FRIDAY, March 7 (HealthDay News) -- Memory loss, where the brain deletes inconsequential information, is in a hyperactive state in people with Alzheimer's disease, a new study suggests.
Researchers at California's Buck Institute for Age Research analyzed human brain tissue and found that people with Alzheimer's disease (AD) showed more signs of cleavage of a molecule called amyloid precursor protein (APP) than people without the disease.
But when they analyzed the brains of younger people without Alzheimer's, the researchers were surprised to find that they had about 10 times as much APP cleavage as Alzheimer's patients. However, younger brains make memories faster than they lose them.
The Buck Institute team believes that the malfunction of a biochemical switch associated with APP cleavage causes the brains of Alzheimer's patients to get stuck in the process of deleting memories. They added that this suggests the disease affects the plasticity or malleability of the brain.
The study was published in the March 7 issue of the Journal of Alzheimer's Disease.
"Young brains operate like Ferraris -- shifting between forward and reverse, making and breaking memories with a facility that surpasses that of older brains, which are less plastic," research group leader Dr. Dale Bredesen said in a prepared statement.
"We believe that in aging brains, AD occurs when the 'molecular shifting switch' gets stuck in the reverse position, throwing the balance of making and breaking memories seriously off kilter," Bredesen said.
Researchers at the Buck Institute are focusing on nerve signaling and efforts to "disconnect" the molecular mechanism that causes this hyperactivation of memory loss in people with Alzheimer's. They're also investigating the mechanisms that support brain cell connections that play a critical role in memory making.
About 5.1 million Americans have Alzheimer's, which costs the country $148 billion a year.
More information
The National Institute on Aging has more about Alzheimer's disease.
SOURCE: Buck Institute, news release, March 7, 2008
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