevents calcium entry and decreases the mitochondrial stress in dopamine-releasing neurons, bringing it to the level of healthy neurons.

The drug has been approved by the Food and Drug Administration for treating high blood pressure, and Northwestern Medicine scientists are now carrying out a clinical trial to find out if it can also be used safely by Parkinson's patients.

Lead author D. James Surmeier, the Nathan Smith Davis Professor and chair of physiology at Northwestern University Feinberg School of Medicine says that “why this small group of neurons dies in Parkinson's disease is the core question we struggled with.

“Our research provides a potential answer by showing this small group of neurons uses a metabolically expensive strategy to do its job.

“This 'lifestyle' choice stresses the neurons' mitochondria and elevates the production of superoxide and free radicals – molecules closely linked to aging, cellular dysfunction and death.”

There is no genetic link in most cases of Parkinson's disease, but the study carried out by Surmeier in mice, showed that mitochondrial stress in dopamine-releasing neurons was aggravated in a genetic model of early-onset Parkinson's disease, which suggests that there might be a similar mechanism in rare familial forms of the illness.

He said that age makes everyone lose their dopamine-releasing neurons, but “by lowering their metabolic stress level, we should be able to make dopamine-releasing neurons live longer and delay the onset of Parkinson's disease.

“For individuals diagnosed with Parkinson's disease, the hope is that this drug can slow disease progression, giving symptomatic therapies a broader window in which to work.”

In the US, Parkinson's disease is the second most common neurodegenerative disease, Alzheimer's being the first one.

People are diagnosed around the age of 60, and over 1 million Americans suffer from it.

The symptoms include tremors, rigidity and slowness of movement and there no current treatment that could prevent or slow down the progression of the disease.

This study was published November 10 in the journal Nature.