Parkinson’s disease related to mitochondrial changes in humans

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Parkinson’s disease related to mitochondrial changes in humans
Parkinson’s disease related to mitochondrial changes in humans

Dr. Xianmin Zeng and colleagues at the Buck Institute for Aging have confirmed that changes in the mitochondria of human cells that produce dopamine are the cause of Parkinson’s disease. The same result was previously seen in fruit flies and has now been confirmed in humans.

Mitochondria produce energy for cells. A mutation in one gene involved with Parkinson’s disease causes the mitochondria in dopamine producing neurons to die. The lack of dopamine produces the characteristic physical and emotional symptoms seen in Parkinson’s disease.

The researchers used induced pluripotent stem cells to recreate the mutation that causes the death of dopamine producing neurons. The laboratory induced destruction of mitochondria was exactly the same as that seen in four people that had Parkinson’s disease. The loss of mitochondria is firmly established as a cause of the symptoms of Parkinson’s disease that is inherited and the variety that is not inherited.

The discovery opens the door to possible stem cell treatments that could prevent the destruction of dopamine producing cells or prevent the destruction of mitochondria in dopamine producing neurons. More than one million people in the United States have Parkinson’s disease. The numbers are expected to increase. The disease is incurable at present.

This development will allow induced pluripotent stem cell treatments to be actively pursued in people. Previously, the use of stem cell treatments was not allowed because the death of mitochondria in dopamine producing neurons had not been linked to Parkinson’s disease in humans. The testing of compounds that prevent mitochondrial death due to Parkinson’s disease is presently being pursued.

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