Disease-causing proteins can migrate from the gastro-intestinal tract to the brain, now shows an experiment with mice.
Parkinson’s disease often manifests itself first of all by balance disorders.
It has long been known that Parkinson’s disease is closely related with the dying off of nerve cells in the midbrain.
The more nerve cells die, the more difficult it is for the patients to control their body motor skills: you will lose the balance, can only go hard, grab, swallow, or speak.
With time, the disease is always severe. In the end, patients are mostly bedridden, and die often, because the autonomic nervous system is working properly.
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Damaged alpha-Synuclein proteins form clumps, here shown in red, in the nerve cells.
Defects in the proteins that destroy nerve cells
Triggered by the death of nerve cells in the brain is folded, probably from defective, mutant proteins, the so-called alpha-Synuclein proteins. These proteins occur in healthy nerve cells in all people and serve as transport proteins.
They are damaged but, they destroy nerve cells in the substantia nigra pars compacta (SNc) – is a core area of the Midbrain. The SNc is responsible for the production of the hormone dopamine, which handles many vital tasks in the body – such as the control of blood flow.
Now, researchers at the Johns Hopkins University School of Medicine were able to prove that such defective proteins can find their way from the stomach up into the brain of mice. They published their study on the 26. June in the journal Neuron.
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The Substantia nigra pars compacta – dopamine-forming brain cells – due to the harmful proteins are destroyed.
Months long way from the stomach to the brain
The researchers injected the mice with the pathogenic forms of proteins in high concentration directly into the nerves between the stomach mucosa and the muscle tissue surrounding the stomach.
After several months, the physicians were able to the disease-causing proteins, as well as the damage to the SNc nerve to demonstrate cells in different brain regions of the mice.
After a month of the alpha-Synuclein-proteins arrived at the brain stem in the Medulla oblongata and Pons areas mentioned above. From there, they migrated further into the Midbrain and into the Striatum. After ten months, the disease-causing proteins had reached the olfactory bulb. He is the front-most area of the brain.
All the indications are that the proteins were transported by the vagus nerve. This is a Central nerve of the autonomic nervous system that extends from the stomach to the brain stem. The doctors severed the nerve and were not able to reach the alpha-Synuclein proteins in the brain in the mice experiment.
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No therapy
The discovery is still no answer to the question of how Parkinson’s can disease stop. Nevertheless, a neurology Professor and study Co-author Ted Dawson considers the discovery a major breakthrough: “Because the Model begins in the stomach, you can use it to the entire development of the Parkinson’s study disease,” he said. “For example, you could test prevention therapies in an animal model, starting from the Phase where there are no symptoms, up to a fully-onset Parkinson’s disease.”
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Parkinson’s movement as a therapy
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Parkinson’s movement as a therapy
Where is the disease?
The neuro-pathologist Walter Schulz-Schaeffer from the University hospital of the Saarland, which was not involved in the study, there is concern that Parkinson’s disease spreads is usually several decades in the body of the patient before the symptoms are clearly visible. The more difficult, in principle, the prevention.
Also, don’t be become by the study are clear, whether the origin of the disease is spent actually in the stomach. The disease-causing proteins could migrate along the nerve in the other direction: “The recognition that the disease process can spread via the gastrointestinal tract, controlling the nerves, it does not mean, therefore, that the disease in the gastro-intestinal tract needs to occur.”
However, Professor Schulz-Schaeffer hopes that the new knowledge opens up maybe the way to developing a Parkinson’s disease-early detection. The “could improve the treatment facilities significantly.”
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