A new class of Alzheimer’s drugs have been found to reduce long-term damage caused by traumatic brain injury, say researchers from Georgetown University Medical Centre.
The drugs called gamma-secretase inhibitors are designed to target amyloid plaque that accumulates in the brains of people with Alzheimer''s disease.
"No one knows why it occurs, but abnormal amounts of amyloid plaque have been found during an autopsy in about a third of brain injury victims, some of whom were children who would ordinarily never have had these deposits," Nature magazine quoted Dr. Mark Burns, an assistant professor at GUMC, as saying.
"Remarkably, these deposits may occur in less than one day after injury," he added.
The researchers found that the same pathways activated chronically in Alzheimer''s disease are activated acutely in traumatic brain injury, and that they appeared to play a very important role in secondary injury.
Moreover, people who suffered a brain injury were at a 400 percent increased risk of developing the disorder.
During the study, the researchers sought to understand whether amyloid peptide contributed to secondary injury. They used two different approaches to blocking activation of the pathway that produces amyloid peptide.
The mice used in the study were genetically altered to lack beta secretase, which meant they were incapable of producing amyloid.
The researchers also treated "normal" mice with the experimental agent DAPT, one of the first gamma secretase inhibitors currently undergoing trails.
As a result, amyloid peptide production was substantially reduced in that group.
They found that in normal control mice, brain injury produced substantially more amyloid peptide, and that the brain region known as the hippocampus, which is also affected in Alzheimer''s disease, was substantially damaged.
They then followed the groups of reduced amyloid mice after injury, and found that three weeks after initial trauma, both groups performed almost equally well on learning tests.
"The experiment with the genetically altered mice shows that amyloid peptide contributes to the secondary damage seen in traumatic brain injury," he said.
"If injured mice that cannot develop amyloid demonstrate reduced signs of secondary trauma, that points to amyloid peptide as a cause of this continuing damage," he added.
The findings appear in the journal Nature Medicine.