A natural antioxdant enzyme called superoxide dismutase (SOD) lacking in mice paves the way towards new treatment for brain degenerative diseases. It is known that oxidative damage plays an important role in brain degeneration of the kind seen in Alzheimer's, Parkinson's and other neurological diseases. Researchers, in California, have developed a mouse model for studying oxidative damage and how to repair it.
This natural antioxidant enzyme called superoxide dismutase (SOD) in mice normally swipe off the free radicals produced by mitochondria, the 'power house' of the cell. Within the mitochondria, oxygen burns glucose to produce energy and produces free radicals as a necessary - but harmful - side product. Left unchecked by antioxidant defences, the free radicals will cause extensive cell damage, of the kind that may set the scene for neurodegenerative disease.
The SOD-deficient mice do indeed develop brain disease and live for only a week. But when they are treated with synthetic antioxidant molecules which take the place of SOD, their lifespan is trebled and they stay healthy. This research has significant implications for human disease.