“Some studies suggest that in some PD patients, α-synuclein aggregation may originate from peripheral organs but not from the brain,” Zhentao Zhang, senior author of the paper, told Medical Xpress.
“These cases are broadly referred to with the term ‘body-first PD.’ To identify the organs where α-synuclein pathology begins, we stained the peripheral organs and found that the kidneys were positive for α-synuclein pathology in some PD patients.”
Essentially, the researchers found that the kidneys of patients presenting renal failure contained a large amount of the protein α-synuclein. They were then able to shed light on how this α-synuclein accumulation could lead to PD, specifically following the spread of this protein to the brain.
Zhang and his colleagues also showed that severing the connections between the kidneys and the brain in male mice blocked the accumulation of α-synuclein in the brain following renal failure. In the future, their study could inspire further research exploring the processes they uncovered, which could contribute to the development of therapeutic interventions aimed at slowing down or stopping the progression of PD and potentially other LBDs.
“The most notable finding of our study is that α-synuclein may originate from the kidney and spread to the brain,” added Zhang. “These observations suggest that eliminating circulating α-synuclein may be a possible way to halt the progression of PD. In our next studies, we will study the molecular mechanisms that mediate the deposition of α-synuclein in the kidney as well as the mechanisms that mediate the spread of α-synuclein pathology from the kidney to the brain.”
More information:
Xin Yuan et al, Propagation of pathologic α-synuclein from kidney to brain may contribute to Parkinson’s disease, Nature Neuroscience (2025). DOI: 10.1038/s41593-024-01866-2.
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The link between renal failure and Parkinson’s disease: Researchers illuminate the underlying mechanisms (2025, February 4)
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