By Julie Steenhuysen (Reuters)

In a study, U.S. researchers said that instead of producing too much of a protein, people with Alzheimer’s disease appear to have trouble getting rid of it.

The finding, published in the journal Science, may help explain why people with Alzheimer’s accumulate sticky clumps of a protein called amyloid beta, and it may help drug companies hone in on potential treatments.

“In people who have Alzheimer’s disease, we know there are very large amounts of amyloid beta in the brain,” said Dr. Randall Bateman of Washington University in St. Louis, who worked on the study.

Bateman said in a telephone interview people with Alzheimer’s disease have between 100 and 1,000 times the normal amount of amyloid in their brains.

“The question was, ‘How did all of that get there?’”

He said the brain normally makes amyloid beta, so the team compared the rate at which the brain produced and got rid of amyloid beta in 12 people with Alzheimer’s disease and 12 healthy people.

They found no difference in the levels of amyloid produced by either group, but they found a 30 percent reduction in the rate at which Alzheimer patients cleared the protein from the brain.

“I think it tells us that is the major mechanism that is awry in Alzheimer’s disease,” Bateman said. “Further, it tells us about how fast things happen.’

The team estimates that a 30 percent decrease in the ability to clear amyloid in the brain would mean the disease starts about 10 years before people start to show signs of mental impairment.

“That may be an ideal time to try to correct that imbalance by clearing that amyloid beta and hopefully delaying or preventing Alzheimer’s disease,” he said.

Alzheimer’s is the most common form of dementia, a fatal brain-wasting disease that affects memory, thinking, behavior and the ability to handle daily activities.

Many researchers think early efforts to make drugs that clear amyloid from the brain have failed because they were tried on people after the disease had progressed too far to do any good.

Current Alzheimer’s drugs such as Eisai Co and Pfizer Inc’s Aricept or donezepil, and Forest Laboratories’ Namenda or memantine, treat symptoms, but so far nothing has been shown to improve memory and thinking in people with the disease.

Diagnostic and drug companies are now looking for ways to diagnose the disease earlier. Last week, General Electric Co’s GE Healthcare and Johnson & Johnson announced a research collaboration to find biological signals to detect Alzheimer’s disease at an earlier stage.

Alzheimer’s affects 26 million people in the world — most of them elderly — and costs $604 billion to treat.

However, U.S. researchers have also claimed that protein reversed memory loss in Alzheimer’s mice.

Boosting levels of a memory-related protein reversed memory loss in mice with Alzheimer’s disease, a finding that could lead to new approaches to treating people..

They said raising levels of CREB-binding protein (CBP) — a protein needed to create long-term memories — improved memory in mice bred to develop Alzheimer’s, a fatal brain-wasting disease that affects memory, thinking, behavior and the ability to handle daily activities.

“We can reverse the learning and memory deficits by increasing the level of this protein called CBP,” said Salvatore Oddo of the University of Texas Health Science Center in San Antonio, whose study appears in the in Proceedings of the National Academy of Sciences.

He said boosting CBP in mice restores activity of a protein called CREB and increases levels of yet another protein called brain-derived neurotrophic factor or BDNF, proteins needed to develop long-term memory.

“In a mouse that develops symptoms like Alzheimer’s disease, these proteins are not activated,” Oddo said in a telephone interview. “They may account for the memory impairment in these mice.”

Oddo’s team used a harmless virus to deliver the protein, then tested learning in memory in the mice using a classic water maze test, in which mice must learn to find an exit platform hidden in a basin of milky liquid.

Alzheimer’s mice that had been given the protein performed as well as healthy mice.

“They showed no memory problems whatsoever. They learned the task they were supposed to learn, and when we probed for memory, they remembered what they learned the day before,” Oddo said.

Alzheimer’s mice given a placebo struggled to learn and remember the task.

Most drugs being developed for Alzheimer’s disease focus on halting or removing an excess buildup of a protein called amyloid beta, which destroys synapses, the sites where brain cells share information.

Enhancing CBP would not alter amyloid beta, but it might make memory formation more efficient.

“Pharmaceutical companies could theoretically work toward finding a new drug that may facilitate the expression of this CBP protein,” he said.

The work is early and the findings would have to be replicated in other labs and eventually in people, but new treatment approaches are important given that no current drugs have been shown to delay progression of Alzheimer’s disease.

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