A newly discovered class of chemical compounds can protect cells in the brain from the kinds of damage inflicted during blast-associated traumatic brain injury (TBI), often suffered by soldiers in combat, researchers say.
About 10 to 20 percent of the approximately 2 million U.S. servicemen and women deployed in Afghanistan or Iraq have been affected by TBI, which can result in long-term neurological complications such as motor and cognitive decline, emergence of psychiatric problems and neuropathological conditions similar to Alzheimer's disease, they say.
Researchers at the University of Iowa say mice treated with a group of compounds known at the P7C3 series 24 to 36 hours following exposure to a TBI-causing blast gained protection from common harmful effects of TBI that affect memory, movement and learning.
In TBI, axons -- tendril-like fibers that sprout from neurons in the brain to form the connections called synapses -- can be damaged, and axon damage can be followed by death of the neuron.
The new compounds can block axon damage and protect normal synapse function following TBI, the researchers relate in the journal Cell Reports.
"The lack of neuroprotective treatments for traumatic brain injury is a serious problem in our society," says senior study author Andrew Pieper, Iowa professor psychiatry and neurology.
"Everyone involved in this work is motivated to find a way to offer hope for patients, which today include both military personnel and civilians, by establishing a basis for a new treatment to combat the deleterious neuropsychiatric outcomes after blast injury."
Optimized variants of the P7C3 compounds -- also known as neuroprotective aminopropyl carbazoles --could be developed to create agents to deal with either damage to axons, the death of neurons, or both, the researchers say.
A significant feature of the treatment involving the compounds is that it was effective even if delayed for up to 36 hours after a blast injury is suffered, which could be a significant benefit in often-chaotic combat situations, they say.
"Seeing protection even when the compound was given this long after injury was important because it represents a liberal window of time within which almost all patients would be expected to be able to access treatment after injury," Pieper says.
The research team reports it has discovered the biological process by which P7C3 compounds operate in the brain, activating molecular pathways that preserve neuronal levels of an energy molecule, nicotinamide adenine dinucleotide.
The role of the molecule in maintaining the health of axons is well established, the researchers say, so the action of the compound in protecting mice suffering from TBI is likely linked to preservation of the levels of the molecules in the brain.
