London, March 24 : Scientists at Memorial Sloan-Kettering Cancer Center (MSKCC) have come closer to a potential cure for Parkinson's disease, by showing that it's possible to treat the degenerative brain disorder with stem cells produced by therapeutic cloning, also known as somatic-cell nuclear transfer (SCNT).
Scientists at Memorial Sloan-Kettering Cancer Center (MSKCC) have come closer to a potential cure for Parkinson's disease, by showing that it's possible to treat the degenerative brain disorder with stem cells produced by therapeutic cloning, also known as somatic-cell nuclear transfer (SCNT).
For the first time, researchers showed that therapeutic cloning or SCNT has been effectively used to treat disease in the same subjects from whom the initial cells were derived.
Though the researchers have tried the technique only on mice, they say that their study is a proof that a similar approach could be successful in humans.
Therapeutic cloning involves creating an embryo in the lab from which researchers extract the stem cells. These master cells have the ability to develop into numerous cell types and are able to replace defective or missing cells in patients. At the stem cell extraction stage, the embryo is a microscopic ball containing a handful of cells.
As the genetic information in the resulting stem cells comes from the donor subject, therapeutic cloning or SCNT would yield subject-specific cells that are spared by the immune system after transplantation.
For the study, the scientists used skin cells from the tail of the animal to generate customized or autologous dopamine neurons, the missing neurons in Parkinson's disease.
The team injected the stem cells into the affected region of the brains of the donor mice and monitored the animals' behaviour for 11 weeks.
The mice that received neurons derived from individually matched stem cell lines exhibited neurological improvement. But when these neurons were grafted into mice that did not genetically match the transplanted cells, the cells did not survive well and the mice did not recover.
The results showed that the treatment brought about a marked improvement in behavioural symptoms of the disease.
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