Transplanting mitochondria shows promise in lab models of Parkinson’s
Intact functional mitochondria eyed as therapeutic strategy for treating diseases
A new treatment that delivers healthy mitochondria to damaged nerve cells showed promise in cell and animal models of Parkinson’s disease, a study shows.
“[T]he study findings provide evidence that mitochondria transplantation can be developed as a novel therapeutic for” Parkinson’s, researchers wrote in “Mitochondrial transplantation exhibits neuroprotective effects and improves behavioral deficits in an animal model of Parkinson’s disease,” which was published in Neurotherapeutics.
Mitochondria are the cells’ powerhouse, cellular structures essential for generating energy. Nerve cells, which need energy for the busy task of sending electrical signals, are especially sensitive to mitochondrial damage and research has shown that mitochondrial dysfunction is a key driver of Parkinson’s disease.
Recent studies have shown that cells can sometimes take in healthy mitochondria from outside a cell and this uptake is particularly pronounced in damaged cells. This finding has raised the possibility of performing a “mitochondrial transplant” to provide new, healthy mitochondria to cells with damaged mitochondria.
Transplanting mitochondria
Here, scientists in Korea tested this idea in laboratory models of Parkinson’s disease.
“With the accumulating evidence of mitochondrial transfer, transplantation of intact functional mitochondria has received attention as an attractive therapeutic strategy for treating various diseases,” wrote the researchers, who said the strategy has shown promise in lab models of brain damage.
For their experiments, the researchers used healthy mitochondria from stem cells in human umbilical cord tissue. These healthy mitochondria are referred to as PN-101.
A feature of Parkinson’s is the dysfunction of dopamine-making, or dopaminergic nerve cells, in the brain. In experiments in human cell models, the researchers showed that damaged dopaminergic cells could take in healthy PN-101 mitochondria, as expected.
Further experiments showed treatment with PN-101 reduced signs of damage in dopaminergic nerve cells. It also reduced markers of inflammation. Increased inflammation in the brain, called neuroinflammation, is thought to be involved in the progression of Parkinson’s.
The scientists next tested PN-101 in a Parkinson’s mouse model that was induced by giving the mice a chemical that’s toxic to dopaminergic neurons. The therapeutic mitochondria were administered by an injection into their bloodstream.
PN-101 treatment led to improvements in motor function in the mouse model. Analyses of the mice’s brains suggested the mitochondrial transplantation also helped reduce inflammation and prevent the death of dopaminergic nerve cells.
“In this study, we demonstrated that mitochondrial transplantation ameliorated dopaminergic cell damage and neuroinflammation in vitro [in dishes] and in vivo [in living animals],” the scientists said. “These results suggest that PN-101 can be a potential therapeutic treatment against [Parkinson’s disease] by mediating both the neuroprotective and anti-inflammatory effects.”
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