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A research team led by Professor Henning Stahlberg of the Biozentrum of the University of Basel challenges a previously common concept in a recent study published in eLife
The arms and legs are constantly trembling, the muscles are becoming weaker and the movements slower – all these symptoms are typical of many Parkinson's patients. There are more than six million people in the world. In people with the disease, dopaminergic nerve cells die slowly in the brain. The resultant deficiency of this messenger alters motor skills and often cognitive abilities.
Are protein fibrils the causative agents?
Previously, it was thought that one of the triggers was the alpha-synuclein protein. It can agglutinate and deposit itself as Lewy bodies in nerve cells. Toxic protein fibers are the basis of brain cells. A research team led by Professor Henning Stahlberg of the Biozentrum of the University of Basel collaborated with researchers from Hoffmann-La Roche Ltd. and ETH Zurich thus artificially generated an alpha-synuclein fibril in a reagent container and made it visible for the first time at an atomic resolution. "Contrary to our expectations, however, the results raise more questions than they answer," says Stahlberg.
It should be remembered that in some congenital forms of Parkinson's, affected individuals have genetic defects in the alpha-synuclein gene. Mutations, it is believed, eventually lead to incorrect protein folding and assembly in dangerous fibrils. "Our 3D structure, however, shows a fibril structure that could not be formed with such a mutated protein," says Stahlberg. "Because of their location, most of these mutations would rather hinder the formation of the fibril structure that we found." In short, if this fibril structure triggered Parkinson's disease, the genetic defect should protect against the disease. But he does not do it. It could be that another form of fibril or another form of the protein triggers the disease in these patients.
The study raises new questions
What mutations in alpha-synuclein cause the formation of other forms of protein aggregates? What role do fibrils play in nerve cells and what do nerve cells eventually die – these questions must now be studied. To date, the exact function of alpha-synuclein is not clear. Since only symptoms can be relieved with the previous medication, new concepts are urgently needed.
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