Removing Amyloid Plaque Does Not Restore Cognitive Loss in Alzheimer's Disease

Researchers have found that while a potential vaccine against Alzheimer's disease clears beta-amyloid plaques from the brain, it fails to repair nerve damage or restore lost cognitive abilities.

Investigators at the University of California, Irvine (USA) worked with a canine model of Alzheimer's disease because beta-amyloid plaques develop naturally in the brains of dogs, and the animals exhibit cognitive declines similar to those seen in humans.

The investigators immunized aged beagles (8.4–12.4 years) with fibrillar beta-amyloid protein formulated with aluminum salt (Alum) for 2.4 years (25 vaccinations). Results of cognitive testing published in the April 2, 2008, issue of the Journal of Neuroscience revealed no improvement during this time in measures of learning, spatial attention, or spatial memory. Examination of the dogs' brains showed that levels of soluble and insoluble beta amyloid protein and the extent of diffuse plaque accumulation were significantly decreased in several cortical regions, with preferential reductions in the prefrontal cortex, which is associated with a maintenance of cognition. Nonetheless, reducing total concentration of amyloid plaque protein demonstrated limited therapeutic benefit to recovery of cognitive decline in this higher mammalian model of human brain aging and disease.

"We have found that reducing plaques is only part of the puzzle to treat Alzheimer's disease,” said first author Dr. Elizabeth Head, assistant professor of neurobiology at the University of California, Irvine. "Vaccines such as this one are a good first step for effective Alzheimer's treatment, but complimentary treatments must be developed to address the complexity of the disease.”


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