Los Angeles, December 3, 2016: For the first time, scientists have showed that Parkinson’s disease may be linked to changes in the gut bacteria and it can even cause the deterioration of motor skills that is the hallmark of the disorder.
Up to 10 million people worldwide is affected by Parkinson’s disease (PD), making it the second most common neurodegenerative disease.
According to PTI, Sarkis Mazmanian, California Institute of Technology in the US said, “The gut is a permanent home to a diverse community of beneficial and sometimes harmful bacteria, known as the microbiome, that is important for the development and function of the immune and nervous systems.”
“Because GI problems often precede the motor symptoms by many years, and because most PD cases are caused by environmental factors, we hypothesised that bacteria in the gut may contribute to PD,” he said.
Parkinson’s disease have symptoms like tremors, difficulty walking, aggregation of a protein called alpha-synuclein (aSyn) within cells in the gut and brain, and the presence of inflammatory molecules called cytokines within the brain. 75 per cent of people with PD have gastrointestinal (GI) abnormalities, primarily constipation
Researchers utilised mice to display symptoms of Parkinson’s.
According to PTI, “One group of mice had a complex consortium of gut bacteria; the others, called germ-free mice, were bred in a completely sterile environment and thus lacked gut bacteria.”
The researchers used both the groups of mice perform several tasks in order to measure their motor skills, such as running on treadmills, descending from a pole and crossing a beam.
The germ-free mice performed significantly better than that of the mice with a complete microbiome.
“Once you remove the microbiome, the mice have normal motor skills even with the overproduction of aSyn,” Sampson said.
“All three of the hallmark traits of Parkinson’s were gone in the germ-free models,” Sampson said.
When the gut bacteria break down dietary fibre, they produce molecules called short-chain fatty acids or SCFAs, such as acetate and butyrate.
Earlier research has shown that these molecules can activate immune responses in the brain. Therefore, Mazmanian’s group hypothesised that an imbalance in the levels of SCFAs regulates the brain inflammation and other symptoms of PD.
So, when germ-free mice were fed SCFAs, cells called microglia – which are immune cells residing in the brain-became activated.
In fact, such inflammatory processes can cause neurons to malfunction or even die.
When the germ-free mice fed SCFAs they showed motor disabilities and aSyn aggregation in the regions of the brain linked to the PD.
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