Does Parkinson's develop in the stomach? | Knowledge & Environment | '

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It has long been known that Parkinson's disease is closely related to the death of nerve cells in the midbrain.

The more nerve cells die, the harder it is for the patient to control their body motor skills: they lose their balance and can only walk, grasp, swallow or speak with difficulty.

Over time, the disease is getting harder. In the end, patients are usually bedridden and die frequently because the autonomic nervous system is no longer functioning properly.

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Nerve cell in Parkinson's disease: Alpha-synuclein proteins have formed lumps called Lewy bodies. (Imago Images / Science Photo Library)

Defective alpha-synuclein proteins form lumps, shown here in red, in the nerve cells.

Defective proteins destroy nerve cells

The death of nerve cells in the brain is probably triggered by incorrectly folded, mutated proteins, so-called alpha-synuclein proteins. These proteins are found in healthy nerve cells in all humans and serve as transport proteins.

But if they are damaged, they destroy nerve cells of the substantia nigra pars compacta (SNc) – a central area of ​​the midbrain. Among other things, SNc is responsible for the production of the hormone dopamine, which performs many vital tasks in the body – such as the control of blood circulation.

Now, researchers at the Johns Hopkins University School of Medicine have been able to prove that such defective proteins can find their way from the stomach to the brain of mice. They published their study on 26 June in the journal Neuron.

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Substantia nigra pars compacta in Parkinson's disease (Imago Images / Science Photo Library)

The substantia nigra pars compacta – dopamine-forming brain cells – are destroyed by the defective proteins.

Month long way from the stomach to the brain

The researchers injected the mice with the high-level pathogenic forms of proteins directly into the nerves between the gastric mucosa and the muscle tissue surrounding the stomach.

After several months, the physicians were then able to detect the pathogenic proteins as well as the damage to the SNc nerve cells in different brain regions of the mice.

After one month, the alpha-synuclein proteins arrived at the brainstem – in the medulla oblongata and pons areas. From there they migrated further into the midbrain and into the striatum. After ten months, the pathogenic proteins had reached the olfactory bulb. It forms the foremost area of ​​the brain.

Infographic creates Parkinson's in the stomach DE

Everything indicates that the proteins were transported through the vagus nerve. This is a central nerve of the autonomic nervous system that extends from the stomach to the brain stem. When the doctors severed this nerve, the alpha-synuclein proteins could no longer reach the brain during a mouse experiment.

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No therapy yet

For now, the discovery does not answer the question of how to stop Parkinson's disease. Nevertheless, neurologist professor and co-author of the study Ted Dawson considers the discovery to be an important breakthrough: "Because the model starts in the stomach, it can be used to study the entire development of Parkinson's disease," he said. "For example, one could test prevention therapies in the animal model, from the phase where there are no symptoms, to a fully erupted Parkinson's disease."

Where does the disease come from?

The neuropathologist Walter Schulz-Schaeffer from the Saarland University Hospital, who was not involved in the study, points out that Parkinson's disease usually spreads to patients' bodies for several decades before the symptoms become clear. This basically makes prevention more difficult.

In addition, the study did not make it clear whether the origin of the disease actually lies in the stomach. The pathogenic proteins could also migrate in the other direction along the nerve pathways: "The recognition that the disease process can spread through stomach and intestine controlling nerves therefore does not mean that the disease must arise in the gastrointestinal tract."

However, Professor Schulz-Schaeffer hopes that the new findings may open the door to developing Parkinson's early detection. The "could significantly improve the treatment options."

More on this: Childhood dementia: similar mechanisms as in adults

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