The replenishment of missing neurons in the brain as a treatment for Parkinson disease reached the stage of human trials over 15 years ago, however the field is still in its infancy. Researchers from Kyoto University have now shown that dopamine-producing neurons (DA neurons) generated from monkey embryonic stem cells and transplanted into areas of the brain where these neurons have degenerated in a monkey model of Parkinson disease, can reverse parkinsonism. Their results appear in the January 3 issue of the Journal of Clinical Investigation.
Studies
of animal models of Parkinson disease as well as clinical
investigations, have shown that transplantation of fetal DA neurons can
relieve the symptoms this disease. However the technical and ethical
difficulties in obtaining sufficient and appropriate donor fetal brain
tissue have limited the application of this therapy.
These researchers previously demonstrated that mouse embryonic stem
cells can differentiate into neurons when cultured under specific
conditions. These same culture conditions, technically simple and
efficient, were recently applied to primate embryonic stem cells and
resulted in the generation of large numbers of DA neurons. In their
current JCI study, Jun Takahashi and colleagues generated neurons from
monkey embryonic stem cells and exposed these cells to FGF20, a growth
factor that is produced exclusively in the area of the brain affected
by Parkinson disease and is reported to have a protective effect on DA
neurons. The authors observed increased DA neuron development and
subsequently transplanted these neurons into monkeys treated with an
agent called MPTP, which is considered a primate model for Parkinson
disease. These transplanted cells were able to function as DA neurons
and diminished Parkinsonian symptoms.
In an accompanying commentary, J. William Langston from the Parkinson's
Institute, California, describes this study as a milestone in the
development of stem cell technology but ca
utions that while the
observations are encouraging, the reported number of surviving DA
neurons was very low, only 1?% of the cells surviving, well below the
estimated number of DA neurons that survive after fetal cell
transplants (approximately 10%). While this may be a difference
observed between transplantation in monkeys and humans, Langston
stresses that it may be necessary for far more DA neurons to survive
and for that survival to be long lasting in order to render this
approach as a useful therapy in humans.
Langston highlights that "clearly the study reported here will advance
research aimed at validating the use of stem cells to treat
neurodegenerative disease" and this is most welcome particularly as
investigators face yet another presidential moratorium endeavoring to
limit the number of human stem cell lines that can be used for future
research and treatment.
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Source:ScienceDaily
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