Parkinson's disease is a progressive neurodegenerative disorder that mainly affects motor functions. This condition is caused primarily by the death of the neurons that produce dopamine, causing the brain abnormality. Within cell degeneration, science has attributed an essential role to alpha-synuclein protein, a protein significantly present in the brain, and some other areas of the central nervous system.
The α-synuclein is abundant in the area where the disorder is generated, the compact black substance — however, the origin of the disease, maybe in another area of the body: the intestine. The pathological form of the α-synuclein after forming in the gut would spread to the brain through the vagus nerve. To support this claim, researchers at Johns Hopkins University used the protein, but in the form of alpha synuclein preformed fibrils.
The α-Synuclein Preformed Fibrils and Parkinson's
It was the German neuroanatomist Heiko Braak who, after his post-mortem studies, proposed in 2003 that the pathology of α-synuclein can spread from the gastrointestinal tract through the vagus nerve. Once housed in the compact black substance, it would eliminate dopamine neurons. Until now, some studies had been published supporting the theory, but there was no sustenance in an animal model.
Research scientists at Hopkins injected the α-synuclein preformed fibrils into mice in the gastrointestinal muscle innervated by the vagus nerve. The results were satisfactory from the outset. Ted Dawson, professor of Neurology and leader of the research, stated: “When we saw that the initial experiments worked, we were totally surprised (...) Now it is a routine for our team”.
The Progress of α-Synuclein
One month after the administration of preformed fibrils protein, the pathological α-synuclein had spread to the vagus dorsal nucleus. After three months, the protein had passed from the brain stem to the blue core (locus ceruleus). It even reached the amygdala, hypothalamus, and prefrontal cortex. After seven months, the pathological protein had reached other areas of the brain, such as the hippocampus, the striatum, and the olfactory bulb. At that point, there was a significant loss of dopamine-producing neurons, both in the compact black substance and in the striated nerve.
In the mice of the experimental model, symptoms of Parkinson's disease appeared, which in addition to motor deficiencies, exhibited signs of depression and anxiety, alterations in the olfactory system, and cognitive defects.
Dawson explains that there are at least three implications: “One: it is likely to galvanize future studies that explore the connection between the gut and the brain. Two: It will stimulate research focused on the factors, molecules, or infections that could initiate incorrect folding and the spread of alpha-synuclein. And three: it suggests treatments that may be aimed at preventing the spread of the pathological protein from the gut to the brain”.
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