Press Releases & Research Commentary
July 28, 2009
A compound strikingly similar to the common food additive that gives M&Ms and Gatorade their blue tint may offer promise for preventing the additional – and serious – secondary damage that immediately follows a traumatic injury to the spinal cord. In an article published online today in the Proceedings of the National Academy of Sciences, researchers report that the compound Brilliant Blue G (BBG) stops the cascade of molecular events that cause secondary damage to the spinal cord in the hours following a spinal cord injury, an injury known to expand the injured area in the spinal cord and permanently worsen the paralysis for patients.
This research builds on landmark laboratory findings first reported five years ago by researchers at the University of Rochester Medical Center. In the August 2004 cover story of Nature Medicine, scientists detailed how ATP, the vital energy source that keeps our body's cells alive, quickly pours into the area surrounding a spinal cord injury shortly after it occurs, and paradoxically kills off what are otherwise healthy and uninjured cells.
This surprising discovery marked a milestone in establishing how secondary injury occurs in spinal cord patients. It also laid out a potential way to stop secondary spinal injury, by using oxidized ATP, a compound known to block ATP's effects. Rats with damaged spinal cords who received an injection of oxidized ATP were shown to recover much of their limb function, to the point of being able to walk again, ambulating effectively if not gracefully.
July 27, 2009
The same blue food dye that gives your Gatorade its turquoise tint and turns your tongue a peculiar shade of purple might also protect your nerves in the case of spinal cord injury.
By lucky accident, researchers discovered that the commonly used food additive FD&C blue dye No. 1 is remarkably similar to a lab compound that blocks a key step in nerve inflammation. When rats with spinal cord injury were given an infusion of blue dye, they recovered much faster than rats that didn't get the treatment. And researchers reported only one adverse effect: The rats turned blue.
"One of the reasons no one had done this before is that food science is very separate from neuroscience," said neuroscientist Maiken Nedergaard of the University of Rochester Medical Center, who co-authored the study published Monday in the Proceedings of the National Academy of Science. "Those two fields don't interact at all."
March 23, 2009
A type of brain cell that was long overlooked by researchers embodies one of very few ways in which the human brain differs fundamentally from that of a mouse or rat, according to researchers who published their findings as the cover story in the March 11 issue of the Journal of Neuroscience.
Scientists at the University of Rochester Medical Center found that human astrocytes, cells that were long thought simply to support flashier brain cells known as neurons that send electrical signals, are bigger, faster, and much more complex than those in mice and rats.
"There aren't many differences known between the rodent brain and the human brain, but we are finding striking differences in the astrocytes. Our astrocytes signal faster, and they're bigger and more complex. This has big implications for how our brains process information," said first author Nancy Ann Oberheim, Ph.D., a medical student who recently completed her doctoral thesis on astrocytes.
- Rapid manifestation of reactive astrogliosis in acute hippocampal brain slices. Glia. 62, 78-95. (2014 Jan 01).
- Ammonia triggers neuronal disinhibition and seizures by impairing astrocyte potassium buffering. Nat Med. 19, 1643-8. (2013 Dec 01).
- α1-Adrenergic receptors mediate coordinated Ca(2+) signaling of cortical astrocytes in awake, behaving mice. Cell Calcium. 54, 387-94. (2013 Dec 01).