Alzheimer’s Researchers Take Big Step Scientists Develop Similar Brain Disease In Mice

In an important step for finding treatments for Alzheimer’s disease, scientists have developed a strain of mice that get a similar brain disease as they age.

Experts said it was the best result yet from years of attempts to reproduce Alzheimer’s in mice, which can be used to study the disease and test treatments.

“It’s a big, big step forward,” said Dr. John Trojanowski of the University of Pennsylvania School of Medicine, who was not involved in the new research. “This clearly stands head and shoulder above all of the other published or unpublished (results with) mice I have seen or read about.”

The work is presented in today’s issue of the journal Nature by scientists at Athena Neurosciences Inc. of South San Francisco and researchers elsewhere.

While the mice show brain abnormalities like those seen in Alzheimer patients, they have not yet been tested to see if their mental performance is affected, said Dr. Ivan Lieberburg, Athena vice president of research.

In the 4 million Americans with Alzheimer’s disease, the condition causes such symptoms as confusion, memory loss, personality changes and impaired judgment. No cause or cure is known.

In the brain, Alzheimer’s disease produces such abnormalities as deposits of a substance called amyloid and characteristic tangles of skeletal fibers within brain cells. While the newly reported mice do not show these tangles, they produce lots of amyloid deposits.

“This is exciting,” said Dr. Donald Price of the Johns Hopkins School of Medicine in Baltimore, who was familiar with the work. “I think that’s a significant step.”

He said scientists can use the mice to look for drugs that hinder the formation of amyloid deposits and see if they make a difference in mental performance. If so, such drugs might be promising for treating Alzheimer’s or delaying its appearance in people, he said.

The amyloid deposits in Alzheimer’s contain a substance called beta amyloid, which the body makes from a protein called APP. To produce the experimental disease in mice, scientists took a flawed human APP gene that causes Alzheimer’s in people, made it overactive and injected it into mouse embryo cells.

Animals with the gene began to show amyloid deposits between six to nine months, which corresponds to early middle-age. As the animals aged, more deposits appeared and they became more dense.