“Antifreeze” Molecules May Stop and Reverse Damage from Brain Injuries
Penn Researchers Uncover Role of N-acetylaspartate, a Molecule that Controls Amyloid Build-Up
The key to better treatments for brain injuries and disease may lie in the molecules charged with preventing the clumping of specific proteins associated with cognitive decline and other neurological problems, researchers from the Perelman School of Medicine at the University of Pennsylvania report.
Concentrations of these brain molecules – called N-acetylaspartate (NAA) – are known to decrease when people suffer from brain injuries and diseases. While NAA has historically been used as a marker of disease, its primary role in the brain has remained a mystery. Now, Penn neuroscience researchers have shown how NAA wedges in between the folds of amyloid-beta fibrils to inhibit them from locking, folding, and clumping together to create harmful amyloid plaques.
“For decades, NAA has been viewed as simply a marker of injury when in fact it could be a part of the rescue process,” said senior author Douglas H. Smith, MD, director of the Center for Brain Injury and Repair and professor of Neurosurgery in Penn’s Perelman School of Medicine. “We found that it’s a type of brain ‘antifreeze’ that works to pause and even reverse the aggregation or misfolding of amyloid-beta proteins, which occurs after a brain injury. In this way, it may protect the brain.”
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