The strong link between the decreases in select memory genes and amyloid accumulation was observed both in mice genetically engineered to develop memory loss and in the brains of deceased Alzheimer's patients. The results are reported in the June 15 issue of the Journal of Neuroscience published online today.
"Blocking the ability of amyloid to inhibit, or down-regulate, these genes may improve memory in patients with early Alzheimer's disease," said principal investigator David Morgan, PhD, professor of pharmacology and therapeutics and director of the Alzheimer's Disease Research Laboratory at USF.
Many experimental approaches to treating Alzheimer's disease, including the vaccine, try to prevent the further formation of amyloid plaques or remove some of them from the brain. But, Dr. Morgan said, by the time memory loss becomes apparent the toxic plaques are probably accumulating too quickly to eliminate enough amyloid needed to restore normal memory.
"Our study suggests a new approach to treating this neurodegenerative disease that would enhance amyloid-lowering approaches," he said. "For instance, you might give a vaccine or some other immune therapy to reduce the amyloid load and then start the patient on a memory-enhancing drug to block the effect of any remaining amyloid on normal learning and memory."
"This interrogation of the genome reveals new targets for both study and intervention," says D. Stephen Snyder, Ph.D., of the Etiology of Alzheimer's Disease-Cell Biology area of the National Institute on Aging, which funded the research. "This study addresses the important question of what genes related to learning and memory are regulated either up or down by amyloid."