In a groundbreaking research achievement, a team from Wuhan University in China has found evidence suggesting that Parkinson’s disease—long believed to originate in the brain—may actually begin in the kidneys. These findings represent a fundamental shift in understanding the disease mechanism and open new horizons for prevention and treatment.
Previous studies have shown that the incidence of Parkinson’s disease is higher in people with chronic kidney failure, but the reasons linking the two conditions were unclear.
The study revealed abnormal accumulations of the protein alpha-synuclein (α-Syn)—the protein associated with the formation of Lewy bodies, which are responsible for neuronal damage in Parkinson’s disease.
In this study, researchers began by examining the kidneys of patients with Lewy body disorders and found significant deposits of α-Syn. They also observed such deposits in both the kidneys and the central nervous system of individuals with end-stage kidney failure, even in the absence of a formal diagnosis of Lewy body disease.
In animal models (male mice), the researchers studied the role of the kidneys in clearing α-Syn from the blood. They found that healthy kidneys can remove this protein, while in kidney failure, the kidneys’ ability to clear α-Syn is reduced. This leads to its accumulation in the kidneys and its subsequent spread to the brain.
To confirm the protein’s movement from kidneys to brain, the researchers injected α-Syn fibrils directly into the kidneys (intrarenal injection). This caused α-Syn to spread from the kidneys to the brain, inducing neural damage similar to that seen in Parkinson’s disease.
Furthermore, cutting the nerves supplying the kidneys (renal denervation) prevented the spread of this protein to the brain, proving that the transmission occurs via neural pathways.
Additionally, the study showed that deleting the α-Syn gene in blood cells of genetically modified mice (α-Syn A53T model) reduced neuronal damage, suggesting that blood cells also play a role in transporting the pathogenic protein.
The results also revealed α-Syn deposits in patients with chronic kidney disease, even in the absence of neurological symptoms. This supports the hypothesis that the kidneys may act as an “early reservoir” of pathogenic proteins, which could later contribute to the development of neurodegenerative disorders.
Although these results are still preliminary and based on small sample sizes, they pave the way for a new phase of research that could transform early diagnostic strategies and therapeutic interventions, with an emphasis on kidney health as a potential protective factor against Parkinson’s disease.
Source:
Yuan, Y., et al. (2025). Peripheral α-synucleinopathy in kidneys contributes to Lewy body pathogenesis. Nature Neuroscience
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