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Kidneys may trigger Parkinson’s disease? Find out what study says

Kidneys may trigger Parkinson’s disease? Find out what study says

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 The landmark discovery was that α-Syn clumps can build up in the kidneys, as well as the brain, suggesting that these abnormal proteins might travel from the kidneys to the brain, possibly triggering the disease.

A new study suggests that Parkinson's disease, which is traditionally linked with neurological damage in the brain, could also begin mushrooming in an unexpected part of the body, like the kidneys. The study was conducted by a team from Wuhan University in China, has also highlighted concerns about the alpha-synuclein (α-Syn) protein, which is closely associated with Parkinson's disease.

It noted that when production goes awry and creates clumps of misfolded proteins, it somehow affects brain function. The landmark discovery was that α-Syn clumps can build up in the kidneys, as well as the brain, suggesting that these abnormal proteins might travel from the kidneys to the brain, possibly triggering the disease.

"We demonstrate that the kidney is a peripheral organ that serves as an origin of pathological α-Syn," Science Alert cited the written report of the researchers. Researchers conducted a series of experiments examining the behaviour of α-Synuclein (α-Syn) in genetically modified mice and human tissue samples, including those from individuals with Parkinson’s disease and chronic kidney disease.

Will a human with kidney dysfunction survive this disease?

Their analysis revealed abnormal α-Syn accumulation in the kidneys of 10 out of 11 patients diagnosed with Parkinson’s and other Lewy body-related dementias, a condition marked by clumping of this protein.

Interestingly, similar protein irregularities were observed in 17 of 20 patients suffering from chronic kidney disease, even though none had any neurological symptoms. This suggests that the kidneys may be an early site for the build-up of harmful α-Syn proteins before brain damage sets in.

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Tests on mice further supported this theory. Healthy mice were able to eliminate injected α-Syn clumps via their kidneys, while mice with kidney dysfunction showed protein accumulation that eventually spread to the brain. However, when the nerve connections between the brain and kidneys were severed, this spread did not occur.

Since α-Syn can also travel through the bloodstream, researchers examined that route as well. They found that reduced α-Syn levels in the blood correlated with decreased brain damage, pointing to another potential transmission pathway.

That said, the study has its limitations. The human sample size was relatively small, and while mice offer valuable insights, their biological responses may not exactly mirror those of humans.