Press Releases & Research Commentary
December 2, 2014
A new study out today in the Journal of Neuroscience shows that traumatic brain injury can disrupt the function of the brain's waste removal system. When this occurs, toxic proteins may accumulate in the brain, setting the stage for the onset of neurodegenerative diseases such as Alzheimer’s and chronic traumatic encephalopathy.
We know that traumatic brain injury early in life is a risk factor for the early development of dementia in the decades that follow,said Maiken Nedergaard, M.D., D.M.Sc., co-director of the University of Rochester Center for Translational Neuromedicine and senior author of the article.
This study shows that these injuries set into motion a cascading series of events that impair the brain's ability to clear waste, allowing proteins like tau to spread throughout the brain and eventually reach toxic levels.
The findings are the latest in a series of new insights that are fundamentally changing the way scientists understand neurological disorders. These discoveries are possible due to a study published in 2012 in which Nedergaard and her colleagues described a previously unknown system of waste removal that is unique to the brain which researchers have dubbed the glymphatic system.
November 17, 2014
Researchers have developed new insight into a rare but deadly brain infection, called progressive multifocal leukoencephalopathy (PML). This disease – which is caused by the JC virus – is most frequently found in people with suppressed immune systems and, until now, scientists have had no effective way to study it or test new treatments.
The JC virus is an example of an infection that specifically targets glia, the brain’s support cells,said neurologist Steve Goldman, M.D., Ph.D., co-director of University of Rochester Center for Translational Neuromedicine and senior author of the paper.
Because this virus only infects human glia and not brain cells in other species, it has eluded our efforts to better understand this disease. To get around this problem, we have developed a new mouse model that allows us to study human glia in live animals.
The new discovery – which appears today in the Journal of Clinical Investigation – was the result of research using a new tool developed at the University of Rochester. Last year, Goldman and Maiken Nedergaard, M.D., D.M.Sc., reported that they had created a mouse model whose brains consisted of both animal neurons and human glia cells. While the previous study focused on the fact that the human cells essentially made the mice smarter, at the same time it created a powerful new platform for researchers to study human glial cells in live adult animals, including diseases that impact these cells.
September 30, 2014
More than $6 million in funding from the National Institute of Mental Health (NIMH) is supporting new research that could fundamentally alter the way we comprehend and, perhaps ultimately, treat schizophrenia.
The research - which is being led by University of Rochester Center for Translational Neuromedicine co-directors Steve Goldman, M.D., Ph.D., and Maiken Nedergaard, M.D., D.M.Sc. - will explore the role that support cells found in the brain, called glia, play in the disease.The new research is possible because of findings published by Goldman and Nedergaard last year that showed that glial cells play an important role in the complex signaling activity that is unique to the human brain. In these experiments the researchers showed that when human glial cells were implanted into the brains of newborn mice the human cells influenced communication within the animals' brains, allowing the mice to learn more rapidly.
January 11, 2014
Sleep seems like a perfectly fine waste of time. Why would our bodies evolve to spend close to one-third of our lives completely out of it, when we could instead be doing something useful or exciting? Something that would, as an added bonus, be less likely to get us killed back when we were sleeping on the savanna?
Sleep is such a dangerous thing to do, when you're out in the wild,Maiken Nedergaard, a Danish biologist who has been leading research into sleep function at the University of Rochester's medical school, told me.
It has to have a basic evolutional function. Otherwise it would have been eliminated.
To read more please see the NY Times article.
- Urokinase-Type Plasminogen Activator Receptor as a Potential PET Biomarker in Glioblastoma.J Nucl Med. 57, 272-8. (2016 Feb 01).
- Purinergic receptor P2RY12-dependent microglial closure of the injured blood-brain barrier.Proc Natl Acad Sci U S A. 113, 1074-9. (2016 Jan 26).
- Ultra-fast magnetic resonance encephalography of physiological brain activity - Glymphatic pulsation mechanisms?J Cereb Blood Flow Metab. (2015 Dec 21).