No other therapy ever managed to halt the disease's progression

Mar 2, 2012 09:48 GMT  ·  By
Positive α-synuclein staining of a Lewy body in a patient with Parkinson's disease
   Positive α-synuclein staining of a Lewy body in a patient with Parkinson's disease

Investigators from the University of California in Los Angeles (UCLA) say that they were recently able to halt the progression of Parkinson's disease in lab animals, primarily through preventing the formation of clumps between neurons.

These clumps are formed by a protein called α-synuclein (alpha-synuclein). When they appear, these structures begin to interfere with the normal functioning of nerve cells in the brain, leading to the symptoms characteristic to Parkinson's.

When these proteic aggregates grow sufficiently, they turn toxic, and begin to kill off neurons. While experts still can't say for certain what causes this condition, they do know that this protein plays an important role in the process.

Currently, doctors have access to a number of therapies that can successfully address the disease's symptoms, but they have no way of treating it, or even halting its progression. This is a very serious situation considering that millions of people suffer from Parkinson's worldwide.

Primarily, it affects the elderly, meaning that the developed world will experience its social and economic effects hardest. A negative rate of natural population increase is now being recorded in nearly all developed countries, meaning that the population is getting older.

This is why the UCLA team sought to discover a way of simply preventing these clumps from forming in the first place. The group was led by professor of neurology Jeff Bronstein and associate professor of neurology Gal Bitan.

Together with their collaborators, they developed a compound called a molecular tweezer, which was able to prevent the formation of alpha-synuclein clumps in animal models of Parkinson's disease.

But the most amazing aspect of the new research is that the molecular tweezer also proved able to reverse the toxic proteic aggregates that had already formed in the brain before it was injected.

Parkinson's, Alzheimer's and Type 2 diabetes are just some of the 30+ dangerous medical conditions triggered by protein aggregation in the brain, researchers report in the latest online issue of the esteemed scientific journal Neurotherapeutics.

The normal function of alpha-synuclein “is not well understood, but it may play a role in aiding communication between neurons,” Bronstein explains.

“The trick, then, is to prevent the α-synuclein protein aggregates and their toxicity without destroying α-synuclein's normal function, along with, of course, other healthy areas of the brain,” he concludes.