What Causes Parkinson’s? It May Start Outside the Brain : The Hearty Soul

Recent studies have redefined our understanding of what causes Parkinson’s disease. This disease is typically associated with neurological damage caused by a drop in dopamine production. However, a new study has indicated that it may actually start in one of the last places you would think of looking: your kidneys. The Chinese team of researchers focused on a protein closely associated with Parkinson’s called the alpha-synuclein (α-Syn) protein. When the production of these proteins experiences an issue, they create misfolded clumps that can affect brain function. 

A New Study on What Causes Parkinson’s to Develop

The most important discovery of the study was that α-Syn clumps can build up in both the brain and the kidneys. The team believes that these protein clumps could actually be travelling from the kidneys to the brain, potentially acting as a trigger for the disease. In their paper, the team wrote that “We demonstrate that the kidney is a peripheral organ that serves as an origin of pathological α-Syn.” They reached this conclusion after running multiple tests in which they examined the behavior of the protein in mice that had been genetically modified. They also ran tests that analyzed human tissue, such as samples from individuals diagnosed with chronic kidney disease and Parkinson’s.

Results of the Study

The results of the study were rather striking, with abnormal growth of the protein reported in the kidneys of 10 out of 11 individuals diagnosed with Parkinson’s and other kinds of dementia-related conditions. Additionally, another sample batch revealed that similar protein abnormalities were discovered in 17 out of 20 chronic kidney disease patients. For the team, this was sufficient evidence that pointed to the kidneys as the place where these proteins gather before damage to the brain occurs. Furthermore, their mouse model studies confirmed these results. 

Mice with healthy kidneys eventually cleared out the injected alpha-synuclein clumps. When their kidneys didn’t work, the protein piled up and later travelled towards the brain. However, if the research team cut the nerves linking the mice’s kidneys and the brain, the protein didn’t manage to spread to the brain. Because these α-Syn proteins can also travel through the blood, the team decided to test this out, too. They found that if they reduced the amount of the protein present in the blood, they observed less damage occurring to the brain. 

Study Limits

As with all studies, this one also had its limitations. The sample base of tissues taken from people was quite small, which may not provide the most accurate depiction of a larger populace. Additionally, mice make for great subjects in laboratory research. However, the results observed in mice don’t always translate to human subjects in subsequent trials. Yet, there is no denying that their findings have raised interesting results that should be investigated in greater depth. This could ultimately lead to the development of breakthrough treatments for Parkinson’s and other disorders of the brain.  

It is most likely true that there are many risk factors that can increase the chances of developing these types of conditions. Previous research had already indicated that the gut also played a part in the potential development of neurological disorders. According to the researchers, “Removal of α-Syn from the blood may hinder the progression of Parkinson’s disease, providing new strategies for therapeutic management of Lewy body diseases.” 

 Potential Implications of these Findings

Early detection is possible if α-Syn accumulates in the kidneys before affecting the brain. In theory, standard blood or urine tests may be developed to detect aberrant versions of the protein long before symptoms emerge. Mouse studies show that lowering α-Syn levels in the bloodstream can reduce brain damage. This study suggests that future treatments could either bind the protein in circulation or help the body eliminate it better. 

Additional proof comes from the neural channel connecting the kidneys and the brain: when this link was severed in mice, the spread slowed. While this is not a cure for humans, it does reveal an entirely new biological pathway that researchers might focus on with nerve signal-modulating drugs. These ideas are not yet ready for clinical trials, but they provide a practical framework for future research. These include finding reliable blood or urine markers, testing medications to reduce circulating α-Syn, and exploring if maintaining kidney function can indirectly benefit the brain.

The Bottom Line

We continue to learn more about the various potential causes of Parkinson’s disease on a regular basis. While we associate the development of neurological disorders with the brain, it seems that the issues can actually stem from other remote organs of the body, such as the kidneys. This information could help us better understand how to both detect and treat these types of conditions in the future. Until then, more studies are required to see if the same results can be observed in humans as have been seen in mouse trials. 

Read More: Scientists Show Early Promise in Reversing Parkinson’s Symptoms Using Lab-Grown Brain Cells