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A Step Forward In the Fight Against Alzheimer's

Researchers have developed a molecular compound that reversed the symptoms of Alzheimer’s in mice. The compound also reduced inflammation of the brain.

The compound, antisense oligonucleotide (OL-1), “reversed learning and memory deficits and brain inflammation in mice that are genetically engineered to model Alzheimer’s disease,” said Susan Farr, Ph.D., research professor of geriatrics at Saint Louis University.

The findings were published in the Journal of Alzheimer’s Disease.

This is the second mouse study that supports the potential therapeutic value of an antisense compound in treating Alzheimer’s disease in humans. Antisense, a strand of molecules, prompts a series of cellular events that ultimately turns off a certain gene.

In this study OL-1 was found to help trigger a process that keeps excess amyloid beta protein from being produced. Amyloid bet protein is believed to be partially responsible for Alzheimer’s. Excess amyloid beta protein is believed to be partially responsible for the formation of plaque in the brain of patients who have Alzheimer’s disease.

“Our findings reinforced the importance of amyloid beta protein in the Alzheimer’s disease process,” Farr said. “They suggest that an antisense that targets the precursor to amyloid beta protein is a potential therapy to explore to reversing symptoms of Alzheimer’s disease.”

Farr emphasized, though, that investigators would have to examine possible toxic effects in humans before the compound could be given in a clinical trial.

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