The trigger is a protein called "beta amyloid" that accumulates within neurons in the mice's brains. Although several researchers have studied the association between beta amyloid and memory, the UCI research team is the first to identify that early beta amyloid accumulation within neurons is the trigger for the onset of memory decline in Alzheimer's.
"This finding has important and useful implications for the pharmaceutical industry in terms of developing drugs that can target beta amyloid as soon as it accumulates within the neurons," said Frank LaFerla, principal investigator of the research project, associate professor of neurobiology and behavior, and co-director of the UCI Institute for Brain Aging and Dementia. "Once the plaques and tangles form, it is too late."
The researchers report their findings in the March 3 issue of Neuron.
Although the production of beta amyloid occurs in all brains, healthy brains are able to clear away excess amounts. Brains with Alzheimer's disease, on the other hand, are unable to control beta amyloid accumulation. In monitoring the mice from birth until six months, the researchers found that the mice had no Alzheimer's disease symptoms at two months of age. At four months, however, the mice showed a decline in their long-term memory retention that the researchers found occurred in combination with the buildup of beta amyloid in neurons of the hippocampus, amygdala and cerebral cortex regions of the mice's brains.
While the hippocampus is thought to play a key role in learning and memory formation, the amygdala is involved in computing the emotional significance of events. The cerebral cortex the outer portion of the brain is where thought processe
Contact: Iqbal Pittalwala
University of California - Irvine