BIZKAIA, Spain, Jan. 26 (UPI) -- Scientists in Spain found a method of limiting beta-amyloid plaques in the brains of mice, which impair memory in Alzheimer's patients as they build up over time, suggesting the effects of the progressive disease could be prevented.
Learning and memory in humans and animals is based on the modulation of information exchange between neurons in the brain. The continuous modulation of neurons, called synaptic plasticity, is interrupted by the buildup of plaques that block synaptic connections in Alzheimer's disease.
While researchers at the University of the Basque Country say there still is not nearly enough understanding of all the changes Alzheimer's causes in the brain, they have started to understand the function of proteins and their effects on people with cognitive diseases.
A 2010 discovery indicated the protein PTEN, thought to be a tumor suppressor, is recruited by synapses during normal brain function. In patients with Alzheimer's, however, the mechanism attracting PTEN runs rampant. This is driven by beta-amyloids driving the protein into synapses excessively, unbalancing synaptic plasticity and impairing memory formation and recall.
For the new study, published in the journal Nature, researchers developed a molecular tool that lets neurons resist the effects of beta-amyloids.
Researchers report blocking beta-amyloids allowed mice with a rodent version of Alzheimer's to maintain their memories.
"Although this is basic research using animal models, these studies contribute to dissect the mechanisms that control our cognitive function, and orient us towards potential therapeutic avenues for mental diseases where these mechanisms are deficient," the researchers said in a press release.