In the brain of mice, Yes, but transplant to the end, and the animals that were suffering a severe disorder of obesity were recovered after the intervention. What did not know until where it was repaired, begins to be revealed.
Researchers that did belong to Harvard University, to the Massachusetts General Hospital (MGH), to the Beth Israel Deaconess Medical Center (BIDMC) and the Harvard Medical School (HMS) United States and Israel. Specifically, they transplanted embryonic neurons in the hypothalamus of mice that could not respond to the action of leptin, a hormone produced by fat cells, or adipocytes regulates metabolism and controlling body weight.
That brain failure was that the mice develop obesity morbid.
After the transplantation of nerve cells and repair of their brain, circuits the brains of rodents started to respond to leptin and as a result, the animals began to lose weight.
This fix in the hypothalamus of mice to a cellular level opens a way for the development of new therapeutic methods, not only for disorders in this region of the brain (regulating processes and behaviors such as hunger or sexuality), but also to other disorders such as epilepsy or spinal cord injuries. Although it also dreams of finding a treatment for Parkinson’s disease or amyotrophic lateral sclerosis.
According to Jeffrey Macklis, Professor of regenerative biology at Harvard University, in the brain there are only two regions in which neural substitutions large-scale during adulthood and occur at the cellular level (by the natural process of neurogenesis): the olfactory bulb and a subregion of the hippocampus known toothed twist. Scientists have now achieved what “reconfigure a system of brain circuit that does not undergo neurogenesis course”, explains the scientist.
Transplanted neurons survived the transplant process and developed at all levels, giving rise to four types of neurons that are already known are key in the brain response to leptin. In addition, these new neurons communicate with neurons in the circuit through normal synaptic contacts. The brains of rodents returned to present a current electrical signaling.
Aged mice treated with this process and engordaron approximately 30% less than animals not treated or treated with methods alternative.
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