Protein reversed memory loss in Alzheimer’s mice
Protein reversed memory loss in AlzheimerProtein reversed memory loss in Alzheimer’s mice’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, US researchers said on Monday.
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, and 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.
Alzheimer’s affects 26 million people worldwide and costs $604 billion to treat. – Reuters
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