Scientists arrest brain cell death in mice
British researchers writing in the journal Nature said they had found a major pathway leading to brain cell death in mice with prion disease, the mouse equivalent of Creutzfeld-Jacob Disease (CJD).
They then worked out how to block it, and were able to prevent brain cells from dying, helping the mice live longer. Kate Kelland of Reuters filed a story May 6 about a story in Nature. Pravin Char edited it. The journal article stated that a prion disease in mice causes premature death of brain cells. A way has been discovered to block the process that kills these cells, an approach that may become effective in fighting diseases like Alzheimer’s and Parkinson’s disease. The mice themselves had a disease equivalent to
Creutzfeld-Jacob disease (CJD).
The research, conducted in Britain at the University of Leicester, shows a common mechanism through which Alzheimer’s, Parkinson’s and CJD inflict damage to the nerve cells.
For these neurodegenerative diseases, certain proteins fold themselves incorrectly, which creates a buildup of misshapen proteins, creating plaques in the brains of Alzheimer’s patients or the Lewy bodies of brains stricken with Parkinson’s disease.
The researchers were able to manipulate the mechanism of the prion disease to protect brain cells from destruction, a success that may eventually lead to treatment of certain brain diseases. About 18 million people in the world have Alzheimer’s, and about one person in 100 over the age of 60 is afflicted with Parkinson’s. These are illnesses in which neurons in the brain die, a mysterious process that has not been solved before this research.
The researchers found that the buildup of misshapen proteins in mice brains with prion disease stimulated a natural defense of the cells, one that switches off any projection of new proteins. This feature would normally switch on again, but continued buildup of misshapen proteins keeps the production of new cells switched off.
This results in brain cell death, since critical proteins needed for cell survival are not made.
Researchers injected a protein that blocks the "off" switch, restoring production of important proteins, stopping the neurodegeneration by protecting the brain celkls, restoring protein levels and re-establishing synaptic transmissions.
'Though the triggers for various neurodegenerative diseases are distinct, they may act through a common mechanism, leading to a target for treating the illnesses.