Enzyme Stymies Alzheimer's Effects In Mice
August 4, 2009
Adapted from the Baylor College of Medicine
A potent antioxidant enzyme made in the mitochondria reduces or prevents the memory and learning impairments of Alzheimer's disease in animals and could provide new direction to treating the disease, said researchers from Baylor College of Medicine (BCM) and New York University in a new report.
Superoxide dismutase (SOD-2), an enzyme made in the cell's mitochondria, also reduced the levels of superoxide (reactive oxygen) that is implicated in Alzheimer's disease, said Dr. Robia Pautler, assistant professor in the department of molecular physiology and biophysics at BCM, and Dr. Eric Klann of New York University.
"This is one of the first reports with so many improvements in cognition in these mice," said Pautler, who is also an assistant professor in the departments of neuroscience and radiology at BCM. She and Klann were senior authors of the report that appears in the current issue of the Proceedings of the National Academy of Sciences. The two began their collaboration on the neurodegenerative disorder when Klann was still at BCM, where he is an adjunct professor.
In this study, the researchers crossbred mice engineered to show features of Alzheimer's disease with mice that produced large amounts of mitochondrial superoxide dismutase. (The mitochondria are the cell's energy source.) The Alzheimer's model mice make too much of a protein that is a precursor to amyloid, the protein complexes that form plaques in the brains of people and animals with the disease and are associated with its disabling effects to think or remember.
In the offspring of the two kinds of mice, the researchers found that high levels of the enzyme superoxide dismutase decreased the amount of superoxide. Even more exciting, in special laboratory tests, the animals did not show the learning and memory deficits found in the Alzheimer's mice. The findings directly link mitochondrial superoxide to the disabling effects of Alzheimer's, the authors said. It also shows that a mitochondrial anti-oxidant enzyme has a beneficial effect, providing new direction for treatment of the neurodegenerative disorder.
"While other anti-oxidant treatments for Alzheimer's disease have not proven effective, we think something more potent might have benefit," said Pautler, who hopes to continue working in that direction. The decrease in the amount of amyloid plaque found in the brain also was encouraging, she said. "We are trying to understand how over-expression of this enzyme contributes to decreased Alzheimer's disease pathology," she said.
She credits post-doc Dr. Cynthia A. Massaad with much of the actual laboratory work in the research. She said she and Klann collaborated on mentoring Massaad, who hoped to gain experience in multiple areas of research.
On behalf of its donors, the Alzheimer's Disease Research program of the BrightFocus Foundation is proud to have funded Dr. Massaad for this very important work.
View all news updates for Alzheimer's disease
Disclaimer: The information provided in this section is a public service of the BrightFocus Foundation, and should not in any way substitute for the advice of a qualified healthcare professional, and is not intended to constitute medical advice. Although we take efforts to keep the medical information on our website updated, we cannot guarantee that the information on our website reflects the most up-to-date research. Please consult your physician for personalized medical advice; all medications and supplements should only be taken under medical supervision. BrightFocus Foundation does not endorse any medical product or therapy.
Some of the content in this section is adapted from other sources, which are clearly identified within each individual item of information.