In a discovery that could reshape our understanding of Parkinson’s disease, scientists have identified the kidney as a surprising potential starting point for the neurodegenerative condition.
The study revealed that pathological α-synuclein, the hallmark protein behind Parkinson’s, can accumulate in the kidneys and then spread to the brain. This overturns the long-held belief that Parkinson’s always originates in the central nervous system.
Using both human samples and mouse models, researchers found α-synuclein deposits in the kidneys of patients with Lewy body diseases and individuals with end-stage renal disease (ESRD), even in the absence of neurological symptoms. In healthy conditions, the kidneys help clear α-synuclein from the blood. But when renal function fails, the protein accumulates and begins migrating toward the brain.
In mice, injecting α-synuclein fibrils into the kidney triggered brain pathology, an effect blocked by renal nerve removal. Mice genetically modified to lack α-synuclein in their blood cells showed reduced signs of Parkinson’s-like brain damage.
“This suggests that the kidney isn’t just collateral damage, it might be the source,” said lead author Zhentao Zhang. “Chronic kidney disease could raise the risk of Parkinson’s through impaired protein clearance and peripheral spread.”
The findings highlight a new disease pathway and may help explain why people with chronic renal failure are at increased risk of developing Parkinson’s. More importantly, they open new possibilities for prevention and early intervention, starting not in the brain, but in the body’s filtration system.
There's a lot to dig into here. A research team from Wuhan Uni., China, ran multiple tests, looking at the behavior of α-Syn in genetically engineered mice, as well as analyzing human tissue – including samples from people with Parkinson's disease and chronic kidney disease.
The team found abnormal α-Syn growth in the kidneys of 10 out of 11 people with Parkinson's and other types of dementia related to Lewy bodies (a commonly seen type of α-Syn protein clumping).
That wasn't all: in another sample batch, similar protein malfunctions were found in 17 out of 20 patients with chronic kidney disease, even though these people had no signs of neurological disorders. This is more evidence that the kidneys are where these harmful proteins begin to gather, before brain damage begins.
The animal tests backed up these hypotheses. Mice with healthy kidneys cleared out injected α-Syn clumps, but in mice with kidneys that weren't functioning, the proteins built up and eventually spread to the brain. In further tests where the nerves between the brain and kidneys were cut, this spread didn't happen. there are lots of interesting findings here that can be explored further, which could eventually aid in the development of new treatments for Parkinson's and other related neurological disorders.
The likelihood is that Parkinson's (in a similar way to Alzheimer's disease) is actually triggered in a variety of ways and through a variety of risk factors. For example, previous studies have also suggested it could get started in the gut – and now it seems the kidneys could be connected in a similar way.

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