Translational Research:

From the laboratory bench to the patient’s bedside, the process of ‘translating’ ideas, insights, and discoveries generated through basic scientific inquiry to the treatment or prevention of human disease.



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A Giant Leap toward Prevention and Treatment
CHORI Scientist Discovers New Therapeutic Target for Alzheimer’s Disease

CHORI scientist, Hani Atamna, PhD has just published a new study in the February 28th issue of the Proceedings of the National Academy of Sciences. The first study to explain how brain cells die in patients with Alzheimer’s Disease, Dr. Atamna's research could lead to a cure for Alzehimer's disease.

The revolutionary study found that alterations in the production of heme (a molecule that contains iron) may be the key to understanding why excessive amyloid-beta is toxic to brain cells. Dr. Atamna had previously discovered that Alzheimer’s patients have abnormal amounts of heme in their brains. In new research results, Atamna’s team showed that amyloid-beta readily binds with heme to form a compound that can be flushed from cells. When there is insufficient heme or too much amyloid-beta, however, the amyloid-beta forms large toxic “clumps” that the cell cannot dissolve and eliminate.

Though heme binding with amyloid-beta can be beneficial, if too much heme is bound up with amyloid-beta, there may be insufficient heme available for the cell to properly function. When this happens, the cell’s mitochondria, which are the tiny structures inside brain cells that produce the energy the cells need to function, begin to decay. Dr. Atamna refers to this phenomenon as a “functional heme deficiency” because the cells are still forming heme, but it is trapped within an amyloid-beta/heme compound.

When they examined the heme/ amyloid-beta compound researchers in the Atamna laboratory were surprised to discover it was a peroxidase—a type of enzyme that reacts harmfully with biological materials essential for proper brain function such as serotonin and L-DOPA. Dr. Atamna believes that the combination of functional heme deficiency, which harms mitochondria needed to produce energy, together with the increase in oxidative damage caused by the peroxidase, is what eventually kills the cell.

“The discovery of the formation of amyloid-beta peroxidase provides a clear picture of why cells die in the brain of Alzheimer’s patients," says Dr. Atamna. "Our next challenge is to develop drugs that directly and selectively target the excessive peroxidase of amyloid-beta, which could lead to the first significant therapy for Alzheimer’s disease.”

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Monday, May 16, 2011 11:33 PM

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