ArticleNature neuroscience2025
Propagation of pathologic α-synuclein from kidney to brain may contribute to Parkinson's disease.
Article in Nature neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Research progress and hotspots of the impact of Mediterranean diet on brain health from 2005 to 2025: a bibliometric and visualization analysis.Frontiers in nutrition · 2026Pooled it
- Allogeneic bone marrow-derived mesenchymal stem cells in the aging kidney: secondary results of a Parkinson's disease clinical trial.Stem cell research & therapy · 2025Trial
- Beyond Kidney Function: A Neuro-Renal Perspective on Personalized Care in Pediatric Chronic Kidney Disease.Medical sciences (Basel, Switzerland) · 2026Review
- Brain-first and body-first subtypes of Lewy body disease.Nature reviews. Neurology · 2026Review
- Parkinson's Disease: Pathophysiology, Treatment Strategies, Wellness Approaches, and Obstacles/Paths Forward.NeuroSci · 2026Review
- Advancing disease-modifying therapies for Parkinson's disease: Current strategies and future directions.Innovation (Cambridge (Mass.)) · 2026Review
- A new paradigm in Parkinson's disease: kidney-origin α-synuclein pathology driven by PKC signaling and aurothioglucose.Inflammopharmacology · 2026Review
- Enrichment and amplification of secreted α-synuclein from cellular model and saliva of patients with synucleinopathies.Biophysics reports · 2026Article
- Glymphatic system impairment in neurological disorders: potential mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Associations of DTI-ALPS index and choroid plexus volume with clinical severity across the Parkinson's disease spectrum.NPJ Parkinson's disease · 2026Article
- α-Synuclein as a molecular link between Parkinson's disease and chronic kidney disease: insights into the kidney-brain axis.Metabolic brain disease · 2026Review
- The APOA1-SNCA Axis as a Molecular Bridge Between CKD and Parkinson's Disease: A Systems Biology Model of Kidney-to-Brain Propagation via Exosomal Pathways.International journal of molecular sciences · 2026Article
- The emerging role and therapeutic targeting of autophagy-lysosome pathway in the pathogenesis of Parkinson's disease.Translational neurodegeneration · 2026Review
- Quantitative measures of total and phosphorylated alpha-synuclein in skin tissue as potential biomarkers for synucleinopathies.Journal of Parkinson's disease · 2026Article
- Macrophage ferritin heavy chain/α-synuclein regulatory axis modulates ferroptosis during kidney injury.JCI insight · 2026Article
- The brain and heart-axis in neurodegeneration and cardiovascular disease.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Rigorous evaluation of pathological α-synucleinopathy transmissibility between animals in an experimental model.Acta neuropathologica communications · 2026Article
- A Pathophysiological Model of Parkinson's Disease Based on Microvascular Flow Disturbance and Leukocyte-Mediated Oxidative Injury in Critical Pigmented Neuronal Niches.Antioxidants (Basel, Switzerland) · 2026Article
- Propagation of α-synuclein pathology: models, mechanisms and future goals.Molecular neurodegeneration advances · 2026Review
- Astrocytes in Parkinson's Disease: From Guardians to Accomplices.Clinical interventions in aging · 2026Review
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Abstract
The pathogenesis of Lewy body diseases (LBDs), including Parkinson's disease (PD), involves α-synuclein (α-Syn) aggregation that originates in peripheral organs and spreads to the brain. PD incidence is increased in individuals with chronic renal failure, but the underlying mechanisms remain unknown. Here we observed α-Syn deposits in the kidneys of patients with LBDs and in the kidney and central nervous system of individuals with end-stage renal disease without documented LBDs. In male mice, we found that the kidney removes α-Syn from the blood, which is reduced in renal failure, causing α-Syn deposition in the kidney and subsequent spread into the brain. Intrarenal injection of α-Syn fibrils induces the propagation of α-Syn pathology from the kidney to the brain, which is blocked by renal denervation. Deletion of α-Syn in blood cells alleviates pathology in α-Syn A53T transgenic mice. Thus, the kidney may act as an initiation site for pathogenic α-Syn spread, and compromised renal function may contribute to the onset of LBDs.
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