By Kim Cumbie
Contact Mary Margaret Colliver

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Alzheimer’s disease (AD) is a progressive, ultimately fatal degenerative disorder characterized by the death of neurons in the brain. Stroke occurs when blood vessels bringing oxygen to the brain burst or become clogged. As a result, the brain does not receive essential blood flow, and a portion will die.

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The research was published in the Jan. 15, 1998 issue of The Journal of Neuroscience, by Mark Mattson, Ph.D., professor of anatomy and neurobiology and a research associate of the UK Sanders-Brown Center on Aging, and colleagues.

Alzheimer’s disease (AD) is a progressive, ultimately fatal degenerative disorder characterized by the death of neurons in the brain. Stroke occurs when blood vessels bringing oxygen to the brain burst or become clogged. As a result, the brain does not receive essential blood flow, and a portion will die.

Oxidative stress is a common factor in AD and stroke, as well as in a variety of other illnesses. It occurs when free radicals, highly reactive molecules, accumulate and cause damage to other molecules within the body. They bind to proteins, accumulate in lipids, and damage nucleic acids.

Antioxidants help control oxidative stress by scavenging free radicals. The enzyme MnSOD is one of the primary antioxidant enzymes in mammalian tissues. Mattson showed that MnSOD increased the efficiency of mitochondria, power-supplying organelles within the cell, by preventing production of a free radical called superoxide.

Mattson’s current findings build upon a series of experiments aimed at determining the protective ability of the human-MnSOD enzyme.

Neurons were removed from brains of rats and humans, and placed in cell cultures. The human-MnSOD gene was introduced into these nerve cells. Subsequently, the neurons began to produce the MnSOD enzyme, and cultures were subjected to processes that mimic injury caused by stroke and Alzheimer’s disease. Cells that produced the enzyme were resistant to death, and were able to prevent accumulation of free radicals.

Neurons expressing the human-MnSOD gene were also protected against amyloid beta peptide, a toxic protein that accumulates in the brains of Alzheimer’s disease sufferers. Amyloid beta peptide kills neurons by production of free radicals.

In the current study, scientists introduced the gene for human-MnSOD into mice. The animals began to overproduce the human MnSOD enzyme in nerve cells. Stroke was induced in both enzyme producing and non-enzyme producing mice. Results clearly indicated that brains of mice with the human-MnSOD gene had a reduction in the extent of brain damage caused by stroke.

Mattson and colleagues have previously demonstrated that MnSOD can be induced in nerve cells by various drugs and growth factors. By combining knowledge garnered from many studies, researchers hope to develop drugs that will confer protection to brain nerve cells by facilitating production of the human MnSOD enzyme.