The National Heart Foundation reports that ischemic strokes account for 87% of strokes in the United States. Ischemic strokes are caused by a blood clot that forms and travels to the brain, preventing the flow of blood and oxygen.
Even when blood and oxygen flow is restored, however, neurotransmitter processes in the brain continue to overcompensate for the lack of oxygen, causing brain cells to be damaged. The damage to brain cells often leads to health complications including visual impairment, memory loss, clumsiness, moodiness, and partial or total paralysis.
Research and drug trials have focused primarily on therapies affecting neurons to limit brain cell damage. Phil Haydon's group at Tufts University School of Medicine have focused on astrocytes, a lesser known type of brain cell, as an alternative path to understanding and treating diseases affecting brain cells.
In animal models, his research team has shown that astrocytes-which outnumber neurons by ten to one-send signals to neurons that can spread the damage caused by strokes. The current study determines that decreasing astrocyte signals limits damage caused by stroke by regulating the neurotransmitter pathways after an ischemic stroke.
The research team compared two sets of mice: a control group with normal astrocyte signaling levels and a group whose signaling was weakened enough to be made protective rather than destructive. To assess the effect of astrocyte protection after ischemic strokes, motor skills, involving tasks such as walking and picking up food, were tested. In addition, tissue samples were taken from both groups and compared.
"Mice with altered astrocyte signaling had limited damage after the stroke," said first author Dustin Hines, Ph.D., a post-doctoral fellow in the department of neuroscience at Tufts University School of Medicine. "Manipulating the astrocyte signaling demonstrates that astrocytes are critical to understanding the spread of damage following stroke."
"Looking into ways to utilize and enhance the astrocyte's protective properties in order to limit damage is a promising avenue in stroke research," said senior author Phillip Haydon, Ph.D. Haydon is the Annetta and Gustav Grisard professor and chair of the department of neuroscience at Tufts University School of Medicine and a member of the neuroscience program faculty at the Sackler School of Graduate Biomedical Sciences at Tufts.
Research reported in this publication was supported by the National Institute of Neurological Disorders and Stroke and the National Institute of Mental Health, both of the National Institutes of Health under award numbers R01NS037585 and R01MH095385, respectively. Dustin Hines was partially funded by the Heart and Stroke Foundation of Canada. Haydon is the co-founder and president of GliaCure Inc., which has licensed a pending patent application filed by Tufts University related to work described in this paper.
Hines, D.J., Haydon, P.G. (2013). Inhibition of a SNARE-Sensitive Pathway in Astrocytes Attenuates Damage following Stroke. The Journal of Neuroscience, vol 33 issue 10, pp 4234-4240; DOI: 10.1523/JNEUROSCI.5495-12.2013
About Tufts University School of Medicine and the Sackler School of Graduate Biomedical Sciences
Tufts University School of Medicine and the Sackler School of Graduate Biomedical Sciences at Tufts Universityare international leaders in innovative medical education and advanced research. The School of Medicine and the Sackler School are renowned for excellence in education in general medicine, biomedical sciences, special combined degree programs in business, health management, public health, bioengineering and international relations, as well as basic and clinical research at the cellular and molecular level. Ranked among the top in the nation, the School of Medicine is affiliated with six major teaching hospitals and more than 30 health care facilities. Tufts University School of Medicine and the Sackler School undertake research that is consistently rated among the highest in the nation for its effect on the advancement of medical science.
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