In a recent study, German researchers find that traffic jams can also occur in the brain, and they can be damaging.
Disrupted transportation routes in nerve cells are a significant cause of Parkinson’s disease.
Nerve fibres give nerve cells their characteristic long shape. Measuring up to one meter in length, they form the contact points to other nerve cells.
In order to carry out the important task of communicating with other nerve cells, the fine branches of these nerve fibers and their ends, called synapses, must be regularly supplied with energy from the cell body.
If this energy supply is interrupted, the synapses are destroyed. Connections between nerve cells are then disrupted, which can lead to the cells dying off.
This process is typical for the development of brain disorders such as Parkinson’s disease.
However, it is unclear which mechanisms are responsible for the loss of nerve cells in Parkinson’s.
In the study, researchers demonstrated that a type of ‘traffic jam’ in the nerve cells could be the cause.
The researchers discovered that the traffic jam is triggered by a protein called alpha-synuclein.
This protein is also found in healthy nerve cells.
In abnormal nerve cells, the protein forms deposits, or even lumps, leading to a delay, disrupting the energy supply of the nerve fibers, and ultimately damaging the synapses.
The researchers also demonstrated this mechanism in cell cultures from patients with Parkinson’s.
A small skin sample was taken from affected patients. These skin cells were then converted into stem cells, which can be developed into any type of cell, and in this case, into nerve cells.
In their study, the researchers suppressed the formation of lumps of alpha-synuclein, thus improving the transportation of information in the nerve fibers.
However, the substance they used has not yet passed clinical trials.
But the team suggests that the finding could help improve the understanding of the mechanisms that cause Parkinson’s and push forward new strategies for treatment during the progression of the disease.
The researchers are from Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU). They were led by Dr. Iryna Prots and Prof. Dr. Beate Winner from the Department of Stem Cell Biology.
The study is published in Proceedings of the National Academy of Sciences.
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Journal reference: Iryna Prots et al, α-Synuclein oligomers induce early axonal dysfunction in human iPSC-based models of synucleinopathies, Proceedings of the National Academy of Sciences (2018). DOI: 10.1073/pnas.1713129115