ine is damaged, the change in its ability to function follows a well-defined pattern. In response to the initial shock, the spine immediately becomes completely nonfunctional but then starts to recover quickly. Over the course of the next few days, in response to the secondary damage, the spine’s function again begins to drop, and within about three days it has leveled off at a point of near non-functionality.
"What our group did was measure the levels of acrolein in the injured spines of 25 guinea pigs for several days following an injury," Shi said. "We found that levels of acrolein peak 24 hours afterward, and they remain high for at least a week. Because acrolein has such a long lifespan and is so toxic, we theorize that it is primarily responsible for the secondary damage that keeps injured spines from healing."
Acrolein's involvement with other conditions suggests that it could be the key to fighting a number of diseases, Shi said.
"When the brain suffers a stroke, for example, it is deprived of oxygen, which is often thought to be the cause of brain damage. But, in fact, you can starve the nervous tissue of oxygen for up to an hour without harm if only you control the acrolein levels," Shi said. "This paper suggests that the body is generally pretty resilient but that acrolein may be something it can't handle."
Shi said that some drugs already under development for other conditions could be used to treat neurodegenerative diseases as well.
"Hypertension drugs, which bind to acrolein and detoxify it, are already under study for their added potential to promote liver health," Shi said. "We would like to see whether they also could be modified to treat the conditions we are interested in."
Further research will be necessary to determine how great a role acrolein actually plays in the process of secondary spinal cord damage, but Shi said that once this role is clarified, drugs that coPage: 1 2 3 4 Related medicine news :1
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