The Parkinson's research community may turn out to be an ally in efforts to develop mitochondrial repair technologies suitable for use in rejuvenation: "genetic mutations causing a hereditary form of Parkinson's disease cause mitochondria to run amok inside the cell, leaving the cell without a brake to stop them. ... Mitochondria, when damaged, produce reactive oxygen species that are highly destructive, and can fuse with healthy mitochondria and contaminate them, too ... Normally, when mitochondria go bad, PINK1 tags Miro, [a protein which literally hitches a molecular motor onto the organelle], to be destroyed by Parkin and enzymes in the cell, the researchers showed. When Miro is destroyed, the motor detaches from the mitochondrion. The organelle, unable to move, can then be disposed of: The cell literally digests it. But when either PINK1 or Parkin is mutated, this containment system fails, leaving the damaged mitochondria free to move about the cell, spewing toxic compounds and fusing to otherwise healthy mitochondria and introducing damaged components. ... The study's findings are consistent with observed changes in mitochondrial distribution, transport and dynamics in other neurodegenerative diseases ... Whether it's clearing out damaged mitochondria, or preventing mitochondrial damage, the common thread is that there's too much damage in mitochondria in a particular brain region. ... [Researchers are] interested in the possibility of helping neurons flush out bad mitochondria or make enough new, healthy mitochondria to keep them viable."