Alzheimer's disease drug may treat traumatic brain injury too

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Washington, July 13 (ANI): A class of drugs used for the treatment of Alzheimer's Disease (AD) has been found to be effective in treating traumatic brain injury as well, according to researchers from Georgetown University Medical Center (GUMC).

The scientists have found that the destructive cellular pathways activated in AD are also triggered after traumatic brain injury, indicating that a new therapy could successfully treat both conditions.

Now, the researchers are all set to show that deactivating these pathways in part by using a class of AD drug, called gamma secretase inhibitor, could reduce loss of neurons in animal models of traumatic brain injury.

The drug also protected the animals against motor and cognitive deficits.

"The goal for both diseases is to prevent neuronal cell death, and this study suggests that one therapy could possibly work for both," said the study's lead author, neuroscientist Dr. Mark Burns.

Both disorders are associated with build-up of beta amyloid, a toxic brain peptide.

Burns says that build-up of beta amyloid occurs in a second wave of damage that follows immediate "necrotic" death of nerve cells after traumatic brain injury.

This secondary injury can last months, if not years, resulting in large holes within brain tissue.

Amyloid peptides are produced when a long brain protein known as the amyloid precursor protein (APP) is cut in two by the enzyme beta secretase, and then cut once again by a second enzyme known as gamma secretase.

Agents that inhibit the activity of gamma secretase are now being studied as treatment for Alzheimer's disease.

In the study, researchers used mice that were either treated with DAPT, an experimental gamma secretase inhibitor, or mice which were "BACE knock-outs" -genetically altered in such a way that they could not produce beta secretase.

It was found that DAPT and BACE knockout mice had brain lesions that were as much as 70 percent smaller than control animals and they experienced minimal impairment.

Burns said that the findings further cement the connection between Alzheimer's disease and traumatic brain injury.

In addition, the study showed that "modulation of beta and gamma secretase may provide novel therapeutic targets for the treatment of traumatic brain injury."

The findings of the study will be presented at the Alzheimer's Association 2009 International Conference on Alzheimer's Disease. (ANI)

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