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publicado em 02/09/2011 às 20h00:00
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Injection of peptide prevents cell death after traumatic brain injury

CDB3 cause short circuit in a path that leads to chronic pain, without interfering with other functions important nerve

 
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A recently discovered peptide, which seems to minimize acute and chronic pain, can also act as a potential tool to prevent cell death after traumatic brain injury.

The discovery by researchers at Indiana University School of Medicine, USA. The results show that CDB3 cause a short circuit in a path that leads to chronic pain, without interfering with other important nerve functions.

The assistant professor of pharmacology and toxicology Rajesh Khanna and colleagues suggested that the peptide may be related to cell death due to another protein that interacts with the brain. "At least 50 years of research have shown that the NMDA receptor, a protein linked to cell death, is active after an injury or trauma leading to toxic influx of calcium into the cells that cause cell death. Our strategy was to regulate this protein to control it but not block it completely, because calcium is required for fundamental cellular functions, "said Khanna.

According to the researchers, a single systemic injection of CDB3 allows the peptide to cross the blood-brain barrier and produce a marked reduction in cell death in the hippocampus, an area important for memory and learning.

Working in the lab, the team has been successful in preventing cell death in a model of blunt traumatic brain injury in rats. "We extend the function of this peptide in addition to pain and the fact that CBD3 protects neurons when administered two hours after the stroke is promising," said Khanna.

The next phase of research is to test the effectiveness of injections at longer intervals after the trauma and with different types of brain injury. The expectation is that the targeting of NMDA receptors with the new method may lead to development of Neurotherapy against traumatic brain injury and other neuronal insults.

Source: Isaude.net
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