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The lab duplicated the genetic defect in the ion channel gene and functionally expressed it in a cell system used for channel analysis in the laboratory

We propose that chronic exposure to mutant huntingtin (HTT) elicits a trajectory of impaired mitochondrial biology that maximally impacts subsets of mitotypes abundant in the striatum and cerebral cortex, which eventually surfaces as the hallmark features of HD

3J, Suppl

10.3390/ijms141224438 Int

But Early Success Doesnt Mean It Works in Humans Even though the results are impressive, this research is still early