November 2nd, 2011

Protein Reduces CP-Like Brain Damage in Mice

In a possible boost to cerebral palsy research, scientists have discovered that a certain protein protects against the death of nerve cells in the brains of mice.  The protective protein is called Nmnat1. The researchers found that high levels of this protein greatly diminished the destruction of brain cells deprived of oxygen and blood flow.  Patients with cerebral palsy often suffer from this kind of brain damage just before, during or after birth when their brain cells don’t receive enough oxygen. Patients with Alzheimer’s, Parkinson’s and other kinds of diseases rooted in degeneration of brain cells might also be helped by the research finding. The scientists speculated that if they could make drugs that would stimulate the production of Nmnat1, they could decrease the number of cells that undergo necrosis.  Necrosis is an injury that, when it occurs in the brain, leads to cells quickly swelling, bursting and dying. The work was done at the Washington University School of Medicine in St. Louis by Dr. David M. Holtzman, the Andrew and Gretchen Jones Professor and the head of the Department of Neurology. The experiment conducted by Dr. Holtzman and his colleagues involved normal mice and mice genetically engineered to make high levels of Nmnat1.  In only six hours after depriving the brains of oxygen and blood flow in the two groups of mice there was a big difference between them. Those with the higher amounts of Nmnat1 had significantly less damage to their brains. At one week’s follow-up, the scientists discovered that the Nmnat1 group had far less brain damage in the areas which are known to be injured in cerebral palsy patients — the hippocampus and the cortex. Further studies using MRI scans found even more impressive results.  The mice with the extra Nmnat1 showed little to no damage to their brains. (Source: Science Daily) If your baby was diagnosed with cerebral palsy and you would like to speak with a cerebral palsy lawyer, please contact us today.

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