Cell Transplants for Parkinson’s Disease
by Karen Vieira, MBA, PhD | May 12, 2008Parkinson’s disease is a disorder that affects the central nervous system and causes an impairment of speech and motor skills. Parkinson’s disease affects 1 in 100 people that are over 60 years of age and has a nearly equal incidence rate in women and men. It is second only to Alzheimer’s disease as the most common neurodegenerative disease. Five to ten percent of Parkinson’s patients have an early onset around the age of 40 or younger.
Parkinson’s disease develops as the result of nerve cell damage or death in the midbrain. The cells that are impaired are responsible for the production of dopamine, this neurotransmitter aids in the transmission of signals from the midbrain to the corpus striatum. The proper transmission of these signals is needed for coordinated movement. Currently, treatment options for Parkinson’s include medications such as L-dopa to treat individual symptoms like stiffness and tremors. There is also an entire class of L-dopa derivatives that perform similar functions and are more efficiently converted into dopamine in the body. Unfortunately, the L-dopa derivatives cause more negative side effects than the traditional L-dopa drugs. In addition, each Parkinson’s case is unique to the patient and the severity of symptoms often varies considerably from patient to patient so treatment must be tailored to each individual.
A study published recently in the journal Glia discusses an exciting discovery of “radial glia-like cells” that lead to the production of dopaminergic neurons in the midbrain. These are the neurons typically affected by Parkinson’s disease. Glial cells nourish, protect, and support neurons. Researchers hope that this discovery may lead to a scientific method that would allow them to artificially reproduce dopaminergic neurons. The transplantation of healthy radial glia-like cells into the brain of Parkinson’s patients may lead to the regeneration of dopaminergic neurons that were damaged or destroyed.
Another study recently published in Nature Medicine showed that in some patients the progression of Parkinson’s disease can affect transplanted dopaminergic neurons that were grafted into an individual’s brain up to one decade earlier. As previously stated, each Parkinson’s case is unique. Some patients may continue to respond positively to the dopaminergic neuron grafts after prolonged periods of time while in other patients the disease will begin to affect the transplanted cells after one decade. Despite this discovery, the benefits of dopaminergic neuron transplantation are quite evident. After a successful transplantation patients usually experience reduced rigidity and an increase in the speed at which they can move. Researchers hope that figuring out why transplanted neurons can be affected in Parkinson’s patients will identify the mechanism of the disease. A better understanding of how this disease develops can lead to treatments that slow or prevent the progression of symptoms.
In conclusion, the contradictory results from these two studies suggest that more research regarding the development and progression of this disease needs to be the focus of treatment. More specifically, discovering how the disease can affect healthy transplanted neurons that were cultured in a clinical setting will undoubtedly lead to the control and prevention of this disease. These types of discoveries may also lead to a better quality of life for Parkinson’s patients.
References
Bonilla, S., Hall, A.C., Pinto, L., Attardo, A., Gotz, M., Huttner, W.B., Arenas, E. (2008). Identification of midbrain floor plate radial glia-like cells as dopaminergic progenitors. Glia, 56(8), 809-820. DOI: 10.1002/glia.20654
Li, J., Englund, E., Holton, J.L., Soulet, D., Hagell, P., Lees, A.J., Lashley, T., Quinn, N.P., Rehncrona, S., Bjorklund, A., Widner, H., Revesz, T., Lindvall, O., Brundin, P. (2008). Lewy bodies in grafted neurons in subjects with Parkinson’s disease suggest host-to-graft disease propagation. Nature Medicine, 14(5), 501-503. DOI: 10.1038/nm1746
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