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Archive for April 27, 2008

Parkinson’s burden rising

last updated: 11 April 2008 A surge of Parkinson’s disease linked to rapidly ageing populations worldwide will severely tax health care systems in coming decades, experts warned ahead of World Parkinson’s Disease Day.

AdvertisementThe burden of Parkinson’s and other neurodegenerative diseases that strike later in life will be amplified, experts say, by breakdown of informal, home-based care networks that are already strained.

“In many countries, overdependence on voluntary care is a key issue caused by lack of appropriate, consistent and affordable institutional resources,” said Mary Baker, president of the European Parkinson’s Disease Society.

“With an ever-increasing elderly global population, the cost to nations will be astronomical if action is not taken now, at the beginning of the 21st century,” she said.

The World Health Organisation (WHO) forecasts a 20 percent jump from 2007 to 2030 in the number of “disability-adjusted life years” (DALYs) attributable to Parkinson’s.

DALYs is a measure that combines years of life lost due to a disability, and years of healthy life lost.

The rate of increase over the same period for Alzheimer’s and other progressive neurological disorders that typically emerge in old age is even higher at 66 percent.

Myths and misconceptions about Parkinson’s
For 2008, World Parkinson’s Disease Day is seeking to overturn myths and misconceptions about the condition, which affects 6.5 million people around the world.

Sufferers of what James Parkinson, the English doctor who first diagnosed the disease, called “the shaking palsy” are sometimes shunned due to awkward and uncontrolled movements, or mistaken for persons under the influence of alcohol or drugs.

Symptoms include muscular rigidity, difficulty with initiating movements, lack of balance, and slowness of voluntary actions.

“In today’s world, it is necessary to move fast, and to communicate through body language and emotions,” commented French Psychiatrist Philippe Nuss of Saint Antoine Hospital in Paris. “Parkinson’s attacks exactly these three areas.”

For Marie Vidhaillet, a neurologist at Pitie Salpetriere Hospital, living with the disease is like the fickle weather of March, with an unpredictable sequence of good days and bad days.

“You have to learn to live with it without succumbing to it,” she added.

Death of brain neurons
Parkinson’s is caused by the death of neurons in the brain that produce dopamine, a chemical neurotransmitter that regulates, among other things, bodily movement.

Several medications compensate for the lack of dopamine that triggers symptoms, but only imperfectly. Neurosurgical treatments also exist, but are only appropriate in five percent of cases.

Among the misconceptions surrounding Parkinson’s is the idea that it is “an old person’s disease,” said Vidhaillet.

At least 10 percent of patients in France are under 45, but “most doctors don’t think of Parkinson’s if a patient is 40 years old.”

“In our society, where one does not have the right to get old, the disease is doubly stigmatising,” she said. ?(Marlowe Hood/Sapa)

New Protein May Slow, Perhaps Reverse Parkinson’s Disease Symptoms

Scientists in Finland believe they have found a protein that can prevent the degeneration of cells that produce dopamine. In a patient with Parkinson’s, these nerve cells, which produce dopamine, are destroyed.

The scientists believe this chemical may lead the way to treatment which would encourage the damaged cells to recover. Drugs today do not prevent the degeneration of nerve cells.

You can read about this study in the journal Nature.

In this study, scientists injected the protein - CDNF (dopamine neurotrophic factor) - into rats with symptoms of Parkinson’s. The rats’ symptoms improved; 96% of their nerve cells were protected from degeneration.

Previous studies had focused on another protein, GDNF. As GDNF raised serious safety concerns, they decided to examine CDNF, a related protein (a growth factor). CDNF was found to be better tolerated.

The researchers discovered that CDNF is specific to brain nerve cells. This is not the case with other similar growth factors.

In a further study, the researchers allowed the rats’ Parkinson’s to progress further. Their aim was to see whether CDNF might help repair damaged nerves. The mice were at a stage similar to a human with Parkinson’s who has lost 70% of his/her ability to produce dopamine. After administering CDNF to these rats, they found that 58% of the dopamine-producing cells were alive, compared to 26% in a control group.

Dr Mart Saarma, team leader, University of Helsinki, said “Our new protein has great potential to be developed as drug for Parkinson’s disease, but we need to do more animal experiments and also toxicology studies before we can start clinical trials.”

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