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Brain Cell Repair Loss disclosed

According to researchers at the University of Stanford, have discovered the point of no return stage at which adult brain cells lose the ability to repair themselves. The investigators said their work should help find new opportunities to reverse this regeneration loss and speed nerve cell growth.

Researcher Ben Barres, a Stanford neurobiologist, felt that they can study any disease that causes// the brain and spinal cord to degenerate multiple sclerosis, spinal cord injury, stroke, the list goes on and on. Thereby provides grounds for optimism that we can come up with new treatments for patients.

Nerve cells, or neurons, first grow by sprouting long "branches" called axons. The cells then switch gears and begin budding many small "twigs" called dendrites that reach out all around them. These long and short branches are what neurons use to talk with one another. Since axons are longer than dendrites, most nerve damage from injury or disease involve axons. Although neurons in the arms and legs can regenerate axons incredibly efficiently, the ones in the brain and spinal cord the central nervous system lose the ability early in development.

Previously, medical scientists thought nerve cell surroundings released streams of growth-stifling proteins that kept neurons from repairing themselves. "A lot of evidence suggests this is true," Barres said. "But we wondered, 'Is that all? Are there other problems? What about the neurons themselves?'"

Barres and lead researcher Jeff Goldberg discovered a neuron's failure to regenerate also may be due to its own internal programming. Once nerve cells start growing dendrites, they apparently cannot switch back. The investigators took lab-grown nerve cells from the retinas of rat embryos and newborns and compared growth rates. Surprising, but even if the cells from newborn rats were given a host of growth-enhancing biochemicals, the embryonic rat cell axons grew about 10 times faster, spro uting out at an average speed of about half a millimeter per day.

"We found out rats lose this ability sharply within the day of birth," Barres noted. Because neurons taken from embryos and grown for weeks never slowed their growth, this meant internal programming was not wholly responsible an outside signal somehow had to activate a switch inside the neurons to make them stop growing. The researchers found the signal originates from neural circuits elsewhere in the retina known as amacrime cells.

"They've showed there is a developmental switch triggered by cell contact, but what we don't know yet is what the mechanism inside the cell is," Lisa McKerracher a neuroscientists at the University of Montreal.


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