Testing Dopamine Neuron Transplants in Rats

Parkinson's disease involves loss of a small population of dopamine generating neurons in the brain. The underlying processes causing this loss happen in all aging brains, but to a greater extent in those who ultimately manifest this condition. One approach to treatment under development is direct replacement of the lost cells, but like many types of cell therapy a lot of work and testing is involved to find the most useful strategies given the cell sources and technologies presently available:

Parkinson's disease is caused, in part, by the death of neurons that release a brain chemical called dopamine, leading to the progressive loss of control over dexterity and the speed of movement. [Researchers have shown] that transplantation of neurons derived from human embryonic stem cells (hESCs) can restore motor function in a rat model of Parkinson's disease, paving the way for the use of cell replacement therapy in human clinical trials.

Another approach involving the transplantation of human fetal cells has produced long-lasting clinical benefits; however, the positive effects were only seen in some individuals and can also cause involuntary movements driven by the graft itself. To rigorously assess an alternative hESC-based treatment approach, [scientists] transplanted hESC-derived dopamine neurons into brain regions that control movement in a rat model of Parkinson's disease. The transplanted cells survived the procedure, restored dopamine levels back to normal within five months, and established the correct pattern of long-distance connections in the brain. As a result, this therapy restored normal motor function in the animals. Importantly, the hESC-derived neurons show efficacy and potency similar to fetal neurons when transplanted in the rat model of Parkinson's disease, suggesting that the hESC-based approach may be a viable alternative to the approaches that have already been established with fetal cells in Parkinson's patients.

Link: http://www.sciencedaily.com/releases/2014/11/141106131845.htm

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