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Drug blocks damage that follows brain injury

U. PITTSBURGH (US) — A new treatment protects against a second round of damage after traumatic brain injury, according to a new study.

Treatment with an agent that blocks the oxidation of an important component of the mitochondrial membrane prevented the secondary damage of severe traumatic brain injury and preserved function that would otherwise have been impaired.

The researchers report their findings in Nature Neuroscience.

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Annually, an estimated 1.7 million Americans sustain a traumatic brain injury (TBI) due to traffic accidents, falls, assaults, and sports participation, says the study’s senior author Hülya Bayir, associate professor in the department of critical care medicine at the University of Pittsburgh School of Medicine.

She adds that 52,000 of those injured die, and 85,000 are left with significant disability.

“We don’t yet have a specific therapy for TBI, but can provide only supportive care to try to ease symptoms,” Bayir says. “Our study drug shows promise as a neuroprotective agent that might help address this important public health problem.”

For the study, the research team conducted a global assessment of all the phospholipids in rat brain cells. This revealed that damage from TBI was nonrandom and mostly involved cardiolipin, a phospholipid that is found in the membranes that form mitochondria, the cell’s powerhouse.

They noted that in the healthy animal, only 10 of the 190 cardiolipin species were modified by oxygen, but after a brain injury, the number of oxidized species rose many-fold.

The researchers then developed an agent, called XJB-5-131, which can cross the blood-brain barrier and prevent the oxidation of cardiolipin. Using an established research model of severe TBI, the agent or a placebo was injected into the bloodstream of rats five minutes and again 24 hours after head injury.

In the weeks that followed, treated animals performed akin to normal on tests of balance, agility, and motor coordination, learning, and object recognition, while placebo-treated animals showed significant impairment. The results indicate that blocking cardiolipin oxidation by XJB-5-131 protected the brain from cell death.

“The primary head injury might not be that serious,” Bayir notes. “But that initial injury can set into motion secondary cellular and molecular events that cause more damage to the brain and that ultimately determine the outcome for the patient.”

She adds that a targeted oxidation-blocker might also be beneficial in the treatment of other neurological disorders, such as Parkinson’s disease, amyotrophic lateral sclerosis (ALS), and stroke.

Lead author of the paper is Jing Ji of the University of Pittsburgh, and additional co-authors contributed from University of Pittsburgh and Noxygen Science Transfer and Diagnostics GmbH in Elzach, Germany.

The study was funded by National Institutes of Health, the National Institute for Occupational Safety and Health, and the US Army.

Source: University of Pittsburgh

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