Renal insufficiency can play a surprising role in the development of Parkinson’s disease (BP), and a new study provides additional information about this connection. Researchers at Renmin Hospital of Wuhan have found that renal dysfunction can contribute to the accumulation of a protein, α-sinuclein , in the kidneys, which subsequently comes to spread to the brain, thus accelerating the development of Parkinson’s disease.
Photo archive
Lewy body disease (LBD), which include Parkinson’s disease, are characterized by abnormal aggregation of α-sinuclein protein in nerve cells, a phenomenon that can lead to neurodegeneration. Although it is known that these diseases mainly affect the brain, recent research suggests that in some cases, the disease could start in peripheral organs, such as the kidneys. “Some studies suggest that in some patients with BP, the aggregation of α-sinuclein may come from peripheral organs, but not from the brain,” said Zhentao Zhang, main author of the work, for Medical Xpress.
In the research, Zhang and his colleagues analyzed kidney samples taken from patients with Parkinson’s disease and people with chronic kidney disease. The results showed that the kidneys of these patients contained a significant amount of α-sinuclein, which suggests a direct connection between renal failure and the development of Parkinson’s disease. Moreover, experiments on mice models have shown that renal failure agrava characteristic pathology of Parkinson. The injection of α-sinuclein fibers in the kidneys favored the spread of protein to the brain, and the elimination of α-sinuclein from blood cells has improved the pathology of Parkinson’s disease in these mice.
Another important aspect of the study was how the interruption of connections between the kidneys and the brain in mice blocked the accumulation of α-sinuclein in the brain, suggesting possible treatment directions to prevent this protein and develop Parkinson’s disease. “The most notable finding of our study is that α-sinuclein can come from the kidneys and spread to the brain,” Zhang added.
In future research, the team of researchers will explore the molecular mechanisms that facilitate the deposit of α-sinuclein in the kidneys and spread it in the brain, in order to contribute to the development of treatments that stop the progression of Parkinson’s disease.
