Research recently conducted at Washington University School of Medicine in St. Louis, Mo, suggests that the protein Nmat1 may protect against the kind of damage that occurs in babies with cerebral palsy and in ischemic stroke.
According to the study, researchers used a mouse model that mimicked cerebral palsy in newborns. High levels of the protective protein Nmnat1, researchers say, substantially reduced damage that develops when the brain is deprived of oxygen and blood flow.
Researchers say they evaluated the effects of oxygen and blood flow deprivation in normal mice and in mice genetically engineered to produce higher-than-normal levels of Nmat1. Within 6 hours, researchers report that the mice with enhanced Nmnat1 exhibited significantly less brain injury than those with lower levels.
One week later, the amount of tissue atrophy in the brain was measured. Results suggested that mice with high levels of Nmnat1 had experienced far less damage to key brain structures like the hippocampus and cortex, known to suffer injury in cerebral palsy.
During follow-up studies, researchers report that MRI scans of the brain indicated the mice with boosted Nnmat1 ultimately suffered little to no brain damage. Laboratory studies suggest the protein prevents a particular type of cell death, explaining its protective behavior against brain damage.
David M. Holtzman, MD, the Andrew and Gretchen Jones professor and head of the department of neurology, explains that there are two types of injury in the developing brain resulting from inadequate oxygen and blood flow. The first is necrosis, in which cells swell, burst, and die and the second apoptosis, in which cells shrink and die. “We found that Nmat1 prevents necrosis.” Holtzman says.
Necrosis is also believed to be responsible for killing brain cells in ischemic stroke in adults. Researchers say that Nmat1 could have implications in future treatments of ischemic stroke and cerebral palsy. Holtzman reiterates this point, “If we can use drugs to trigger the same protective pathway as Nmnat1, it may be possible to prevent brain damage that occurs from these conditions as well as from neurodegenerative diseases.” Holtzman says.
Source: Washington University School of Medicine