Mounting evidence is pointing to an association between the good and Parkinson's disease. The new research coming out of the Johns Hopkins University School of Medicine has added some weight to the connection to the neurodegenerative disorder.
In human studies, Johns Hopkins scientists found that misfolded alpha-synuclein protein-which scientists believe in the brain and drives Parkinson's can from the good to the brain. They published the findings in the journal Neuron.
Back in 2003, German neuroanatomist Heiko Braak and colleagues found that in postmortem samples of Parkinson's patients, clumps of alpha-synuclein also appeared in the nervous system that controls the well, known as the enteric nervous system Patients often develop gastrointestinal disorders. They are characteristic of Parkinson's disease. Braak hypothesized that Parkinson's might originate in the good.
But there's a big question: Are these synapses in the enteric nervous system? In other words, do the aggregates actually travel? To answer this, Johns Hopkins neurologist Ted Dawson and colleagues injected synthetic misfolded alpha-synuclein into the guts of dozens of healthy mice.
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Dawson's team tested the animals' brain at one, three, seven, and ten months after injection of the protein that started the vagus nerve, which connects the brain to the brain. Lund University-led team described in a 2014 study in the journal Acta Neuropathologica.
The researchers said they were in a group of mice, the animals said they were not.
But how does that translate into Parkinson's-related behavioral changes? The researchers set out to study the mice with nest building and exploring new environments.
Mice with the misfolded alpha-synuclein and intact vague nerves used to be less and more messing materials, as well as the control mice and those with severed vague nerves. Parkinson's plays out in people, said Han Seok Ko, a co-author of the study, said in a statement.
In another test, the researchers say they are responding to a new environment. The healthy mice and those with their vagus nerve removed spent about 20 to 30 minutes exploring mostly the center of the box, while the others spent less than five minutes doing so and moved towards sheltered borders. What were the mice that received alpha-synuclein and had intact vagus nerves were more anxious, a symptom consistent with Parkinson's, the researchers said.
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Accruing evidence of the good's possible role in neurological disorders is the basis of several biotech startups. These include Axial Biotherapeutics, which recently netted $ 25 million to fund its programs that target the best microbiome to treat Parkinson's and autism. New York-based Kallyope is leveraging the good-brain axis to find small molecules for metabolic and neurological diseases.
Targeting alpha-synuclein is therefore a popular strategy in Parkinson's research. AbbVie and Voyager Therapeutics recently expanded their partnership to use "vectorize" antibodies against the toxic protein clump. A team at Georgetown University found that Novartis 'blood cancer drug Tasigna might work for Parkinson's after that the drug can reduce levels of alpha-synuclein clumps and increase the levels of dopamine in Parkinson's patients' brains.
Last case, Parkinson's team found that they have their appendixes removed. They also discovered alpha-synuclein clumps in the appendix tissue they examined.
Dawson's team at Johns Hopkins has previously identified a protein called c-Abl as a suspected driver of alpha-synuclein clumping in Parkinson's.
Dawson hopes his team's latest discovery could offer a model to study Parkinson's progression. The researchers are now planning to explore what parts of the vagus nerve allow the misfolded protein to travel to the brain. All told, the new evidence of a link between the good and the brain "presents a target for early intervention in the disease," he said.